Re: Ooops forgot the 2nd question

May 29, 2011

Onc surgeons do a bit of adrenal stuff.Most today will do minimally invasive surgery so you want one who had done a lot. As common as PA is they should not be hard to find.The adrenals were put in a hard place to get to using general surgery. Easier with Band Aid surgery approach if experienced.CE Grim MDThe other question was about adrenalectomies. The endocrinologist at Dartmouth as well as the one here in Maine that I see think I should have an adrenalectomy. One suggests a general sugeon at Dartmouth by the name of Laycock and the other is suggesting a Maine Oncology surgeon (I'veheard a lot of good about the oncology surgeon) by the name of MacGilvary. My question is what type of surgeon should I be seeing ? I would rather not go back to Dartmouth for several reasons but someof you told me before that my local endo was foolish for sending me to the oncology surgeon. The endo is only sending me to him because she believes he is a good surgeon.Any input would be helpful at thgis point. I apreciate it. Lettie PA in ton Maine

May 30, 2011

You might want to search postings by paulkabrna

> > > > > > >

> > > > > > > > The other question was about adrenalectomies. The

> > > > > > endocrinologist at

> > > > > > > > Dartmouth as well as the one here in Maine that I see think I

> > > > > > should

> > > > > > > > have an adrenalectomy. One suggests a general sugeon at

> > > > > > Dartmouth by

> > > > > > > > the name of Laycock and the other is suggesting a Maine

> > > > > > > > Oncology surgeon (I'veheard a lot of good about the oncology

> > > > > > > > surgeon) by the name of MacGilvary. My question is what type of

> > > > > > > > surgeon should I be seeing ? I would rather not go back to

> > > > > > Dartmouth

> > > > > > > > for several reasons but someof you told me before that my local

> > > > > > endo

> > > > > > > > was foolish for sending me to the oncology surgeon. The endo is

> > > > > > only

> > > > > > > > sending me to him because she believes he is a good surgeon.Any

> > > > > > > > input would be helpful at thgis point. I apreciate it.

> > > > > > > > Lettie PA in ton Maine

> > > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > >

> > >

> >

>

May 31, 2011

The only time I've had to get up at night to pee is while heavily pregnant. It's

never been a problem at any other time. I didn't have a high bp between

pregnancies. I have had absolutely no other symptoms of PA beyond the high bp

that was diagnosed 18 months ago or so.

What does renin do? Given that I don't appear to have any....

H

> > > > > > > >

> > > > > > > > > The other question was about adrenalectomies. The

> > > > > > > endocrinologist at

> > > > > > > > > Dartmouth as well as the one here in Maine that I see think I

> > > > > > > should

> > > > > > > > > have an adrenalectomy. One suggests a general sugeon at

> > > > > > > Dartmouth by

> > > > > > > > > the name of Laycock and the other is suggesting a Maine

> > > > > > > > > Oncology surgeon (I'veheard a lot of good about the oncology

> > > > > > > > > surgeon) by the name of MacGilvary. My question is what type

of

> > > > > > > > > surgeon should I be seeing ? I would rather not go back to

> > > > > > > Dartmouth

> > > > > > > > > for several reasons but someof you told me before that my

local

> > > > > > > endo

> > > > > > > > > was foolish for sending me to the oncology surgeon. The endo

is

> > > > > > > only

> > > > > > > > > sending me to him because she believes he is a good

surgeon.Any

> > > > > > > > > input would be helpful at thgis point. I apreciate it.

> > > > > > > > > Lettie PA in ton Maine

> > > > > > > > >

> > > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > >

> > >

> >

>

May 31, 2011

Hmm - have had a quick read through. From what I can see, he was diagnosed with

bilateral in 1977 but had an adrenalectomy anyway?? And has been on Spiro ever

since? Not really the same scenario but my fall back will be to be on drugs for

many, many years (unless I get hit by a car). So it could be a similar story -

surgery doesn't work so back on drugs. But I can't see a reason not to give it a

go. The only part which I agree is a risk is skipping AVS.

H

> > > > > > > >

> > > > > > > > > The other question was about adrenalectomies. The

> > > > > > > endocrinologist at

> > > > > > > > > Dartmouth as well as the one here in Maine that I see think I

> > > > > > > should

> > > > > > > > > have an adrenalectomy. One suggests a general sugeon at

> > > > > > > Dartmouth by

> > > > > > > > > the name of Laycock and the other is suggesting a Maine

> > > > > > > > > Oncology surgeon (I'veheard a lot of good about the oncology

> > > > > > > > > surgeon) by the name of MacGilvary. My question is what type

of

> > > > > > > > > surgeon should I be seeing ? I would rather not go back to

> > > > > > > Dartmouth

> > > > > > > > > for several reasons but someof you told me before that my

local

> > > > > > > endo

> > > > > > > > > was foolish for sending me to the oncology surgeon. The endo

is

> > > > > > > only

> > > > > > > > > sending me to him because she believes he is a good

surgeon.Any

> > > > > > > > > input would be helpful at thgis point. I apreciate it.

> > > > > > > > > Lettie PA in ton Maine

> > > > > > > > >

> > > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > >

> > >

> >

>

May 31, 2011

Hmm - have had a quick read through. From what I can see, he was diagnosed with

bilateral in 1977 but had an adrenalectomy anyway?? And has been on Spiro ever

since? Not really the same scenario but my fall back will be to be on drugs for

many, many years (unless I get hit by a car). So it could be a similar story -

surgery doesn't work so back on drugs. But I can't see a reason not to give it a

go. The only part which I agree is a risk is skipping AVS.

H

> > > > > > > >

> > > > > > > > > The other question was about adrenalectomies. The

> > > > > > > endocrinologist at

> > > > > > > > > Dartmouth as well as the one here in Maine that I see think I

> > > > > > > should

> > > > > > > > > have an adrenalectomy. One suggests a general sugeon at

> > > > > > > Dartmouth by

> > > > > > > > > the name of Laycock and the other is suggesting a Maine

> > > > > > > > > Oncology surgeon (I'veheard a lot of good about the oncology

> > > > > > > > > surgeon) by the name of MacGilvary. My question is what type

of

> > > > > > > > > surgeon should I be seeing ? I would rather not go back to

> > > > > > > Dartmouth

> > > > > > > > > for several reasons but someof you told me before that my

local

> > > > > > > endo

> > > > > > > > > was foolish for sending me to the oncology surgeon. The endo

is

> > > > > > > only

> > > > > > > > > sending me to him because she believes he is a good

surgeon.Any

> > > > > > > > > input would be helpful at thgis point. I apreciate it.

> > > > > > > > > Lettie PA in ton Maine

> > > > > > > > >

> > > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > >

> > >

> >

>

May 31, 2011

The risk of not knowing what side is making to much aldo is if they remove wrong

side you have lost the chance to not be on meds for the rest of your life.

> > > > > > > > >

> > > > > > > > > > The other question was about adrenalectomies. The

> > > > > > > > endocrinologist at

> > > > > > > > > > Dartmouth as well as the one here in Maine that I see think

I

> > > > > > > > should

> > > > > > > > > > have an adrenalectomy. One suggests a general sugeon at

> > > > > > > > Dartmouth by

> > > > > > > > > > the name of Laycock and the other is suggesting a Maine

> > > > > > > > > > Oncology surgeon (I'veheard a lot of good about the oncology

> > > > > > > > > > surgeon) by the name of MacGilvary. My question is what type

of

> > > > > > > > > > surgeon should I be seeing ? I would rather not go back to

> > > > > > > > Dartmouth

> > > > > > > > > > for several reasons but someof you told me before that my

local

> > > > > > > > endo

> > > > > > > > > > was foolish for sending me to the oncology surgeon. The endo

is

> > > > > > > > only

> > > > > > > > > > sending me to him because she believes he is a good

surgeon.Any

> > > > > > > > > > input would be helpful at thgis point. I apreciate it.

> > > > > > > > > > Lettie PA in ton Maine

> > > > > > > > > >

> > > > > > > > >

> > > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > >

> > >

> >

>

May 31, 2011

Clearly a risk but one I'm willing to take. One side is a perfectly normal

looking adrenal gland with no abnormalities (so they'd be unlikely to remove it,

even if AVS said it was doing something odd), the other has a 21mm growth on it.

You can reserve the right to 'I told you so' if it doesn't work but the odds are

somewhere over 95% that it is the right side.

> > > > > > > > > >

> > > > > > > > > > > The other question was about adrenalectomies. The

> > > > > > > > > endocrinologist at

> > > > > > > > > > > Dartmouth as well as the one here in Maine that I see

think I

> > > > > > > > > should

> > > > > > > > > > > have an adrenalectomy. One suggests a general sugeon at

> > > > > > > > > Dartmouth by

> > > > > > > > > > > the name of Laycock and the other is suggesting a

Maine

> > > > > > > > > > > Oncology surgeon (I'veheard a lot of good about the

oncology

> > > > > > > > > > > surgeon) by the name of MacGilvary. My question is what

type of

> > > > > > > > > > > surgeon should I be seeing ? I would rather not go back to

> > > > > > > > > Dartmouth

> > > > > > > > > > > for several reasons but someof you told me before that my

local

> > > > > > > > > endo

> > > > > > > > > > > was foolish for sending me to the oncology surgeon. The

endo is

> > > > > > > > > only

> > > > > > > > > > > sending me to him because she believes he is a good

surgeon.Any

> > > > > > > > > > > input would be helpful at thgis point. I apreciate it.

> > > > > > > > > > > Lettie PA in ton Maine

> > > > > > > > > > >

> > > > > > > > > >

> > > > > > > > >

> > > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > >

> > >

> >

>

May 31, 2011

Not that I belive this is true But from the medical stand point the odds of

adrenal Adenoma fould on CT is 80% are Nonfunctiona.

With this in mind Don't know how one can say the odds are somewhere over 95%

with out more testing. AVS isn't the only test that can be done to increase the

odds that the gland is the right one.

> > > > > > > > > > >

> > > > > > > > > > > > The other question was about adrenalectomies. The

> > > > > > > > > > endocrinologist at

> > > > > > > > > > > > Dartmouth as well as the one here in Maine that I see

think I

> > > > > > > > > > should

> > > > > > > > > > > > have an adrenalectomy. One suggests a general sugeon at

> > > > > > > > > > Dartmouth by

> > > > > > > > > > > > the name of Laycock and the other is suggesting a

Maine

> > > > > > > > > > > > Oncology surgeon (I'veheard a lot of good about the

oncology

> > > > > > > > > > > > surgeon) by the name of MacGilvary. My question is what

type of

> > > > > > > > > > > > surgeon should I be seeing ? I would rather not go back

to

> > > > > > > > > > Dartmouth

> > > > > > > > > > > > for several reasons but someof you told me before that

my local

> > > > > > > > > > endo

> > > > > > > > > > > > was foolish for sending me to the oncology surgeon. The

endo is

> > > > > > > > > > only

> > > > > > > > > > > > sending me to him because she believes he is a good

surgeon.Any

> > > > > > > > > > > > input would be helpful at thgis point. I apreciate it.

> > > > > > > > > > > > Lettie PA in ton Maine

> > > > > > > > > > > >

> > > > > > > > > > >

> > > > > > > > > >

> > > > > > > > >

> > > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > >

> > >

> >

>

May 31, 2011

As msmith found out she has a know adrenal adenoma on one side and nothing

showing on the other. AVS shows both sides making to much aldo. Now there is a

chance the AVS wasn't done right. Even if it is right the question is would

removing adrenal adenoma reduce the amount of meds she has to take?

> > > > > > > > > > > >

> > > > > > > > > > > > > The other question was about adrenalectomies. The

> > > > > > > > > > > endocrinologist at

> > > > > > > > > > > > > Dartmouth as well as the one here in Maine that I see

think I

> > > > > > > > > > > should

> > > > > > > > > > > > > have an adrenalectomy. One suggests a general sugeon

at

> > > > > > > > > > > Dartmouth by

> > > > > > > > > > > > > the name of Laycock and the other is suggesting a

Maine

> > > > > > > > > > > > > Oncology surgeon (I'veheard a lot of good about the

oncology

> > > > > > > > > > > > > surgeon) by the name of MacGilvary. My question is

what type of

> > > > > > > > > > > > > surgeon should I be seeing ? I would rather not go

back to

> > > > > > > > > > > Dartmouth

> > > > > > > > > > > > > for several reasons but someof you told me before that

my local

> > > > > > > > > > > endo

> > > > > > > > > > > > > was foolish for sending me to the oncology surgeon.

The endo is

> > > > > > > > > > > only

> > > > > > > > > > > > > sending me to him because she believes he is a good

surgeon.Any

> > > > > > > > > > > > > input would be helpful at thgis point. I apreciate it.

> > > > > > > > > > > > > Lettie PA in ton Maine

> > > > > > > > > > > > >

> > > > > > > > > > > >

> > > > > > > > > > >

> > > > > > > > > >

> > > > > > > > >

> > > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > >

> > >

> >

>

June 1, 2011

:-D For right side = correct side (it is on the left side)

> > > > > > > > > > > >

> > > > > > > > > > > > > The other question was about adrenalectomies.

> > The

> > > > > > > > > > > endocrinologist at

> > > > > > > > > > > > > Dartmouth as well as the one here in Maine

> > that I see think I

> > > > > > > > > > > should

> > > > > > > > > > > > > have an adrenalectomy. One suggests a general

> > sugeon at

> > > > > > > > > > > Dartmouth by

> > > > > > > > > > > > > the name of Laycock and the other is

> > suggesting a Maine

> > > > > > > > > > > > > Oncology surgeon (I'veheard a lot of good

> > about the oncology

> > > > > > > > > > > > > surgeon) by the name of MacGilvary. My

> > question is what type of

> > > > > > > > > > > > > surgeon should I be seeing ? I would rather

> > not go back to

> > > > > > > > > > > Dartmouth

> > > > > > > > > > > > > for several reasons but someof you told me

> > before that my local

> > > > > > > > > > > endo

> > > > > > > > > > > > > was foolish for sending me to the oncology

> > surgeon. The endo is

> > > > > > > > > > > only

> > > > > > > > > > > > > sending me to him because she believes he is a

> > good surgeon.Any

> > > > > > > > > > > > > input would be helpful at thgis point. I

> > apreciate it.

> > > > > > > > > > > > > Lettie PA in ton Maine

> > > > > > > > > > > > >

> > > > > > > > > > > >

> > > > > > > > > > >

> > > > > > > > > >

> > > > > > > > >

> > > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > >

> > >

> >

>

June 1, 2011

It also has this quote

Radiologists are constantly seeking ways to differentiate adenomas from

carcinomas on CT scan. The most recent method uses Hounsfield units. The density

of the lesion or mass found on the CT scan is compared against the density of

water, which is assigned the value of 0 Hounsfield units. Adenomas typically

have low attenuation values of & #8804;10 units; some studies report values up to

14 units, but <10 units almost certainly indicates an adenoma (3). CT scans,

however, cannot determine if a mass is hyperfunctioning vs nonfunctioning or

benign vs malignant.

So if CT can't tell if mass is hyperfunctioning vs nonfunctioning. How do you

tell?

> > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > The other question was about adrenalectomies.

The

> > > > > > > > > > > > > > endocrinologist at

> > > > > > > > > > > > > > > > Dartmouth as well as the one here in Maine that

I see think I

> > > > > > > > > > > > > > should

> > > > > > > > > > > > > > > > have an adrenalectomy. One suggests a general

sugeon at

> > > > > > > > > > > > > > Dartmouth by

> > > > > > > > > > > > > > > > the name of Laycock and the other is

suggesting a Maine

> > > > > > > > > > > > > > > > Oncology surgeon (I'veheard a lot of good about

the oncology

> > > > > > > > > > > > > > > > surgeon) by the name of MacGilvary. My question

is what type of

> > > > > > > > > > > > > > > > surgeon should I be seeing ? I would rather not

go back to

> > > > > > > > > > > > > > Dartmouth

> > > > > > > > > > > > > > > > for several reasons but someof you told me

before that my local

> > > > > > > > > > > > > > endo

> > > > > > > > > > > > > > > > was foolish for sending me to the oncology

surgeon. The endo is

> > > > > > > > > > > > > > only

> > > > > > > > > > > > > > > > sending me to him because she believes he is a

good surgeon.Any

> > > > > > > > > > > > > > > > input would be helpful at thgis point. I

apreciate it.

> > > > > > > > > > > > > > > > Lettie PA in ton Maine

> > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > >

> > > > > > > > > > > > > >

> > > > > > > > > > > > >

> > > > > > > > > > > >

> > > > > > > > > > >

> > > > > > > > > >

> > > > > > > > >

> > > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > >

> > >

> >

>

June 1, 2011

I can't - but I do have PA. So the probabilities I'm quoting come from the

correlation between having PA, being under 40 and having a 20mm adrenal adenoma

based on historical cases.

Not from accidentally finding an adenoma and trying to identify from that what

type it is - which is what this paper is all about. It starts from the other end

of diagnosis.

So like I've said before, I don't KNOW that this adenoma is the problem. But the

probability is that it is - and a high enough probability to be OK about going

straight for surgery (based on advice here and supported by this from the

American Association of Endocrine Surgeons

http://endocrinediseases.org/adrenal/hyperaldosteronism_diagnosis.shtml)

> > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > The other question was about adrenalectomies.

The

> > > > > > > > > > > > > > > endocrinologist at

> > > > > > > > > > > > > > > > > Dartmouth as well as the one here in Maine

that I see think I

> > > > > > > > > > > > > > > should

> > > > > > > > > > > > > > > > > have an adrenalectomy. One suggests a general

sugeon at

> > > > > > > > > > > > > > > Dartmouth by

> > > > > > > > > > > > > > > > > the name of Laycock and the other is

suggesting a Maine

> > > > > > > > > > > > > > > > > Oncology surgeon (I'veheard a lot of good

about the oncology

> > > > > > > > > > > > > > > > > surgeon) by the name of MacGilvary. My

question is what type of

> > > > > > > > > > > > > > > > > surgeon should I be seeing ? I would rather

not go back to

> > > > > > > > > > > > > > > Dartmouth

> > > > > > > > > > > > > > > > > for several reasons but someof you told me

before that my local

> > > > > > > > > > > > > > > endo

> > > > > > > > > > > > > > > > > was foolish for sending me to the oncology

surgeon. The endo is

> > > > > > > > > > > > > > > only

> > > > > > > > > > > > > > > > > sending me to him because she believes he is a

good surgeon.Any

> > > > > > > > > > > > > > > > > input would be helpful at thgis point. I

apreciate it.

> > > > > > > > > > > > > > > > > Lettie PA in ton Maine

> > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > >

> > > > > > > > > > > > > >

> > > > > > > > > > > > >

> > > > > > > > > > > >

> > > > > > > > > > >

> > > > > > > > > >

> > > > > > > > >

> > > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > >

> > >

> >

>

June 1, 2011

Look at this study.

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Adrenal Vein Sampling: How to Make It Quick, Easy, and Successful1

Daunt, MBBS, FRCR, FRACR

+ Author Affiliations

1From the X-Ray Department, Greenslopes Private Hospital, Newdegate Street, Greenslopes, Queensland 4120, Australia. Recipient of a Cum Laude award for an education exhibit at the 2004 RSNA Annual Meeting. Received March 14, 2005; revision requested April 15 and received June 13; accepted June 17. The author has no financial relationships to disclose.

Address correspondence tothe author (e-mail: dauntnic@...).

Next Section

Abstract

Adrenal vein sampling has a reputation as a difficult procedure. However, it is being performed more frequently at some institutions due to the realization that primary aldosteronism is more common than previously believed. At the author's institution, adrenal vein sampling with computed tomographic (CT) and laboratory correlation has been performed more than 800 times in the past 10 years. Adrenal vein sampling is used to determine whether autonomous hormone production is unilateral or bilateral; unilateral secretion can be treated with surgery. The venous drainage of each adrenal gland is predominantly via a central vein. Recognition of the right adrenal vein is the crux of adrenal vein sampling. CT is useful in planning adrenal vein sampling by demonstrating the anatomy and positions of the adrenal veins. A small amount of contrast material is injected gently and slowly into the adrenal vein; it is not necessary to perform formal venography to outline the entire gland. To confirm that the vein is draining the majority of adrenal cortical blood, the adrenal vein sample should have a significantly higher level of cortisol than a peripheral sample. Adrenal glands that are producing aldosterone demonstrate an aldosterone-cortisol ratio that is higher than the peripheral value.

Previous SectionNext Section

Introduction

There is an increasing requirement for adrenal vein sampling, which is driven by the appreciation that primary aldosteronism is far more common than previously recognized (1–3). Many centers throughout the world are reporting a prevalence of between 5% and 10% in unselected hypertensive patients (4–8).

Historically, adrenal vein sampling has been problematic, with many authors reporting difficulties with obtaining good samples, particularly from the right adrenal vein (9–11). This results from the small size of the right adrenal vein and the resulting difficulty in obtaining an adequate specimen, recognizing the typical vascular patterns, and distinguishing other vessels that may arise from the posterior wall of the inferior vena cava (IVC) close by. Lastly, the long anatomic segment that may give rise to the right adrenal vein may result in a prolonged search pattern. Superimposed on this is the frequency of anatomic variations of the left renal vein or left adrenal vein (12).

Furthermore, the realization that computed tomography (CT) is unreliable as a screening test, with increasing reports of inappropriate conclusions drawn from CT examinations (13–20), supports the premise that most patients with syndromes of adrenocortical excess production should undergo adrenal vein sampling to determine if the overproduction is unilateral or bilateral. Cure of hypertension occurs in 50%–80% of patients after adrenalectomy for an aldosterone-producing adenoma, and most of the remaining cases show improvement (1–3,21,22). Cases of bilateral aldosterone hypersecretion can usually be controlled simply with specific medications (1–3). The community cost benefit resulting from a reduction in hypertension medications and hypertension-associated morbidity is evident (23).

This article covers all aspects of adrenal vein sampling. Specific topics discussed are the reasons for performing the study, our clinical experience, aldosteronism, the shortcomings and value of CT, the anatomy of the adrenal veins, variations of the left renal vein, how to recognize the right adrenal vein, how to perform adrenal vein sampling, analysis of the results, and complications.

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Why Perform Adrenal Vein Sampling?

Adrenal vein sampling is performed to assess whether autonomous hormone production is unilateral or bilateral. Adrenal vein sampling is most commonly performed in primary aldosteronism, as this is the most common hypersecretory adrenal disease (24–26). Less commonly, it is performed in biochemically proved pheochromocytoma when no source is visible at CT or other cross-sectional imaging. Rarely, it may be performed in adrenal Cushing disease or for syndromes of androgen excess (27).

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Clinical Experience

Queensland X-Ray has been performing adrenal vein sampling at Greenslopes Private Hospital since November 1994. Up to the end of August 2004, we had performed 800 examinations. Of these procedures, 716 were performed by two radiologists and 792 were performed for primary aldosteronism. Both cortisol and aldosterone were assayed in each sample (see the "Analysis of the Results" section). Because adrenal venous blood is rich in cortisol, this is used as a marker of successful adrenal vein sampling. Empirically, a cortisol gradient of 3 between the adrenal sample and a peripheral sample was considered to indicate adequate sampling (3); if the cortisol gradient was under 2, the sample was excluded from further analysis, as such levels have on occasion proved to be misleading. Cortisol gradients between 2 and 3 are assessed on their individual merits. Over the past 7 years, for the two experienced radiologists, the success rate has been 97% for left-sided samples and 96.6% for right-sided samples, with success defined as sample adequacy as outlined earlier (ie, an adequate gradient) and a study on the basis of which ongoing management can be planned.

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Aldosteronism

Jerome Conn first described primary aldosteronism in 1954, the same year that the chemical structure of aldosterone was identified (28).

In April 1954, Conn managed the case of a 34-year-old housewife with severe hypokalemia, generalized muscle weakness, tetany, and hypertension, salient features of the soon to be recognized Conn syndrome. At surgery, a 4-cm cortical adenoma was removed from her right adrenal gland, resulting in cure of the hypertension. Over the next 10 years, it became evident that primary aldosteronism could be present even with normal potassium levels. By the mid-1960s, Conn suggested that the overall prevalence of aldosteronism among hypertensive persons was at least 7.6%. This idea aroused heated debate and was generally rejected by the medical community. Even today, some textbooks still suggest that the prevalence of aldosteronism among hypertensive persons is less than 1%.

In 1981, Hiramatsu and colleagues (29) described a screening test—the aldosterone-to-renin ratio—and found aldosterone-producing adenomas in 2.6% of hypertensive patients. Because only those cases with a positive nuclear medicine (iodine 131 iodocholesterol) or CT study were accepted as positive cases, this figure would have underestimated the number of patients with primary aldosteronism, as all those cases with bilateral hyperplasia or small adenomas would have been missed.

There are now numerous published reports from all major continents and in many racial groups that confirm Conn's original hypothesis, suggesting that the true prevalence of primary aldosteronism may be between 5% and 10% of all hypertensive persons (1–8).

Types of Primary Aldosteronism

The pathologic pattern of primary aldosteronism is very variable (1–3). The most common type is bilateral adrenal cortical hyperplasia, which may demonstrate several patterns including diffuse, micronodular, macronodular (30), or occasionally giant macronodular. Less frequent is unilateral secretion from a solitary adenoma, hyperplasia (23,31,32), or rarely carcinoma. When unilateral secretion is found and an adenoma is present, there is usually associated hyperplasia of the zona glomerulosa, the aldosterone-secreting portion of the adrenal gland, on the same side.

However, the macroscopic appearance, whether it be hyperplasia, nodular disease, or other, is irrelevant; the main differentiation is whether secretion is unilateral or bilateral, as those with unilateral secretion can be offered surgery (3).

There are two main types of familial hyperaldosteronism. Type 1 is glucocorticoid-remediable primary aldosteronism and is inherited as an autosomal dominant disease (1–3,21).

The second form of familial hyperaldosteronism, type 2, is now realized to be more common than type 1 (3). Type 2 familial hyperaldosteronism may be expressed as unilateral or bilateral disease and therefore needs to be investigated in the same manner as apparently sporadic primary aldosteronism.

Effects of Aldosterone and Rationale for Screening

Screening for primary aldosteronism by means of the aldosteronerenin ratio in venous blood is straightforward and reliable. Levels of renin and aldosterone are often within the normal range, but a ratio of the two levels is a robust screening test for primary aldosteronism (29). It requires care in interpretation, as there are numerous causes of false-positive and false-negative studies, particularly resulting from antihypertensive medication and diuretics (33). All of our cases are confirmed by use of a fludrocortisone suppression test (2,3,28).

A further important consideration is that inappropriate aldosterone secretion in excess appears to have direct cardiac effects that are independent of blood pressure elevation (34–38). A disproportionate extent of myocardial hypertrophy and fibrosis has been reported in patients with aldosteronism.

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Shortcomings and Value of CT

Previously, many had suggested that if primary aldosteronism was diagnosed and CT demonstrated a clear-cut adenoma, then surgery could be performed without adrenal vein sampling (39,40). It has become realized that such a process may lead to inappropriate surgery (13–20). In the most recent of these studies (13–20), Magill et al (20) compared adrenal vein sampling and CT in 62 patients and showed that CT results were inaccurate or noncontributory in 68%. Indeed, adenomas less than 1 cm in diameter account for nearly 50% of aldosterone-producing adenomas surgically removed at our center (3), and below this size detection at CT can become difficult. We have had several patients with adenomas at CT in whom disease was localized to the contralateral side at adrenal vein sampling (Fig 1).

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Figure 1. CT scan shows a 13-mm-diameter nonhyperfunctioning adenoma in the lateral limb of the left adrenal gland (arrow). At adrenal vein sampling, the patient's disease was lateralized to the right adrenal gland. (The adrenal vein sampling was repeated to confirm the unexpected finding.) The patient's hypertension was cured with right adrenalectomy.

However, the value of CT is twofold: (a) It allows assessment of mass lesions. A large adrenal mass greater than 2.5–4 cm in diameter may warrant consideration for surgical removal in its own right, on the basis of possible malignant potential, unless radiologic appearances are characteristic of other benign lesions such as myelolipoma or there are other clinical considerations such as metastatic disease. ( CT demonstrates the anatomy and position of the adrenal veins, especially the right adrenal vein (Fig 2).

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Figure 2. CT scan clearly shows the right adrenal vein (arrow).

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Anatomy of the Adrenal Veins

The venous drainage of the adrenal glands is predominantly via a central vein on both sides (Fig 3) (41–44). On the right, the central vein drains directly into the IVC on its midposterior wall, and one researcher remarked on the constancy of this relationship in cadaver studies (42). Monkhouse and Khalique (44) noted that the central vein on the right may be duplicated and rarely triplicated; although some of these multiple veins may drain to the inferior phrenic or right renal vein, these authors noted that there was always a central vein entering the IVC. At least two authors have reported significant proportions of adrenal veins entering hepatic venous structures (43,45), with Bookstein (45) suggesting a frequency of 10%. The frequency stated in these two sources appears out of step with the frequency in other references, with none being reported in cadaver studies (42,44), and with the frequency in our experience, in which no convincing cases have been observed.

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Figure 3. Diagram shows the anatomy of the adrenal veins.

The central vein on the left is also extremely constant (41–44), taking a caudal or downward path into the superior margin of the left renal vein and taking a tributary, the inferior phrenic vein with a variable-length common trunk, before entering the left renal vein. Rarely, the left adrenal and inferior phrenic veins enter the left renal vein separately (probably no more than 1% of cases). Both adrenal glands also have a number of superficial, emissary, or capsular veins that extend from the surface of the gland into the perirenal fat, even on occasion penetrating the renal capsule, particularly on the right (45). Such veins not infrequently communicate with inferior phrenic or intercostal veins; in addition, in two of our 800 cases, a connection with superficial hepatic veins was seen on the right (Figs 4, 5). On the right, they may enter the right renal vein (Fig 6). On the left, communications may be seen to the left renal vein as well as the azygos or hemiazygos vein. Visualization of these veins is an excellent method of confirming intraadrenal positioning.

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Figure 4. Fluoroscopic image obtained with injection into the right adrenal vein shows opacification of small peripheral hepatic vessels (arrow).

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Figure 5. Fluoroscopic image shows a Mikaelsson catheter passed distally in the right adrenal vein to superselect a medial limb branch; with this catheter position, drainage from a lateral limb adenoma could be missed. The wedged position of the catheter tip (open arrow) has resulted in some extravasation or staining around small branches inferiorly (arrowheads). More cephalad, there is possible filling of a hepatic branch (solid arrow).

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Figure 6. Fluoroscopic image obtained with a C2 catheter in the central right adrenal vein shows superficial communications superolaterally and inferolaterally (arrows) and to the right renal vein (arrowhead).

Stack et al (46) recently described an anomalous central left adrenal vein draining directly into the IVC. I could find no other example of this in the literature, although we have seen several cases of superficial veins entering the IVC (Fig 7).

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Figure 7. Fluoroscopic image obtained with injection into the left adrenal vein shows two separate left adrenal veins and extensive communicating veins draining into the left renal vein (1) and IVC (2).

In cadaver studies, the right adrenal vein may be 1–15 mm in length and averages 3.5–5 mm in caliber. The left adrenal vein measures 1–4 cm to the inferior phrenic confluence and 1–3 cm from there to the left renal vein and is usually 4–5 mm in caliber (42,44).

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Variations of the Left Renal Vein

A recent study by Trigaux et al (12) evaluated anomalies of the IVC and left renal vein with spiral CT, with bilateral IVCs recognized in 0.3% of patients. Ten percent had left renal vein variants, with 38 cases (3.7%) of retroaortic renal veins and 64 cases (6.3%) of circumaortic venous rings (Fig 8). Occasionally, the approach to the left adrenal vein will have to be made via a lower-positioned (usually at L3) retroaortic left renal vein (Fig 9). Retroaortic left renal veins usually lie some 4 cm below a normally sited vein.

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Figure 8. Fluoroscopic image obtained with injection into the left adrenal vein shows numerous adrenal branches. Also noted is a renal vein ring, with a normal preaortic vein (top arrow) and a retroaortic vein inferiorly (bottom arrow).

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Figure 9. Fluoroscopic image shows a C2 catheter passed via a retroaortic renal vein into the left adrenal vein, with injected contrast material draining into the normal preaortic renal vein.

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How to Recognize the Right Adrenal Vein

Recognition of the right adrenal vein is the crux of adrenal vein sampling. In cadaver studies, it is usually some 4–5 mm in caliber (42,44). It often funnels down to the hilum of the gland. In our experience, it is usually angled caudally, although Monkhouse and Khalique (44) reported that 26 of 68 veins entered from above. We see five different patterns:

A glandlike pattern with a main central stem and numerous branches (Figs 10, 11), usually with angles of less than 90° between the branches and the main stem, forming a characteristic glandlike pattern. This can occasionally be difficult to differentiate from an accessory hepatic vein (Fig 12).

A delta pattern with little filling of internal structure (Figs 13–15).

A triangular pattern with vessels fairly crowded together and a "blush-like" appearance (Figs 16, 17).

No discernible adrenal vessels, but the main vessel position and attitude are characteristic and fit in with the position estimated at CT (Figs 18–20). Surprisingly, this occurs with some frequency, about one in 30 cases.

A central vein leading to thin stellate or spidery branches (Figs 21–23).

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Figure 10. Fluoroscopic image shows the classic glandlike pattern of injection into the right adrenal vein.

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Figure 11. Fluoroscopic image shows the classic glandlike pattern of injection into the right adrenal vein with prominent lateral communicating veins.

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Figure 12. Fluoroscopic image shows what appears to be a right adrenal vein injection but is actually injection into a hepatic radicle. The subtle upsloping vessel (arrow) arising from the superficial lateral border of the adrenal gland is the giveaway.

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Figure 13. Fluoroscopic image shows the delta pattern of injection into the central adrenal vein. There are two or three major branches with acute angles between them.

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Figure 14. Fluoroscopic image shows injection into the right adrenal vein with a reverse catheter. There is a basic delta pattern with extensive communications from superficial veins into the retroperitoneum and an intercostal vein (arrow).

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Figure 15. Fluoroscopic image obtained with injection into the right adrenal vein shows mainly the central vein. The early branches of a delta configuration are also seen (arrows), thus confirming good catheter position; no more contrast material needs to be injected.

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Figure 16. Fluoroscopic image obtained with adrenal vein injection shows a triangular pattern of veins (arrows) and minor blush with communicating superficial veins inferiorly.

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Figure 17. Fluoroscopic image obtained with adrenal vein injection shows vessels in a triangular configuration with subtle background blush and an extremely large communicating superficial vein.

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Figure 18. Fluoroscopic image obtained with injection into the right adrenal vein. It is difficult to make out any background adrenal structure; however, positive cortisol ratios were found at sampling.

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Figure 19. Fluoroscopic image shows a right adrenal gland with an irregular intraglandular structure. Although no normal adrenal structure is discernible, there are large communicating vessels laterally.

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Figure 20. Fluoroscopic image obtained with injection into the right adrenal vein. It is difficult to make out a normal background adrenal structure; however, the extensive inferolateral communicating veins support the premise of good catheter position.

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Figure 21. Fluoroscopic image shows a barely discernible adrenal structure. However, there is a background spidery pattern with thin vessels and some communicating veins, which are also of small caliber.

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Figure 22. Fluoroscopic image shows the spidery pattern of adrenal vein injection. There is a central adrenal vein with straight branches at multiple angles and with lateral communicating veins.

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Figure 23. Fluoroscopic image obtained with injection into the right adrenal vein shows a poorly defined stellate or spidery pattern with inferior communicating veins.

Perhaps the most important finding is communication with superficial or emissary veins from the adrenal capsule; if appropriate, this finding gives a high confidence level for a satisfactory position (45). The emissary veins most commonly course laterally, medially, or inferiorly (Figs 6, 11, 16, 17, 20, 24) but sometimes pass cephalad in a straight fashion toward the IVC. They may communicate with the right renal vein (Fig 6), intercostal veins (Figs 14, 16, 17, 20, 24), phrenic vein, or IVC (Figs 6, 24). They must be contrasted with the sweeping, curvilinear, upward-passing veins that extend into the main hepatic veins in patients in whom a small accessory hepatic radicle has been injected (Fig 25). These accessory hepatic radicles often demonstrate marked tissue staining without patient discomfort, whereas injection into an adrenal gland, or for that matter, sometimes suction on a syringe to aspirate blood, may cause poorly defined upper quadrant or lower chest discomfort, particularly posteriorly. Tissue staining in the adrenal gland (Fig 5), which should be avoided at all costs, is also associated with acute discomfort or low-grade pain.

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Figure 24. Fluoroscopic image obtained with right adrenal vein injection through a reverse 1 catheter shows no discernible adrenal structure. However, the large communicating veins extending into intercostal veins make it highly likely that the sample will be positive. At sample analysis, good cortisol gradients were obtained.

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Figure 25. Fluoroscopic image obtained with right-sided venous injection shows what appears to be the delta pattern of an adrenal gland. However, the veins coursing upward and to the right are suggestive of hepatic vessels. Samples obtained at this point showed low cortisol values, findings typical of hepatic drainage.

Another major point is that the position of the adrenal gland at CT should have been assessed prior to the study and the area of gland filling should obviously not extend beyond the anticipated margins of the adrenal gland.

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How to Perform Adrenal Vein Sampling

CT Scanning

High-quality CT examination is of enormous benefit in planning adrenal vein sampling. On a modern multisection scanner with reconstruction at 2 or 3 mm, the right adrenal vein can be identified in more than 50% of patients (Figs 2, 26). When we identify the right adrenal vein, we accurately assess its position in relation to the vertebral column and assign a disk end-plate or pedicle level as necessary. We then plan to place the catheter 1 cm higher to allow for the inspiration used for CT of the adrenal glands. This dramatically reduces the time taken for the search. If no vein can be identified, then the midpoint of the adrenal gland is used as the potential adrenal vein position.

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Figure 26. Three sequential thin CT sections show the caudal alignment of the right adrenal vein (arrow), which drains into the mid posterior wall of the IVC.

Stimulation

Many authors use adrenocorticotropic hormone (ACTH) infusions before and during adrenal sampling to stimulate aldosterone release (24–26). The unit at Greenslopes Private Hospital has treated over 1,000 patients with primary aldosteronism over the past 20 years and for many years also used ACTH stimulation. However, we suspect that it increased the number of cases diagnosed as bilateral, perhaps falsely, and this will have eliminated the therapeutic possibility of unilateral adrenalectomy in some patients. Thus, we do not use ACTH stimulation for our adrenal vein sampling.

Peripheral Line

When each adrenal vein sample is obtained, it requires a peripheral blood sample for correlation of the cortisol and aldosterone levels. Although we routinely place a peripheral line for obtaining this blood, a sheath sample could equally well be used.

Catheters

We use 5- or 5.5-F catheters. Although many use a reverse catheter for the right adrenal vein, our unit has traditionally used a C2 Cobra catheter with one side hole 3 mm from the tip. With this catheter and the use of prior CT, the catheter normally drops immediately into the vein, with a very short search required. One side hole is used to facilitate drawing back of blood. We have found that using two side holes increases the number of samples with a low cortisol ratio, which may be a result of dilution by IVC blood. In a narrow IVC, a C1 catheter may often be helpful. Rarely, a reverse catheter such as a 1 or Mikaelsson may be required. The C2 catheter can often be used for accessing the left adrenal vein. However, more frequently we use an MK1B catheter (Cook, Bloomington, Ind), as this is purpose made for the left adrenal vein.

Puncture

In general, a right femoral vein puncture is performed. Occasionally, a referring endocrinology or hypertension department insists on bilateral adrenal vein sampling simultaneously. In such cases, after the initial femoral vein puncture, then under fluoroscopic guidance in the right inguinal region, a needle can be passed down toward the guidewire or catheter and a quick, easy second puncture can be performed within half a centimeter of the first. It is advisable to use a sheath for one of the catheters, preferably the right venous catheter, to prevent displacement of one catheter when the second is moved.

Often, a Valsalva maneuver aids in venous puncture. Very rarely, ultrasonographic guidance has been required.

Technique of Contrast Material Injection

It is important to inject gently into the adrenal veins, particularly that on the right, to prevent hemorrhage due to rupture of small intraglandular veins. A small amount of contrast material is used, perhaps 3 mL and no more. The injection is started slowly, and if satisfactory confirmation of adrenal position is obtained, then no more contrast material need be injected; a formal diagnostic venogram to outline the entire adrenal gland is not necessary (Fig 27). If little venous structure is seen due to backflow into the IVC (or into the left renal vein on the left), then the speed of injection and pressure are increased slightly in order to visualize the necessary vessels. When tumors are present, staining or a tumor outline is often seen, but this should not be aimed for (Figs 28, 29).

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Figure 27. Fluoroscopic image obtained with injection into the central adrenal vein shows virtually no intraglandular structure (same patient as in Fig 12). This injection technique reduces the risk of extravasation to the minimum.

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Figure 28. Fluoroscopic image obtained with right adrenal vein injection through a C2 catheter shows extensive distortion of the adrenal venous structure due to a large adenoma (arrows). At surgery, a 2.3-cm-diameter adenoma was removed.

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Figure 29. Fluoroscopic image obtained with left adrenal vein injection shows the rounded configuration of an adenoma (arrow) in the lateral limb of the gland (same patient as in Fig 1).

Sampling Techniques

We are required by our laboratory service to provide a minimum of 5 mL and preferably 6 mL. We use a 10-mL syringe for aspiration. On the right, it is often difficult to obtain an adequate quantity of blood from the adrenal vein, as suction on the syringe results in presumed collapse of the vessel wall around the catheter tip. The presence of side holes in the catheter helps allay this problem, as may the following techniques: (a) intermittent gentle suction, ( suction on the syringe with air in the syringe to reduce the effective suction pressure, and © free drainage (ie, letting blood drip from the catheter end into the sample bottle).

A recent article has also identified potential problems with too high a concentration of iodinated contrast material in the sample forming a gel layer that may alter concentrations (47). Therefore, it is advisable to eliminate all contrast material from the system before sampling.

Strategies for the Right Adrenal Vein

The C2 catheter is passed to the predetermined level (from CT) and rotated to the posterior wall of the IVC. Often, the catheter will "drop in" almost immediately. Catheter probing starts on the posterior wall and extends in an arc of 45° to the right and less so to the left. Although the catheter often appears to be pointing significantly one way or the other, CT suggests that this is illusory, as the vein always arises from the posterior wall. Occasionally, the search has to be extended a little cephalad, but rarely caudally. In this fashion, up to 90% of right adrenal veins are found within 5 minutes.

During this initial phase, the catheter usually engages a number of different vessels, such as short accessory hepatic vessels, retroperitoneal vessels, and phrenic vessels.

If the initial search fails, then the catheter can be exchanged for a C1 pattern; the tighter curve allows a more downward approach that may help in steeper right adrenal veins or narrower IVCs (Fig 30). If no vein is found with an extended search and by using these catheters, a reverse catheter such as a 1 or Mikaelsson may prove helpful. On at least two occasions, the MK1B catheter that I use for the left side has easily entered the right adrenal vein despite its inappropriate design (Fig 31). A reverse catheter may extend deeply into the right adrenal gland; this can potentially result in too selective sampling, which could result in missing the drainage from an adenoma (Figs 5, 32), and also could promote a wedged injection, which could increase the likelihood of extravasation (Fig 5).

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Figure 30. Fluoroscopic image obtained with a C1 catheter in the central adrenal vein shows spindly intraglandular adrenal veins with superficial communications laterally.

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Figure 31. Fluoroscopic image shows a reverse catheter (MK1B) deeply engaged within the central right adrenal vein.

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Figure 32. Fluoroscopic image shows a reverse catheter (Mikaelsson) placed too selectively in the adrenal vein, with the catheter tip in the main medial limb branch (arrow).

In view of possible cephalic orientation of the right adrenal vein (44), other catheter shapes may on occasion be helpful.

If all else fails, an IVC sample obtained with the catheter tip on the mid posterior wall a few millimeters above the anticipated orifice may prove successful. The laminar flow of slow venous return that is characteristically observed from the renal veins at CT will also be observed from the adrenal veins, and this should promote a high likelihood of success with this method. This further highlights the importance of careful analysis of a good-quality CT study before adrenal vein sampling.

Strategies for the Left Adrenal Vein

After at least two right-sided samples are obtained, the C2 catheter is withdrawn to the left renal vein level. By gentle pushing, sometimes with a little rotation or twisting of the catheter around the wire, the C2 can often be advanced down the left renal vein. With the C2 catheter some 3–4 cm into the left renal vein, rotation on the catheter to direct the tip cephalad will result in this catheter engaging the left adrenal vein in at least 50% of patients. (Actually, the common trunk of the left adrenal and inferior phrenic veins is engaged, but I will refer to it as the left adrenal vein, as this is where sampling is usually performed.) The C2 catheter usually experiences some torque trying to expel it from this vein, but holding the catheter and applying an opposite torque should result in retention of a good position.

In those cases where the C2 catheter will not pass down the left renal vein, a guidewire—we use a double-ended wire to give us two options—can often be directed deep into the renal veins and the catheter advanced over the wire, often again with a rotary force applied to the catheter stem. The C2 catheter is advanced or pulled back and rotated to try to select the left adrenal vein, as described earlier.

If the C2 catheter cannot be persuaded down the left renal or adrenal vein, a reverse catheter is required. An MK1B catheter is ideal and was designed for the job (Fig 33). This should be deployed over the guidewire with the wire deeply seated in the left renal vein. If this proves difficult, sometimes success can be achieved by using the right renal vein. On occasion, an adequate length of guidewire cannot be passed down either renal vein, in which case the catheter can be re-formed down the left common iliac vein. The MK1B catheter is then passed up the IVC with the guide-wire at the apex of the catheter until the tip is just above the left renal vein. The wire is advanced to the tip of the catheter, causing the main convexity of the catheter to open, pushing the tip of the MK1B against the left lateral wall of the IVC. On pulling back from this position, the MK1B catheter always engages the left renal vein.

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Figure 33. Fluoroscopic image shows an MK1B catheter in the left adrenal vein (common trunk). Although the catheter points slightly toward the inferior phrenic vein (arrow), there is excellent filling of only the adrenal venous structure with contrast material injection.

The wire is then withdrawn several centimeters, and the catheter is slowly pulled back while its tip is watched with fluoroscopy. It enters the adrenal vein in most cases; occasionally, a little advancing of the catheter is required to obtain a good stable position. The left adrenal vein is usually about 3 cm from the confluence of the left renal vein and IVC. It is very rare that the left adrenal vein is not found in this way. Once in the common trunk, sampling is performed, preferably with the catheter tip pointing toward the central adrenal vein rather than the inferior phrenic vein (Figs 33–35). I advance the catheter into the central vein only rarely (Figs 36, 37), only in repeat studies, as passage deeper into the gland must increase risk and poor studies are so uncommon.

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Figure 34. Fluoroscopic image shows an unusually large common trunk and central left adrenal vein with good demonstration of the entire intraglandular venous system.

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Figure 35. Fluoroscopic image shows an MK1B catheter in the common trunk just beyond the confluence and pointing laterally toward the adrenal veins. An unusual aberrant vein joins the central vein at the confluence (arrow).

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Figure 36. Fluoroscopic image obtained with an MK1B catheter deep in the central left adrenal vein shows extensive communicating veins laterally, medially, and inferiorly. The catheter position is too deep (arrow); as a result, venous supply from some parts of the left adrenal gland could be missed.

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Figure 37. Fluoroscopic image shows a catheter deep in the central adrenal vein, past some of the early branches. In addition, the inferior phrenic vein is filled by an unusual communicating superficial vein superiorly (arrow).

In our experience, there have been only eight cases where the left adrenal vein could not be selected in this way: five cases of retroaortic veins with or without a vascular ring, one case where no vein was found in the normal position, and two cases of complex venous anomalies.

If no left adrenal vein can be cannulated in this way, a retroaortic vein is looked for at L2–3; this will often be apparent at CT. If one is present, a guidewire can often be passed up the vein. A C2 catheter is passed over the guidewire (Fig 9), which may require a combination of twisting and advancing, and contrast material is injected to identify the position of the adrenal vein. Lastly, if all else fails, a left renal vein sample is obtained in the same way as in the IVC on the right; that is, medially to the anticipated adrenal vein orifice on the cephalic border of the renal vein.

When contrast material is injected on the left side, numerous communicating veins are seen to the phrenic vein, retroperitoneal fat, hemiazygos system, left renal vein, and even IVC (46) (Figs 36–40).

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Figure 38. Fluoroscopic image obtained with left adrenal vein injection shows the tip of the catheter just past the confluence and in the central adrenal vein. An unusual, extensive varicose branch arises from the common trunk and passes inferiorly.

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Figure 39. Fluoroscopic image shows injection into the common trunk with no inferior phrenic vein seen. Extensive corkscrew communicating veins extend from the gland inferiorly and laterally.

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Figure 40. Fluoroscopic image obtained with injection into the common trunk shows filling of left adrenal venous structures and communicating veins, with extension into an aberrant branch draining retroperitoneal structures (arrow).

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Analysis of the Results

For each adrenal vein sample collected, a peripheral sample is simultaneously obtained (3). The adrenal vein sample should have significantly higher levels of cortisol than the peripheral sample if the vein selected is truly draining the majority of adrenal cortical blood. On rare occasions, despite an obviously adequate position with good demonstration of adrenal vasculature, cortisol levels are only slightly raised, if at all, over those of the peripheral samples. In these cases, it may be that the majority of the blood is draining via a different "central" vein or via superficial or emissary veins. Oddly enough, in our experience, this is more commonly a problem on the left side and may be due to the occasionally extraordinary size of communicating or emissary veins on the left ( Rutherford, FRACS, oral communication, 1995) (Figs 38, 39). Monkhouse and Khalique (44) reported a positive case from right atrial sampling due to azygos inflow from a pheochromocytoma on the left side when adrenal vein samples were negative.

Ideally, our referral hypertension unit seeks a cortisol ratio that is three times the peripheral value from the selected vein (3). In practice, ratios between 2 and 3 often provide useful information even though they are not ideal. Ratios below 2 have the potential to create a false diagnostic impression. To correct for dilution from inflow of adjacent veins, the ratio of aldosterone to cortisol is calculated in the selected venous sample and compared to those in the corresponding peripheral sample. Adrenal glands that are producing aldosterone show an aldosterone-cortisol ratio higher than the peripheral value; normal glands give a ratio equal to or less than the peripheral value. In the case of an adenoma on one side, the contralateral normal adrenal gland shows suppressed aldosterone excretion.

Rarely, adrenal vein sampling results in aldosterone-cortisol ratios that are no higher than the peripheral value, despite good cortisol gradients confirming successful adrenal vein catheterization. Possibilities that might be considered are (a) a quiescent phase of aldosterone production, ( venous drainage of an aldosterone-producing adenoma being via veins other than those cannulated (eg, superficial emissary veins), © superselective sampling from an area of gland that does not house an adenoma (Figs 5, 32), or (d) an ectopic source of aldosterone overproduction. More detail can be found in the article by Stowasser et al (3).

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Complications

The major complication of adrenal vein cannulation is rupture of an adrenal vein and subsequent intraglandular and widespread periadrenal hemorrhage. Bookstein (45) quotes a complication rate of some 4% and suggests that complications are more common with Conn and Cushing syndromes due to vein fragility. Walters and Thomson (48) suggest that complications including adrenal infarction and venous rupture occur in 5%–10% of patients, more commonly on the right.

Gross et al (10) suggest that hematoma, infarction, adrenal vein thrombosis and perforation, as well as hypertensive crisis and adrenal insufficiency are not infrequent. Doppman and Gill (25) outline the occasional occurrence of painful extravasation or rarely bilateral infarction. The sequence of events indicating intraadrenal hemorrhage is persistent pain after an injection, increasing in intensity over 30–60 minutes and requiring large doses of analgesics with pain and fever often persisting for 24–48 hours. This sequence of events is frequently associated with complete and permanent destruction of the gland. With the move away from venography and only small injections, the complication rate is undoubtedly much lower. We have had only one documented case of intraadrenal hemorrhage in the past 8 years, for a frequency of less than 0.2% over that time.

It should be noted that local hemorrhage makes laparoscopic surgery far more difficult due to the extensive retroperitoneal adhesions that are found.

Previous SectionNext Section

Conclusions

Adrenal vein sampling should be a rapid, safe, and reliable procedure. In our experience, most studies are performed within 15–25 minutes from local anesthetic infiltration to the finish of the procedure, and indeed our quickest procedure took 7 minutes. Avoidance of strong injections and adrenal venography gives a very tolerable complication rate that should be well under 1%.

The procedure should be reliable and accurate. With CT planning on the right and with a thorough appreciation of different right adrenal vein patterns, catheterization should be achieved in 90% of cases within 5 minutes, although it is admitted that obtaining good volume from the right adrenal vein can be a frustrating experience. The rationale for adrenal vein sampling particularly in primary aldosteronism should be appreciated, and the importance of the procedure in the treatment of these patients is emphasized. Abbreviation: IVC = inferior vena cava

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References

â†µ

GordonRD. Mineralocorticoid hypertension. Lancet1994;344:240–243.

CrossRefMedline

â†µ

GordonRD. Primary aldosteronism. J Endocrinol Invest1995;18:495–511.

Medline

â†µ

StowasserM, Gordon RD, Rutherford JC, Nikwan NZ, Daunt N, Slater GJ. Diagnosis and management of primary aldosteronism. J Renin Angiotensin Aldosterone Syst2001;2:156–169.

FREE Full Text

â†µ

LohKC, Koay ES, Khaw MC, Emmanuel SC, Young WF Jr. Prevalence of primary aldosteronism among Asian hypertensive patients in Singapore. J Clin Endocrinol Metab2000;85:2854–2859.

Abstract/FREE Full Text

BerniniG, Moretti A, Argenio G, Salvetti A. Primary aldosteronism in normokalaemic patients with adrenal incidentalomas. Eur J Endocrinol2002;146:523–529.

Abstract

CalhounDA, Nishizaka MK, Zaman MA, Thakkar RB, Weissmann N. Hyperaldosteronism among black and white subjects with resistant hypertension. Hypertension2002;40:892–896.

Abstract/FREE Full Text

StrauchB, Zelinka T, Hampf M, Berhardt R, Widimsky J Jr. Prevalence of primary hyperaldosteronism in the central Europe region. J Hum Hypertens2003;17:349–352.

CrossRefMedline

â†µ

VeglioF, Morello F, Rabbia F, Leotta G, Mulatero P. Recent advances in diagnosis and treatment of primary aldosteronism. Minerva Med2003;94:259–265.

Medline

â†µ

YoungWF, Klee GG. Primary aldosteronism: diagnostic evaluation. Endocrinol Metab Clin North Am1988;17:367–395.

Medline

â†µ

GrossMD, Falke THM, Shapiro B, Sandler MP. Adrenal glands. In: Endocrine imaging. Norwalk, Conn: Appleton & Lange, 1992; 271, 349.

â†µ

ReznekRH, Armstrong P. The adrenal gland. Clin Endocrinol (Oxf)1994;40:561–576.

Medline

â†µ

TrigauxJP, Vandroogenbroek S, De Wispelaere JF, Lacrosse M, Jan J. Congenital anomalies of the inferior vena cava: evaluation with spiral CT. J Vasc Interv Radiol1998;9:339–345.

Medline

â†µ

RadinDR, Manoogian C, Hadler JL. Diagnosis of primary hyperaldosteronism. AJR Am J Roentgenol1992;158:553–557.

Abstract/FREE Full Text

DoppmanJL, Gill JR, DL, et al. Distinction between hyperaldosteronism due to bilateral hyperplasia and unilateral aldosteronoma: reliability of CT. Radiology1992;184:677–682.

Abstract/FREE Full Text

RossiGP, Chiesura-Corona M, Tregnaghi A, et al. Imaging of aldosterone secreting adenomas: a prospective comparison of computed tomography and magnetic resonance imaging in 27 patients with suspected primary aldosteronism. J Hum Hypertens1993;7:357–363.

Medline

McAlisterFA, Lewanczuk RZ. Primary hyperaldosteronism and adrenal incidentaloma: an argument for physiologic testing before adrenalectomy. Can J Surg1998;41:299–305.

Medline

HarperR, Ferrett CG, McKnight JA, et al. Accuracy of CT scanning and adrenal vein sampling in the preoperative localisation of aldosterone secreting adrenal adenomas. QJM1999;92:643–650.

Abstract/FREE Full Text

GlodnyB, Kuhle C, Cromme S, Brockmann J, Winde G. An assessment of diagnostic procedures preparatory to retroperitoneoscopic removal of adenoma in cases of primary hyperaldosteronism. Endocr J2000;47:657–665.

Medline

JL, Walther MM, Pezzullo JC, et al. Predictive value of preoperative tests in discriminating bilateral adrenal hyperplasia from an aldosterone producing adrenal adenoma. J Clin Endocrinol Metab2000;85:4526–4533.

Abstract/FREE Full Text

â†µ

MagillSB, Raff H, Shaker JL, et al. Comparison of adrenal vein sampling and computed tomography in the differentiation of primary aldosteronism. J Clin Endocrinol Metab2001;86:1066–1071.

Abstract/FREE Full Text

â†µ

BlumenfeldJD, Sealey JD, Schlussel Y, et al. Diagnosis and treatment of primary hyperaldosteronism. Ann Intern Med1994;121:877–885.

Abstract/FREE Full Text

â†µ

McMahonGT, Dluhy RG. Glucocorticoid remediable aldosteronism. Cardiol Rev2004;12:44–48.

CrossRefMedline

â†µ

SywakM, Pasieka JL. Long-term follow-up and cost benefit of adrenalectomy in patients with primary hyperaldosteronism. Br J Surg2002;89: 1587–1593.

CrossRefMedline

â†µ

DunnickNR, Doppman JL, Mills SR, Gill JR. Preoperative diagnosis and localization of aldosteronomas by measurement of corticosteroids in adrenal venous blood. Radiology1979;133:331–333.

Abstract/FREE Full Text

â†µ

DoppmanJL, Gill JR Jr. Hyperaldosteronism: sampling the adrenal veins. Radiology1996;198: 309–312.

FREE Full Text

â†µ

YoungWF, Stanson AW, Grant CS, GB, van Heerden JA. Primary aldosteronism: adrenal venous sampling. Surgery1996;120:913–920.

CrossRefMedline

â†µ

KaltsasGA, Mukherjee JJ, Kola B, et al. Is ovarian and adrenal venous catheterisation and sampling helpful in the investigation of hyperandrogenic women? Clin Endocrinol (Oxf)2003;59:34–43.

CrossRefMedline

â†µ

StowasserM. Primary aldosteronism [PhD thesis]. Brisbane, Australia: University of Queensland, 1997.

â†µ

HiramatsuK, Yamada T, Yukimura Y, et al. A screening test to identify aldosterone-producing adenoma by measuring plasma renin activity. Arch Intern Med1981;141:1589–1593.

Abstract/FREE Full Text

â†µ

DoppmanJL. The dilemma of bilateral adrenocortical nodularity in Conn's and Cushing's syndromes. Radiol Clin North Am1993;31:1039–1050.

Medline

â†µ

HaenelLC 4th, Hermayer KL. A case of unilateral adrenal hyperplasia: the diagnostic dilemma of hyperaldosteronism. Endocr Pract2000;6:153–158.

Medline

â†µ

OmuraM, Sasano H, Fujiwara T, Yamaguchi K, Nishikawa T. Unique cases of unilateral hyperaldosteronism due to multiple adrenal micronodules, which can only be detected by selective adrenal venous sampling. Metabolism2002;51:350–355.

CrossRefMedline

â†µ

GordonRD. The challenge of more robust and reproducible methodology in screening for primary aldosteronism. J Hypertens2004;22:251–255.

Medline

â†µ

Fritsch NevesM, Schiffrin EL. Aldosterone: a risk factor for vascular disease. Curr Hypertens Rep2003;5:59–65.

Medline

GerlingIC, Sun Y, Ahokas RA, et al. Aldosteronism: an immunostimulatory state precedes proinflammatory/fibrogenic cardiac phenotype. Am J Physiol Heart Circ Physiol2003;285:H813–H821.

Abstract/FREE Full Text

KozakovaM, Buralli S, Palombo C, et al. Myocardial ultrasonic backscatter in hypertension: relation to aldosterone and endothelin. Hypertension2003;41:230–236.

Abstract/FREE Full Text

SchmidtBM, Schmieder RE. Aldosterone-induced cardiac damage: focus on blood pressure independent effects. Am J Hypertens2003;16:80–86.

CrossRefMedline

â†µ

Du CailarG. Cardiac consequences of primary hyperaldosteronism. Ann Cardiol Angeiol (Paris)2004;53:147–149.

Medline

â†µ

FrancisIR, Gross MD, Shapiro B, Korobkin M, Quint LE. Integrated imaging of adrenal disease. Radiology1992;184:1–13.

FREE Full Text

â†µ

DunnickNR, Leight GS, Roubidoux MA, Leder RA, son E, Kurylo L. CT in the diagnosis of primary aldosteronism: sensitivity in 29 patients. AJR Am J Roentgenol1993;160:321–324.

Abstract/FREE Full Text

â†µ

AnsonBJ, Cauldwell EW, Pick JW, Beaton LE. The blood supply of the kidneys, suprarenal gland and associated structures. J Urol1948;60:714–737.

Medline

â†µ

GagnonR. The venous drainage of the human adrenal gland. Rev Can Biol1956;14:350–359.

Medline

â†µ

stoneFR. The suprarenal veins. Am J Surg1957;94:615–620.

CrossRefMedline

â†µ

MonkhouseWS, Khalique A. The adrenal and renal veins of man and their connections with azygos and lumbar veins. J Anat1986;146:105–115.

Medline

â†µ

BooksteinJJ. The roles of angiography in adrenal disease. In: Abram's angiography. 3rd ed. Boston, Mass: Little, Brown, 1983; 1395–1424.

â†µ

StackSP, Rosch J, Cook DM, Sheppard BC, Keller FS. Anomalous left adrenal venous drainage directly into the inferior vena cava. J Vasc Interv Radiol2001;12:385–387.

Medline

â†µ

SpiritusT, Zaman Z, Desmet W. Iodinated contrast media interfere with gel barrier formation in plasma and serum. Clin Chem2003;49:1187–1189.

FREE Full Text

â†µ

WaltersNA, Thomson KR. Urogenital venography. In: Rifkin MD, Thomson K, Rickards D, S, eds. Practical interventional uroradiology. Edinburgh, Scotland: Arnold, 1993; chap 11.

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Abstract

Introduction

Why Perform Adrenal Vein Sampling?

Clinical Experience

Aldosteronism

Shortcomings and Value of CT

Anatomy of the Adrenal Veins

Variations of the Left Renal Vein

How to Recognize the Right Adrenal Vein

How to Perform Adrenal Vein Sampling

Analysis of the Results

Complications

Conclusions

References

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> > > > > > > > > > > > > > > > >> > > > > > > > > > > > > > > > > > The other question was about adrenalectomies. The > > > > > > > > > > > > > > > > endocrinologist at> > > > > > > > > > > > > > > > > > Dartmouth as well as the one here in Maine that I see think I > > > > > > > > > > > > > > > > should> > > > > > > > > > > > > > > > > > have an adrenalectomy. One suggests a general sugeon at > > > > > > > > > > > > > > > > Dartmouth by> > > > > > > > > > > > > > > > > > the name of Laycock and the other is suggesting a Maine> > > > > > > > > > > > > > > > > > Oncology surgeon (I'veheard a lot of good about the oncology> > > > > > > > > > > > > > > > > > surgeon) by the name of MacGilvary. My question is what type of> > > > > > > > > > > > > > > > > > surgeon should I be seeing ? I would rather not go back to > > > > > > > > > > > > > > > > Dartmouth> > > > > > > > > > > > > > > > > > for several reasons but someof you told me before that my local > > > > > > > > > > > > > > > > endo> > > > > > > > > > > > > > > > > > was foolish for sending me to the oncology surgeon. The endo is > > > > > > > > > > > > > > > > only> > > > > > > > > > > > > > > > > > sending me to him because she believes he is a good surgeon.Any> > > > > > > > > > > > > > > > > > input would be helpful at thgis point. I apreciate it.> > > > > > > > > > > > > > > > > > Lettie PA in ton Maine> > > > > > > > > > > > > > > > > >> > > > > > > > > > > > > > > > > >> > > > > > > > > > > > > > > > > >> > > > > > > > > > > > > > > > >> > > > > > > > > > > > > > > >> > > > > > > > > > > > > > > >> > > > > > > > > > > > > > > >> > > > > > > > > > > > > > >> > > > > > > > > > > > > >> > > > > > > > > > > > > > > > > > > > > > > > > >> > > > > > > > > > > >> > > > > > > > > > >> > > > > > > > > >> > > > > > > > >> > > > > > > >> > > > > > >> > > > > >> > > > >> > > >> > >> >>

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|2001 Archive

|March 2001

|Magill et al. 86 (3): 1066

Comparison of Adrenal Vein Sampling and Computed Tomography in the Differentiation of Primary Aldosteronism1

B. Magill,

Hershel Raff,

ph L. Shaker,

C. Brickner,

E. Knechtges,

E. Kehoe and

W. Findling

- Author Affiliations

Endocrine-Diabetes Center, Departments of Medicine and Radiology, St. Luke's Medical Center, Milwaukee, Wisconsin 53215

Address correspondence and requests for reprints to: Dr. B. Magill, Endocrinology and Diabetes, 2801 West Kinnickinnic River Parkway, Suite 245, Milwaukee, Wisconsin 53215. E-mail: steven_magill@....

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Abstract

Determination of the etiology of primary aldosteronism remains a diagnostic challenge. The most common types of primary aldosteronism are bilateral adrenal hyperplasia (BAH), aldosterone-producing adenomas (APA), and primary adrenal hyperplasia. Computed tomography (CT) and adrenal vein sampling (AVS) are the primary modalities used to differentiate these subtypes. The purpose of this study was to compare AVS and CT imaging of the adrenal glands in patients with hyperaldosteronism in whom CT imaging was normal or in whom focal unilateral or bilateral adrenal abnormalities were detected.

The diagnosis of primary aldosteronism was made in 62 patients based on an elevated plasma aldosterone to PRA ratio and an elevated urinary aldosterone excretion rate. Thirty-eight patients had CT imaging and successful bilateral adrenal vein sampling and were included in the final analysis. AVS was considered the gold standard in determining the specific subtype of primary aldosteronism.

There were 15 patients with APA, 21 patients with BAH, and 2 patients with primary adrenal hyperplasia. Plasma aldosterone was significantly higher in patients with APA (46.3 ± 8.5 ng/dL; 1284 ± 235 pmol/L) than in those with BAH (29.3 ± 2.4 ng/dL; 813 ± 11 pmol/L; P < 0.05). Plasma potassium was significantly lower in patients with APA (3.1 ± 0.1 mmol/L) than in patients with BAH (3.5 ± 0.1 mmol/L; P < 0.02). There was considerable overlap in the other biochemical indices (e.g. PRA and urinary aldosterone) in patients with the different subtypes.

In patients with APA proven by AVS, eight had concordant findings with CT imaging, four had discordant findings, and three had normal CT imaging. In patients with BAH proven by AVS, four had concordant findings with CT imaging, eight had discordant findings, and nine had normal CT imaging. Compared with AVS, CT imaging was either inaccurate or provided no additional information in 68% of the patients with primary aldosteronism.

We conclude that adrenal CT imaging is not a reliable method to differentiate primary aldosteronism. Adrenal vein sampling is essential to establish the correct diagnosis of primary aldosteronism.

PRIMARY ALDOSTERONISM is the most common form of secondary hypertension. Patients with primary aldosteronism classically present with poorly controlled hypertension associated with hypokalemia (1). However, it has become apparent that many patients with primary aldosteronism present with normokalemia (2). Based on previous reports, 1–2% of patients with hypertension have primary aldosteronism (3, 4). However, the prevalence of primary aldosteronism in patients evaluated in a primary care clinic for hypertension has been reported to be approximately 10% (5). An even higher prevalence has been found in a referral clinic specializing in treatment of hypertension (6). Therefore, more widespread screening for primary aldosteronism appears to be warranted.

The appropriate treatment of primary aldosteronism depends on the correct differential diagnosis. Of the various subtypes of primary aldosteronism, aldosterone-producing adenomas (APA) and bilateral adrenal hyperplasia (BAH), also known as idiopathic aldosteronism, account for over 95% of all cases. Primary adrenal hyperplasia (PAH) or unilateral hyperplasia is an unusual subtype that physiologically and biochemically mimics APA (7). Glucocorticoid-remediable aldosteronism is a rare familial subtype with an autosomal dominant inheritance pattern (8, 9). Primary aldosteronism has uncommonly been associated with adrenal carcinoma (10).

APAs are typically amenable to unilateral adrenalectomy, which corrects the hypokalemia and can attenuate the hypertension (11). Medical management of BAH is generally recommended, as total or subtotal adrenalectomy results in cure rates of only 20–38% (11, 12).

After the diagnosis of primary aldosteronism, imaging of the adrenal glands with computed tomography (CT) is recommended to help delineate the subtype (13). Magnetic resonance is a promising technique in subtype evaluation, but is not as cost-effective as CT (14). With improved spatial resolution of CT imaging, an increasing number of adrenal abnormalities are being detected (15).

Adrenal vein sampling (AVS) was initially described in the 1960s and appeared useful in the delineation of primary aldosteronism (16). The technique fell into disfavor due to the technical difficulty of cannulating both adrenal veins (17). With improved radiological and angiographic techniques, AVS has reemerged and is considered the gold standard in determining the etiology of hyperaldosteronism (17, 18). Other methods, including saline suppression testing, posture studies, captopril challenge, and the use of biochemical markers, lack the requisite sensitivity necessary to differentiate the etiology of hyperaldosteronism (2).[ 6-Î²-131I]Iodomethyl-19-norcholesterol scanning, an alternate method of differentiating the cause of hyperaldosteronism (19), is not universally available and lacks sensitivity if the adrenal nodule is less than 1–1.5 cm in diameter (20). Adrenal venography has essentially been abandoned because of the high risk of adrenal hemorrhage from the contrast load (18).

The current study compared CT imaging with bilateral adrenal vein sampling in the differentiation of primary aldosteronism. We hypothesize that CT imaging is not a dependable approach in the differential diagnosis of primary aldosteronism.

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Subjects and Methods

Patients

This was a retrospective analysis of patients who were referred for evaluation of suspected primary aldosteronism from 1987–1997. The patients had a history of poorly controlled hypertension, which was often, but not always, associated with hypokalemia. Many of the patients were taking two or more antihypertensive agents and potassium supplements. Patients taking spironolactone or amiloride were switched to other antihypertensive agents at least 4 weeks before evaluation.

A plasma aldosterone to PRA ratio (Aldo/PRA) of 20 or greater in conjunction with a PRA less than 1.0 ng/mL·h (<0.278 ng/L·s) was used as the initial screening criteria (2). Patients were instructed to liberalize daily salt intake for 72 h, and a 24-h urine collection was obtained on the third day. A urinary aldosterone excretion rate of 14 Î¼g/day or greater (â‰¥38.8 nmol/day) (3, 21), confirmed the diagnosis of primary aldosteronism in 62 patients. Urinary sodium excretion of 150 mmol/day or greater indicated adequate salt loading.

CT imaging

In almost all cases, noncontrast CT imaging of the adrenal glands with contiguous 3- to 5-mm cuts were obtained. A GE 9800 scanner was used for CT imaging of adrenal glands for the majority of patients. Three patients who did not undergo AVS had CT scans completed at other institutions and were not included in the accuracy calculations.

AVS

AVS is a direct assessment of hormonal secretion and is more specific than anatomical imaging modalities. Based on extensive past literature, we defined bilaterally successful AVS as the gold standard for differentiation of subtype of hyperaldosteronism. AVS was accomplished via the femoral vein approach (17). Blood samples were obtained from the inferior vena cava (IVC) and the right and left adrenal vein. Samples for aldosterone, cortisol, and epinephrine concentrations were obtained from all three sites. Six of 15 patients with APA, 9 of 21 patients with BAH, and 0 of 2 patients with PAH received cosyntropin infusion [250 Î¼g Cortrosyn (Organon Pharmaceuticals, West Orange, NJ) in 500 mL 5% dextrose at a rate of 100 mL/h] during AVS. Successful AVS was determined by at least a 3-fold elevation in adrenal vein epinephrine and cortisol levels compared with the IVC.

For each sample, the aldosterone concentration was divided by the cortisol concentration to correct for dilutional effects of adrenal vein drainage and herein will be referred to as normalized aldosterone. The diagnoses of APA and PAH were based on the assumption that the ratio of dominant to nondominant normalized aldosterone would be 4 or greater, and the nondominant normalized aldosterone would be less than or equal to the normalized aldosterone in the IVC. For the definition of BAH, the normalized aldosterone in each adrenal vein was equal to or greater than the normalized aldosterone from the IVC. There was no cut-off point of the ratio of dominant to nondominant normalized aldosterone in defining BAH.

Assays

Plasma aldosterone was measured by solid phase RIA (Diagnostic Products, Los Angeles, CA). Intra- and interassay coefficients of variation for measurement of aldosterone were 6% and 9%, respectively (22). Plasma cortisol was measured by an immunofluorometric method. PRA was determined by RIA of angiotensin I generated in vitro (lower limit of detection,âˆ¼ 0.13 ng/mL·h; 0.036 ng/L·s; INCSTAR Corp., Stillwater, MN). Intra- and interassay coefficients of variation for measurement of PRA were 5% and 10%, respectively (22). Plasma epinephrine was measured by high pressure liquid chromatography electrochemical detection (Kline Beecham, Schaumburg, IL).

Data were analyzed by unpaired t tests for comparison, with P < 0.05 considered a significant difference. Ratios of dominant to nondominant normalized aldosterone were analyzed by the Mann-Whitney test. Data are shown as the mean ± sem.

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Results

Patients excluded from AVS

Sixty-two patients were identified as having primary aldosteronism based on clinical and biochemical evaluation. AVS was not performed in 13 patients. Two of these 13 patients had a well defined unilateral adrenal nodule and a normal contralateral gland with CT imaging suggestive of a clinical diagnosis of APA. Unilateral adrenalectomy confirmed the presence of adrenal cortical adenoma in these 2 patients. Both patients had an improvement in control of blood pressure after adrenalectomy. AVS could not technically be performed in 2 patients due to morbid obesity. Another patient developed chest pain just before AVS, and the procedure was aborted. Eight additional patients did not undergo AVS because they refused to undergo the procedure or were lost to follow-up before the sampling could be arranged. The 11 patients who did not undergo AVS were managed with antihypertensive therapy.

Patients who had incomplete AVS

Eleven of 49 patients in whom AVS was attempted had incomplete catheterization of the adrenal glands due to anatomical variation and technical difficulties. Seven had unsuccessful right AVS, and 4 had incomplete sampling due to difficulty in cannulating the left adrenal vein. Despite the technical difficulty, AVS generated sufficient data to provide a diagnosis in 5 of 11 patients who had incomplete AVS. Four of these 11 patients underwent unilateral adrenalectomy, and final pathology demonstrated the presence of an adrenal cortical adenoma. Three of 4 patients with APA who underwent adrenalectomy had improvement or normalization of blood pressure after surgery. Another patient was diagnosed with BAH based on the incomplete AVS findings and was treated medically. Two patients with equivocal AVS results underwent unilateral adrenalectomy, and pathology demonstrated adrenal hyperplasia. These latter 2 patients had no improvement in control of blood pressure after adrenalectomy and were retrospectively thought to have BAH. Four patients had no further differentiation of hyperaldosteronism and also were treated medically. Routine postoperative or post-AVS measurement of plasma aldosterone and PRA was not performed in these patients.

Successful bilateral AVS

Thirty-eight patients had successful bilateral AVS based on the criteria described in the methods. Fifteen patients had APA, 2 patients had PAH, and 21 patients had BAH. Clinical characteristics and data of the patients with APA and BAH are shown in Table 1â‡". There were no differences in gender or age between the 2 groups. The majority of patients identified with primary aldosteronism were male.

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Table 1.

Subject characteristics and clinical data

There were no differences in the effective control of systolic or diastolic blood pressure in the two groups before AVS (Table 1â‡`). PRA levels in patients with APA and BAH were similar. Plasma aldosterone and potassium were lower in the APA group than in the BAH group. Aldo/PRA and the urinary aldosterone excretion rate tended to be higher in patients with APA, but the difference was not statistically significant. Three of 15 patients with APA and 11 of 21 patients with BAH were eukalemic (normal range for plasma potassium, 3.5–5.0 mmol/L) at the time of biochemical evaluation. The 2 patients with PAH had plasma potassium levels of 3.2 and 3.5 mmol/L, respectively. Both of the patients with PAH were Caucasian.

There was no significant difference in normalized aldosterone levels (from the dominant and nondominant adrenal glands) between patients with APA or BAH who did vs. those who did not receive cosyntropin infusion during bilateral AVS. In the APA group, 6 patients received cosyntropin (normalized aldosterone, 14.8 ± 4.7; range, 5.0–30.0), and 9 patients did not (normalized aldosterone, 38.1± 9.8; range, 3.3–86.2; P = 0.090). In the patients with BAH, 9 patients received cosyntropin (normalized aldosterone, 1.6 ± 0.2; range, 1.0–3.2), and 12 patients did not (normalized aldosterone, 2.6 ± 0.5; range, 1.1–7.0; P = 0.137).

APAs based on AVS

There was a significant difference between the mean dominant to nondominant normalized aldosterone levels in APA vs. BAH (Tables 2â‡" and 3â‡"). The ratio of dominant to nondominant normalized aldosterone was greater than 4 in all but 1 patient with APA (Table 2â‡"). In patient 10 the dominant to nondominant normalized aldosterone ratio was 3.8. However, the contralateral normalized aldosterone was less than the normalized aldosterone in the IVC and therefore met the criteria for APA. One patient had a contralateral normalized aldosterone level equal to that in the IVC, but the dominant to nondominant corrected aldosterone ratio was 10 (patient 9, Table 2â‡"). This patient was found to have an adenoma with adrenalectomy and had resolution of hypokalemia and improvement in control of blood pressure after adrenalectomy. There was no difference in the nondominant divided by IVC normalized aldosterone levels in APA vs. BAH.

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Table 2.

Comparison of CT imaging and adrenal vein sampling: APAs and PAH

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Table 3.

Comparison of CT imaging and adrenal vein sampling: BAH

The adrenal glands appeared normal with CT imaging in 3 patients with APA. Another 4 patients had incongruent results in comparison of CT imaging and AVS (patients 12–15, Table 2â‡`). For example, CT imaging demonstrated an ipsilateral adrenal nodule and a plump contralateral adrenal gland in patients 13 and 15 (Table 2â‡`). Aldosterone production lateralized with AVS, and findings were discordant with the CT imaging results in these 2 patients. Confirmation of the presence of an adrenocortical adenoma was obtained in 13 patients who underwent unilateral adrenalectomy. The majority of these patients had improvement of blood pressure control after adrenalectomy (Table 2â‡`). Ten of 13 patients with APA who underwent adrenalectomy had resolution of hypokalemia within 1 week after surgery. Two patients with APA who had successful sampling did not undergo surgery. One of these patients was lost to follow-up, and it is uncertain whether adrenalectomy was completed. Another patient refused surgery and was treated medically (Table 2â‡`).

Primary adrenal gland hyperplasia based on AVS

The ratios of dominant to nondominant normalized aldosterone were 21 and 8 in the two patients with PAH (patients 16 and 17, Table 2â‡`). One patient had normal-appearing adrenal glands on CT. The second patient with PAH had bilateral adrenal enlargement. Both patients underwent unilateral adrenalectomy based on AVS, and pathology confirmed the presence of adrenal hyperplasia. These patients had improvement in blood pressure control and were eukalemic after surgery (Table 2â‡`).

Bilateral adrenal hyperplasia based on AVS

The ratio of dominant to nondominant normalized aldosterone was less than 4 in all but three patients with BAH (Table 3â‡`). Eleven patients had equivalent normalized aldosterone levels between the left and right adrenal glands. In the three patients who had a dominant to nondominant normalized aldosterone ratio of 4 or greater (patients 7, 9, and 21, Table 3â‡`), the ipsilateral and contralateral normalized aldosterone was greater then the normalized aldosterone in the IVC; therefore, these patients met the criteria for BAH. Patient 21 was inappropriately referred for unilateral adrenalectomy based on a dominant to nondominant corrected aldosterone of 4 or more. Two additional patients underwent unilateral adrenalectomy despite evidence of bilateral aldosterone production (patients 3 and 11, Table 3â‡`). None of these three patients had improvement in blood pressure control or resolution of hypokalemia after surgery. These outcomes suggest that the patients did indeed have bilateral aldosterone production, confirming the validity of AVS.

Of the patients with BAH, 8 of 21 had discordance between CT imaging and AVS (patients 14–21, Table 3â‡`). For example, patient 17 had a 2.4-cm diameter left adrenal nodule, but AVS demonstrated bilateral aldosterone production consistent with BAH. Another 9 patients with BAH had normal adrenal glands based on CT imaging. After AVS, 18 of 21 patients with BAH were treated medically with spironolactone or amiloride in combination with other antihypertensive agents. These patients had improvement in control of blood pressure with diuretic therapy and did not undergo further evaluation of PRA or plasma aldosterone.

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Discussion

Primary aldosteronism is diagnosed more frequently with the recognition that the presence of normokalemia does not exclude the disease (23). In addition, utilization of the Aldo/PRA ratio as the primary screening method has enabled more patients to be diagnosed with this secondary form of hypertension (24, 25). A 24-h urinary aldosterone of 14 Î¼g/day or more (â‰¥38.8 nmol/day) obtained during a 3-day high salt diet or salt loading confirms the diagnosis of primary aldosteronism (3, 21).

Adrenal imaging with CT or magnetic resonance is typically performed after confirmation of the diagnosis. CT imaging reportedly has a sensitivity of 58–75% in detecting adrenal adenomas (26, 27). More recent literature suggests that high resolution CT scanning has a sensitivity approaching 80–85% in distinguishing between APA and BAH (28).

Most previous studies demonstrated superiority of AVS over CT scanning in correctly differentiating hyperaldosteronism. In experienced hands, AVS is highly accurate and rarely yields false positive or negative results. Direct comparison of the two methods in one study found only 67% sensitivity with CT imaging and 92% sensitivity using AVS (28). The same group did report one instance in which the AVS falsely suggested the presence of an APA. After adrenalectomy, PRA was persistently suppressed, and plasma aldosterone was elevated, indicating the presence of BAH (28). Another group reported a sensitivity of 70% with CT imaging and 96% with AVS in correctly determining the subtype of hyperaldosteronism (26). Gleason and colleagues determined the correct differential diagnosis of hyperaldosteronism and found 84% sensitivity with CT scanning and 92% sensitivity with AVS (29). Sheaves et al. advocate using CT alone for differentiation of primary aldosteronism based on the reported 100% sensitivity with that modality. They suggest reserving AVS for cases in which there are no adrenal abnormalities identified with CT scanning (30). On the other hand, another group recently found a high degree of inaccuracy with CT imaging. AVS altered management in one third of the cases in this study and was recommended for routine management of primary aldosteronism (31).

Patients with APA are thought to have more dramatic biochemical abnormalities and severe hypertension than patients with BAH (25). However, the present study found a surprising degree of overlap between these groups. The only statistically significant differences were lower plasma potassium and higher plasma aldosterone concentrations in the patients with APA compared with those with BAH. Thirty-seven percent of all patients and 52% of the patients with BAH had normokalemia. Based on these data, screening of patients suspected as having primary aldosteronism should be considered even in the presence of normokalemia.

We found no statistical difference between APA and BAH in control of blood pressure, PRA, Aldo/PRA ratio, or urinary aldosterone excretion rates. Furthermore, there was no particular cut-off level in these indices to separate one subtype of hyperaldosteronism from another. The lack of difference in biochemical features makes the determination of subtypes even more difficult.

Thirty-eight of 49 patients referred for selective catheterization had successful bilateral AVS (78%). Even though bilaterally successful adrenal vein catheterization was not achieved in 11 of 49 patients, interpretable data from unilateral AVS in 5 patients allowed determination of the subtype of primary aldosteronism. Therefore, 88% of patients who underwent AVS in our study had correct differentiation of hyperaldosteronism. Recently, investigators at the Mayo Clinic reported successful bilateral adrenal vein catheterization in 33 of 34 patients evaluated for primary aldosteronism (23). Other groups have reported successful bilateral AVS rates of 63% (32) and 75% (30), respectively, in evaluation of hyperaldosteronism.

We used a normalized aldosterone from each adrenal gland to correct for venous dilution from the right and left adrenal veins during AVS (27). A normalized aldosterone in the dominant divided by the nondominant adrenal gland of 4 or more was used to define the presence of APA or PAH. Fourteen of 15 patients met these criteria for APA. The remaining patient had a dominant to nondominant adrenal, normalized aldosterone ratio of 3.8, and was found to have an adenoma after adrenalectomy. Two patients with APA or PAH had contralateral normalized aldosterone levels equal to that in the IVC, indicating incomplete suppression of contralateral aldosterone production by the APA. In each of these cases, the dominant to nondominant aldosterone ratio was well above the diagnostic cut-point of 4, however. These 2 patients had improvement in blood pressure control and were eukalemic after adrenalectomy.

Doppman et al. used a dominant to nondominant normalized aldosterone ratio of 5 or greater to define APA (28). Young et al. found that 14 of 17 patients with APA had normalized aldosterone ratios of 5 or greater. The remaining 3 patients had normalized aldosterone ratios between 3 and 5 (23).

We found the ratio of dominant to nondominant normalized aldosterone was 4 or more in 3 of 21 patients with BAH, and this could be interpreted as consistent with presence of APA. However, these 3 patients each had nondominant normalized aldosterone levels greater than the corrected aldosterone in the IVC. This is consistent with bilateral autonomous aldosterone production with relative overproduction by 1 dominant adrenal gland. Three of the patients categorized as BAH underwent unilateral adrenalectomy based on slight lateralization of normalized aldosterone. Pathology confirmed the presence of adrenal hyperplasia in each case. Because these patients did not have an improvement in blood pressure after surgery, we retrospectively concluded that these patients did not have PAH, but, rather, BAH. Bilateral adrenalectomy would have had to be performed to actually prove this point.

Previous groups have recommended synthetic ACTH infusion before and during AVS to minimize the pulsatile variation in aldosterone release (17, 33). A potential weakness of the present study is that routine use of cosyntropin infusion during AVS was not instituted in our institution until 1996. Any patient who underwent AVS before that date did not receive cosyntropin infusion. However, the use of synthetic ACTH in the present study did not significantly improve the differentiation of hyperaldosteronism, contrary to previous reports (17, 33).

Fifty-five percent of the patients in this study had a final diagnosis of BAH, 40% had APA, and 5% had a diagnosis of PAH. None of the patients we evaluated had onset of hypertension in the first or second decade of life or a characteristic family history suggestive of glucocorticoid-remediable aldosteronism. Recent literature suggests that BAH accounts for 25–43% of all cases of primary aldosteronism (2, 30). PAH has been reported to represent 1–6% of all cases of hyperaldosteronism (18, 23, 34), and APA constitutes the majority. The higher percentage of patients with BAH in the current study may have been influenced by referral bias. Patients with an obvious unilateral adrenal nodule and dramatic features of primary aldosteronism may undergo adrenalectomy without having AVS or evaluation by an endocrinologist. On the other hand, bilateral adrenal hyperplasia may be recognized more frequently. This may be especially true if patients with milder forms of the disease, such as those with normokalemia, are properly screened for primary aldosteronism.

In this study CT imaging was concordant with pathology results after adrenalectomy in two patients with APA who did not undergo AVS. CT imaging was concordant with AVS in 5 of 11 patients who had unilaterally successful catheterization and 12 of 38 patients who had bilaterally successful AVS. This yields an accuracy of 37% overall for CT scanning in the present study. Adrenal imaging with CT provided no additional information or discordant findings in 68% of the patients who underwent bilaterally successful AVS. The presence of a unilateral adrenal nodule did not preclude a diagnosis of BAH in the present study (patients 14, 17, and 19–21; Table 3â‡`). All of these patients could have been mistakenly diagnosed with APA based on CT imaging, but AVS indicated bilateral aldosterone production consistent with BAH. There is no definable size criterion for unilateral adrenal nodules that absolutely indicates the presence of APA. Despite improved resolution, CT is an insensitive test to define the subtype of primary aldosteronism in the majority of cases.

In conclusion, these results indicate that CT imaging is unreliable in the differentiation of primary aldosteronism. CT imaging has a discordance rate of 34% and can lead to improper therapy of hyperaldosteronism. For complete diagnostic certainty, AVS is essential to define the specific subtype of primary aldosteronism so that appropriate treatment can be recommended.

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Footnotes

â†µ1 Presented in part at the 24th International Aldosterone Conference, New Orleans, Louisiana, June 23, 1998.

Received November 11, 1999.

Revision received June 8, 2000.

Revision received November 15, 2000.

Accepted November 17, 2000.

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References

â†µ

Conn JW. 1955 Presidential address. I. Painting background. II. Primary aldosteronism, a new clinical syndrome. J Lab Clin Med. 45:3–17.

â†µ

Young Jr WF. 1997 Primary aldosteronism: update on diagnosis and treatment. Endocrinologist. 7:213–221.

â†µ

Ganguly A. 1998 Primary aldosteronism. N Engl J Med. 339:1828–1834.

â†µ

Streeten DHP, Tomycz N, GH. 1979 Reliability of screening methods for the diagnosis of primary aldosteronism. Am J Med. 67:403–413.

â†µ

Lim PO, Rodgers P, Cardale K, AD, Mc TM. 1999 Potentially high prevalence of primary aldosteronism in a primary-care population. Lancet. 353:40.

â†µ

Gordon RD, Stowasser M, Tunny TJ, Klemm SA, Rutherford JC. 1994 High incidence of primary aldosteronism in 199 patients referred with hypertension. Clin Exp Pharmacol Physiol. 21:315–318.

â†µ

Banks WA, Kastin AJ, Biglieri EG, Ruiz AE. 1984 Primary adrenal hyperplasia: a new subset of primary hyperaldosteronism. J Clin Endocrinol Metab. 58:783–785.

â†µ

Sutherland DJ, Ruse JL, Laidlaw JC. 1966 Hypertension, increased aldosterone secretion, and low plasma renin activity relieved by dexamethasone. Can Med Assoc J. 95:1109–1119.

â†µ

Dluhy RG, Lifton RP. 1994 Glucocorticoid-remediable aldosteronism. Endocrinol Metab Clin North Am. 23:285–297.

â†µ

Farge D, Chatellier G, Pagny JY. 1987 Isolated clinical syndrome of primary aldosteronism in four patients with adrenocortical carcinoma. Am J Med. 83:635–640.

â†µ

Auda SP, Brennan MF, Gill Jr JR. 1980 Evolution of the surgical management of primary aldosteronism. Ann Surg. 191:1–7.

â†µ

Ferriss JB, Brown JJ, Fraser R, et al. 1975 Results of adrenal surgery in patients with hypertension, aldosterone excess, and low plasma renin concentration. Br Med J. 1:135–138.

â†µ

White EA, Schambelan M, Rost CR, Biglieri EG, Moss AA, Korobkin M. 1980 Use of computed tomography in distinguishing the cause of primary aldosteronism. N Engl J Med. 303:1503–1507.

â†µ

Rossi GP, Chiesura-Corona M, Tregnaghi A, et al. 1993 Imaging of aldosterone-secreting adenomas: a prospective comparison of computed tomography and magnetic resonance imaging in 27 patients with suspected primary aldosteronism. J Hum Hyperten. 7:357–363.

â†µ

Kloos RT, Gross MD, Francis IR, Korobkin M, Shapiro B. 1995 Incidentally discovered adrenal masses. Endocr Rev. 16:460–484.

â†µ

Melby JC, Spark RF, Dale SL, Egdahl RH, Kahn PC. 1967 Diagnosis and localization of aldosterone-producing adenomas by adrenal-vein catheterization. N Engl J Med. 277:1050–1056.

â†µ

Doppman JL, Gill JR, Jr. 1996 Hyperaldosteronism: sampling the adrenal veins. Radiology. 198:309–312.

â†µ

Melby JC, Azar ST. 1993 Adrenal steroids and hypertension: new aspects. Endocrinologist. 3:344–351.

â†µ

Conn JW, Cohen EL, Herwig KR. 1976 The dexamethasone-modified adrenal scintiscan in hyporeninemic aldosteronism (tumor versus hyperplasia). A comparison with adrenal venography and adrenal venous aldosterone. J Lab Clin Med. 88:841–856.

â†µ

Nomura K, Kusakabe K, Maki M, Ito Y, Aiba M, Demura H. 1990 Iodomethylnorcholesterol uptake in an aldosteronoma shown by dexamethasone-suppression scintigraphy: relationship to adenoma size and functional activity. J Clin Endocrinol Metab. 71:825–830.

â†µ

Bravo EL, Tarazi RC, Dustan HP, et al. 1983 The changing clinical spectrum of primary aldosteronism. Am J Med. 74:641–651.

â†µ

Findling JW, Waters VO, Raff H. 1987 The dissociation of renin and aldosterone during critical illness. J Clin Endocrinol Metab. 64:592–595.

â†µ

Young Jr WF, Stanson AW, Grant CS, GB, van Heerden JA. 1996 Primary aldosteronism: adrenal venous sampling. Surgery. 120:913–920.

â†µ

Lins PF, on U. 1986 Plasma aldosterone-plasma renin activity ratio: a simple test to identify patients with primary aldosteronism. Acta Endocrinol (Copenh). 113:564–569.

â†µ

Weinberger MH, Fineberg NS. 1993 The diagnosis of primary aldosteronism and separation of two major subtypes. Arch Intern Med. 153:2125–2129.

â†µ

Geisinger MA, Zelch MG, Bravo EL, et al. 1983 Primary hyperaldosteronism: diagnosis, comparison of CT, adrenal venography, and venous sampling. Am J Radiol. 141:299–302.

â†µ

Dunnick NR, Doppman JL, Gill Jr JR, Strott CA, Keiser HR, Brennan MF. 1982 Localization of functional adrenal tumors by computed tomography and venous sampling. Radiology. 142:429–433.

â†µ

Doppman JL, Gill JR, Jr, DL, et al. 1992 Distinction between hyperaldosteronism due to bilateral hyperplasia and unilateral aldosteronoma: reliability of CT. Radiology. 184:677–682.

â†µ

Gleason PE, Weinberger MG, Pratt JH, et al. 1993 Evaluation of diagnostic tests in the differential diagnosis of primary aldosteronism: unilateral adenoma versus bilateral micronodular hyperplasia. J Urol. 150:1365–1368.

â†µ

Sheaves R, Goldin J, Reznek RH, et al. 1996 Relative value of computed tomography scanning and venous sampling in establishing the cause of primary hyperaldosteronism. Eur J Endocrinol. 134:308–313.

â†µ

Harper R, Ferrett CG, McKnight JA, et al. 1999 Accuracy of CT scanning and adrenal vein sampling in the pre-operative localization of aldosterone-secreting adrenal adenomas. Q J Med. 92:643–650.

â†µ

Blumenfeld JD, Sealey JE, Schussel Y, et al. 1994 Diagnosis and treatment of primary aldosteronism. Ann Intern Med. 121:877–885.

â†µ

Tokunaga K, Nakamura H, Marukawa T, et al. 1992 Adrenal venous sampling analysis of primary aldosteronism: value of ACTH stimulation in the differentiation of adenoma and hyperplasia. Eur Radiol. 2:223–229.

â†µ

Irony I, Kater CE, Biglieri EG, Shackleton CHL. 1990 Correctable subsets of primary aldosteronism. Primary adrenal hyperplasia and renin responsive adenoma. Am J Hyperten. 3:576–582.

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doi: 10.1210/jc.86.3.1066 The Journal of Clinical Endocrinology & Metabolism March 1, 2001 vol. 86 no. 3 1066-1071

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Primary Hyperaldosteronism

Effect of Adrenal Vein Sampling on Surgical Outcome

Fiemu E. Nwariaku, MD; Barbra S. , MD; Auchus, MD, PhD; Shelby Holt, MD; Lori Watumull, MD; Bart Dolmatch, MD; a Nesbitt, MD; Wanpen Vongpatanasin, MD; Victor, MD; Wians, PhD; Livingston, MD; H. Snyder III, MD

Arch Surg. 2006;141:497-503. ABSTRACT

Hypothesis Adrenal vein sampling is superior to computed tomography for subtype differentiation of primary hyperaldosteronism.

Design Retrospective review.

Setting University medical center.

Patients Forty-eight patients (32 men and 16 women) with biochemically confirmed primary hyperaldosteronism.

Main Outcome Measures We compared demographic factors, results of biochemical and imaging studies (computed tomography and adrenal vein sampling), therapy, and patient outcomes.

Results Mean ± SEM adrenal nodule size was 1.54 ± 0.2 cm. Adrenal vein sampling was performed in 41 (85%) of 48 patients, and it was successful in 39 (95%) of those 41 patients. Concordance between computed tomography and adrenal vein sampling was observed in 22 (54%) of the 41 patients. Thirty-two patients underwent successful laparoscopic adrenalectomy. There was 1 complication and no deaths. All 32 patients were cured of hypokalemia.

Conclusion Adrenal vein sampling is superior to image-based techniques for subtype differentiation of primary hyperaldosteronism.

INTRODUCTION

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Introduction

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Discussion

Primary hyperaldosteronism (PH) is a common cause of secondary hypertension, and recent evidence suggests that the prevalence of PH may be increasing.1-3 Although assays needed to establish the biochemical diagnosis have become routinely available, subtype differentiation is particularly challenging. Aldosterone-producing adenomas (APAs), bilateral hyperplasia (BH), primary unilateral hyperplasia, and familial hyperaldosteronism comprise the major subtypes, but APA and BH represent most cases of PH.4 Subtype differentiation is particularly important because surgical therapy for APA is curative, whereas the other subtypes are better managed with potassium-sparing diuretics or aldosterone receptor antagonists. Early studies5 suggested that the use of imaging studies to identify unilateral adrenal enlargement in patients with PH was sufficient to make this distinction. However, modern computed tomographic (CT) scanners detect incidental adrenal nodules (incidentalomas) in 0.35% to 5% of CT scans and contribute to the diagnostic dilemma.6-8 Many of these are nonfunctioning incidental nodules found at the time of evaluation for symptoms unrelated to adrenal origin.7-10

The diagnosis of APA and its localization in patients with PH can be attempted using a variety of techniques, including saline suppression, captopril stimulation, adrenal scintigraphy 6--[131I]iodomethyl-19-norcholesterol, and adrenal vein sampling (AVS). However, the accuracy of these techniques is variable, with the best results being those for AVS.11 Scintigraphy is of limited utility in PH because of the poor image resolution in nodules smaller than 1.5 cm,12 and most APAs are smaller than 15 mm.13-14 Enthusiasm for AVS has been dampened by the relative dearth of technical expertise required and the invasiveness of the technique. However, improved experience with interventional radiologic procedures and catheter-based vascular therapy has caused a resurgence of interest in AVS.

Few large studies13, 15-17 have examined the accuracy of image-based diagnosis of APA using AVS. Some of these studies report an advantage of AVS over image-guided diagnosis; however, the variability in patient selection,15 limits on nodule size,16 and AVS technique (use of corticotropin and cutoff values for positive test results)17 limit conclusions. Furthermore, few of these studies focus on surgical therapy and outcomes of patients with APA.

We examined the utility of CT and AVS in all patients with biochemically confirmed PH seen at the affiliated hospitals and clinics of the University of Texas Southwestern Medical Center between February 1, 2001, and September 30, 2005. Specifically, we determined the accuracy of AVS compared with CT, examined the predictive value of AVS-derived biochemical ratios, and assessed the outcomes for surgically and nonsurgically managed patients.

METHODS

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We retrospectively reviewed the medical records of patients who underwent AVS for PH during a 4-year period (2000-2004). Demographic data, such as patient age, sex, and blood pressure (BP), were examined, as were the use of antihypertensive medications, potassium supplementation, results of biochemical and imaging studies (CT and AVS), and therapy. The biochemical diagnosis of PH was made by using plasma aldosterone concentration–plasma renin activity (PAC/PRA) screening test ratios and was confirmed by saline suppression. Screening test results were considered positive if there was a failure to suppress PAC in the presence of suppressed PRA, as described by other researchers.15-19 Patients with positive screening results underwent confirmation by measurement of 24-hour urinary aldosterone levels (>14.0 µg/24 h [>39 nmol/d]) after saline suppression.

ADRENAL CT Most patients underwent abdominal CT at the University of Texas Southwestern Medical Center by a single radiologist (L.W.) using an Aquilon Super 4 (Toshiba Corp, Tokyo, Japan). Our protocol for adrenal CT is as follows. Scan mode is helical from the diaphragm through the middle of the kidneys. The patient undergoes initial noncontrast CT with 2x2-mm sections followed by injection of 100 mL of Omnipaque 300 (Sanofi Winthrop Markham, Ontario) at 3 mL/s using 2x2-mm sections with a 70-second delay and then 2x2-mm sections with a 10- to 15-minute delay.

ADRENAL VEIN SAMPLING Adrenal vein sampling was performed by 4 interventional radiologists using the same technique, but 1 of these radiologists (B.D.) performed most of the AVS procedures. Our AVS protocol is as follows. When the patient arrives in the radiology suite, a peripheral venous blood sample is obtained for a baseline cortisol level, and corticotropin stimulation is commenced by administration of 0.25 mg of corticotropin1-24 (Cortrosyn; Amphastar Pharmaceuticals Inc, Rancho Cucamonga, Calif) in 300 mL of 5% dextrose in water at a rate of 100 mL/h for the duration of the procedure. This infusion is started at least 20 minutes before obtaining samples.

Bilateral 5F sheaths are inserted into the common femoral veins. Through 1 of these sheaths, a -2 catheter with 2 small side holes is placed in the left renal vein. Then, a search for the right adrenal vein is performed using 5F catheters. Catheterization is confirmed by venography. A 10-mL blood sample is slowly obtained from the right adrenal vein. Immediately thereafter, the left renal vein catheter is repositioned into the left adrenal vein and confirmed by venography before slowly withdrawing a 10-mL blood sample. Once adrenal vein specimens are obtained, either the left- or right-sided catheter is repositioned into the inferior vena cava (IVC) for a 10-mL IVC blood sample, and finally, both catheters are removed, and a 10-mL peripheral venous sample is obtained from 1 of the sheaths. Aldosterone and cortisol levels are measured by radioimmunoassay.

We consider adrenal vein cannulation to be successful when the cortisol levels in both adrenal veins are 3 times (or more) higher than the cortisol level in the IVA, whereas lateralization is considered positive when the adrenal vein aldosterone-cortisol (A/C) ratio in the dominant side is 4 times greater than the A/C ratio in the contralateral side.

STATISTICAL ANALYSIS Results are expressed as mean ± SEM. Comparisons between 2 groups were performed using the t test and among multiple groups using analysis of variance with post hoc analysis. We also compared the sensitivity and specificity of adrenal vein A/C ratios and the A/C ratio of the higher (dominant) vs lower (nondominant) adrenal glands at various thresholds.

RESULTS

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PATIENT CHARACTERISTICS AND PREOPERATIVE FACTORS Forty-eight patients (32 men and 16 women) had biochemically confirmed PH. Forty-one patients (85%) underwent AVS for PH during the 56 months between February 1, 2001, and September 30, 2005. Mean patient age was 52 ± 2 years. All the patients were hypertensive and were being treated with an average of 3 antihypertensive medications. Their mean BP was 157/96 mm Hg. Furthermore, 79% of the patients required potassium supplementation for hypokalemia (mean serum potassium level, 3.5 ± 1 mEq/L). The mean PAC was 52.4 ± 15 ng/dL (1.4±0.4 nmol/L), and the mean PRA was 1.26 ± 0.3 pg/mL (0.03±0.007 pmol/L) per hour. The mean aldosterone-renin ratio was 167 ± 61. Patients with APAs had higher serum aldosterone levels and PRA than patients with bilateral aldosterone hypersecretion (58.0 vs 22.0 ng/dL [1.6 vs 0.6 nmol/L] and 1.36 vs 0.7 pg/mL (0.032 vs 0.016 pmol/L), respectively).

ADRENAL GLAND CT Interpretable CT reports were available for 47 patients and revealed 10 right-sided abnormalities, 18 left-sided abnormalities, 14 bilateral abnormalities, and 5 normal adrenal glands. The mean size of the adrenal nodules in this study was 1.5 ± 0.2 cm.

ADRENAL VEIN SAMPLING Adrenal vein sampling was performed in 41 (85%) of 48 patients. Bilateral adrenal vein cannulation was successful in 39 (95%) of the 41 patients. The right adrenal vein was not cannulated initially in 6 patients but was successfully accessed in 4 patients who underwent another AVS procedure. Procedure-related adrenal hemorrhage occurred in 1 patient, and it resolved spontaneously, with no apparent adverse outcome. Overall, the mean adrenal vein–IVA A/C ratio was 20. The mean right adrenal vein A/C ratio was 30 in patients with right-sided hypersecretion, and the mean left adrenal vein ratio was 14 in patients with left-sided hypersecretion.

Using the criteria mentioned previously herein (adrenal vein A/C ratio in the dominant side is 4 times greater than that in the contralateral side), unilateral aldosterone hypersecretion was identified in 29 (71%) of 41 patients. Fourteen patients lateralized to the right adrenal gland, and 15 lateralized to the left adrenal gland. Twelve patients had bilateral adrenal hyperaldosteronism. The A/C ratio in the unilateral hypersecreting adrenal gland was 34 times the ratio in the contralateral side. The mean dominant-nondominant A/C ratio in patients with BH was 1.9.

AVS RATIOS We examined the predictive value of 3 biochemical ratios (adrenal vein A/C ratio, dominant-nondominant A/C ratio, and contralateral adrenal vein–IVA A/C ratio) for predicting the presence of unilateral aldosterone hypersecretion. The adrenal vein A/C ratio greater than 4 had the best predictive value. The mean dominant-nondominant A/C ratio was higher in patients who underwent surgery, but this difference did not achieve statistical significance (Figure 1).

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Figure 1. Box plots illustrating the dominant-nondominant aldosterone-cortisol ratios in patients who underwent surgery vs patients who were managed medically. The boundary of the box closest to zero indicates the 25th percentile, the line within the box marks the median, and the boundary of the box farthest from zero indicates the 75th percentile. Whiskers above and below the box indicate the 90th and 10th percentiles. Solid circles are outliers.

PREDICTIVE VALUE OF CT VS AVS Forty patients underwent both CT and AVS. The side of abnormality seen on CTs was compared with AVS results of hypersecretion to determine concordance between the 2 studies. Overall, 22 (55%) of 40 patients had concordance between CT and AVS. Twenty patients had unilateral CT abnormalities, and 14 (70%) of them lateralized to the same side (concordant). Of the remaining 6 patients with unilateral CT abnormalities (3 left and 3 right), 1 patient each lateralized to the opposite side and 2 patients each had bilateral hypersecretion. Only 5 of 15 patients (33%) with bilateral CT abnormalities showed concordant bilateral aldosterone hypersecretion. The other 10 patients (67%) demonstrated unilateral hypersecretion. Of the 5 patients with normal-appearing adrenal glands on CT, 1 patient each lateralized to 1 side, and the other 3 patients had bilateral hypersecretion. We found no significant difference between the CT/AVS concordance in patients with micronodules (<1 cm, 67% concordance) and macronodules (>1 cm, 60% concordance). However, the mean age of patients with bilateral CT abnormalities was significantly higher than that of patients with unilateral abnormalities (58 ± 14 vs 47 ± 10 years; P=.008).

Patients with BH diagnosed by AVS were compared with those with a unilateral APA. There was no significant difference in mean age (51.0 vs 51.7 years) or male-female ratio (2:1) between patients with BH and APA. However, the mean PAC/PRA ratio for those with BH vs APA was 50 vs 196.

THERAPY AND OUTCOME Adrenalectomy Thirty-two patients (21 men and 11 women; 14 right adenomas and 18 left adenomas) underwent laparoscopic adrenalectomy for PH: 25 underwent AVS and localized to 1 side for excess aldosterone production and 7 underwent adrenalectomy without previous AVS. Mean operative time was 102 ± 55 minutes, and the mean hospital stay was 1.7 ± 1 days. Mean estimated blood loss was 46 ± 34 mL. All but 1 of the 32 patients were cured of hypokalemia (none required potassium supplements), 6 patients (19%) completely stopped using antihypertensive medication, whereas an additional 15 patients (47%) were normotensive (systolic BP <140 mm Hg) when taking a reduced dosage of antihypertensive medication. Compared with preoperative BPs, the mean postoperative BPs were significantly lower in surgical patients (157/96 vs 127/79 mm Hg; P=.007). Patients were taking an average of 1.8 antihypertensive medications after surgery compared with 3 medications before surgery. The mean potassium level was 4.3 mEq/L after surgery and 3.5 mEq/L before surgery. One patient developed a postoperative deep vein thrombosis that resolved without sequela after anticoagulation therapy. There were no intraoperative complications, conversions to open adrenalectomy, or perioperative deaths. Pathological examination findings revealed 13 adrenal adenomas that averaged 1.32 cm. Of the 2 patients with normal-appearing adrenal glands on CT who underwent adrenalectomy, 1 had a 0.9-cm cortical adenoma and the another had cortical nodular hyperplasia. Both patients had resolution of hypokalemia after surgery.

We compared 25 patients who underwent AVS before adrenalectomy with 7 patients who underwent adrenalectomy without AVS. In the former cohort, 4 patients stopped taking all antihypertensive medications (16%), and 2 (29%) of the 7 patients without AVS were cured of hypertension. Six of these 7 patients were cured of hypokalemia. These patients all had unilateral nodules seen on CT. The mean size of these nodules was 1.9 cm (vs 1.5 cm in the AVS group). One of these 7 patients did not improve after surgery. This patient experienced recurrent hypertension (BP, 194/120 mm Hg) and hypokalemia several months after a laparoscopic adrenalectomy consistent with a wrong diagnosis of APA. This patient's CT initially demonstrated a 0.8-cm cortical nodule in the right adrenal gland, and she had an elevated PAC/PRA ratio of 55.6. Her hypertension is currently controlled with 3 antihypertensive drugs and potassium supplementation. Another patient in the non-AVS group required an increased dosage of antihypertensive medication after surgery. The mean preoperative serum potassium level was 3.4 mEq/L in the AVS group and 2.7 mEq/L in the non-AVS group.

Medical Therapy Fifteen patients (12 with BH and 3 with APA) were treated medically (8 with spironolactone and 4 with eplerenone) because of AVS-diagnosed BH or refusal of surgery. Hypertension improved in 8 of these patients, whereas 2 patients developed worsening hypertension. There were no significant differences between the surgical and nonsurgical groups (Table).

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Table. Comparison Between Surgical Patients and Medically Managed Patients

Based on these findings, a CT-based approach to the evaluation of patients with PH would have led to inappropriate therapy in 45% of the patients. Specifically, 12 (60%) of 20 patients would have been incorrectly excluded from having surgery, whereas nonindicated surgery or wrong side surgery would have been performed in 6 (30%) of 20 patients (Figure 2).

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Figure 2. Projected effects of computed tomography (CT)–guided therapy. BH indicates bilateral hyperplasia; PH, primary hyperaldosteronism; and Tx, treatment.

COMMENT

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This study demonstrates that AVS is markedly superior to abdominal CT in localizing APAs in patients with PH. Successful bilateral adrenal vein cannulation is feasible, and the procedure is associated with low morbidity. The sole use of image-based methods for diagnosing APA or BH would have resulted in inappropriate or suboptimal treatment in almost half of the patients in this study.

These findings are similar to those of previous studies,15-16 which confirm an important role for AVS in patients with PH. Rossi and colleagues16 found AVS to be highly diagnostic of APA in patients with equivocal CT or magnetic resonance imaging results. Although their results remain important, patients with "unequivocal" imaging studies were excluded, as were those with tumors larger than 1.8 cm. Outcomes in patients who underwent surgery are also lacking in their study. We believe that the inclusion of all patients with PH in the present study provides information that is easier to extrapolate to all patients with biochemically confirmed PH, regardless of CT findings. Young and associates15 imposed no CT-based restriction criteria in their study of 203 patients with PH, 92 of whom underwent adrenalectomy. They also noted a high rate of bilateral adrenal cannulation (95%) despite the relatively more stringent criteria used to document successful adrenal vein cannulation (>5 times the IVC cortisol level). They concluded that using CT alone would have led to unnecessary surgery in 24% of the patients and that another 22% of the patients would have been denied surgery inappropriately. We found similar discordant findings between CT and AVS in 30% of the patients with unilateral adrenal abnormalities and in 67% of those with bilateral abnormalities. The former group is of particular concern because of the potential for removal of the biochemically normal adrenal gland. We found no relationship between patient age and the prevalence of micronodules, perhaps because of the smaller sample size; however, the average age of patients with bilateral adrenal lesions was significantly higher than that of those with unilateral lesions, supporting the premise that older patients have a tendency to develop incidental adrenal abnormalities.

Adrenal vein sampling is accurate for predicting the side of aldosterone hypersecretion in APA, and it confirms BH; however, the biochemical ratio with the best predictive value is unclear. Adrenal vein aldosterone levels are unreliable; therefore, most studies suggest the use of A/C ratios, sometimes referred to as the corrected aldosterone.4, 14, 16, 19-20 This ratio is necessary to account for fluctuations in aldosterone secretion due to the invasive procedure and to correct for "dilution" of the adrenal vein sample with blood aspirated from the IVC or left renal vein. However, whether one should use the raw corrected aldosterone from the suspected adrenal gland, the A/C ratio of dominant-nondominant aldosterone, or the suppressed aldosterone from the contralateral adrenal gland is still debated.

Doppman et al18, 21 found that after corticotropin infusion, most patients with APA or primary adrenal hyperplasia demonstrated a corrected aldosterone (A/C ratio) greater than 5:1 between the dominant and nondominant sides. However, more recently, Rossi et al16 found that the ratio of corrected aldosterone in the dominant compared with the nondominant adrenal gland provided the best sensitivity, and the threshold of greater than 2 had the best combination of sensitivity and false-positive rates. We noted a similar trend in the present study. The adrenal vein corrected aldosterone–IVC and the dominant-nondominant ratios performed well (at a threshold of >3 or 4) in predicting APA during this study. At these thresholds, both studies demonstrated high sensitivity and specificity. As expected, increasing the threshold beyond 4 reduced the sensitivity. Using these criteria, AVS and CT findings correlated in 22 of 41 patients, for a concordance rate of 54%. In those with APA, the concordance rate was 70%. This is similar to the 51% to 65% concordance rate in patients with APA described by Young et al.15 We identified a much lower concordance rate (33%) for patients with bilateral CT abnormalities. Specifically, two thirds of this group demonstrated unilateral hypersecretion, underscoring the importance of AVS in patients with any bilateral abnormalities. Finally, we noted a 60% concordance rate in 5 patients with normal findings on adrenal CT, that is, bilateral hypersecretion. This is similar to findings by Young et al,15 who noted a 41% unilateral hypersecretion rate in patients with normal findings on adrenal CT.

Laparoscopic adrenalectomy was associated with low morbidity rates and a short hospital stay in the present study. As with other studies,22-23 hypokalemia resolved in all the patients who underwent adrenalectomy; however, the effect of adrenalectomy on hypertension was variable.23-24 Although the mean postoperative BPs were significantly lower than the mean preoperative levels and the average number of antihypertensive drugs used was lower, individual responses varied. This is similar to findings by others and probably reflects the underlying prevalence of essential hypertension in these patients and the development of fixed hypertension in patients with a secondary cause. However, recent evidence suggests significant cardiovascular benefit by reducing circulating aldosterone levels despite persistent hypertension.25-30 Therefore, we believe that the advantage of reducing aldosterone levels in these patients goes beyond resolution of hypokalemia and hypertension.

A group of 7 highly selected patients seen early in our experience had good outcomes despite not undergoing AVS for localization. These patients had larger nodules and more severe hypokalemia, but 2 of them developed worsening hypertension. We would consider offering unilateral adrenalectomy to patients with large unilateral nodules and completely normal contralateral adrenal glands in the presence of severe PH.

This study did not address the additional cost of AVS, a factor that should be considered in evaluating the approach to therapy. The recent availability of a selective aldosterone receptor antagonist, eplerenone, provides a safe and effective means of preventing the deleterious effects of excess circulating aldosterone. As the cost of such drugs decreases, and the safety profile improves, enthusiasm to treat patients with APA with these agents may ensue. In fact, studies31-32 have documented improvement in BP, and hypokalemia in patients with APA managed medically using aldosterone receptor antagonists. Although many researchers believe that the cost-benefit analysis favors adrenalectomy in patients who can withstand surgery, few direct comparisons exist. Sywak and Pasieka33 suggested a cost-benefit advantage for adrenalectomy compared with life-long medical therapy in patients with PH; however, that study was underpowered.

The age of the patient, the severity of hypertension, and comorbidity must be considered in the therapeutic decision for individual patients. The lack of long-term surveillance of patients in this study is a limitation because the beneficial effects of therapy could occur long after surgery. However, we have used the resolution of hypokalemia as a surrogate for relief of hyperaldosteronism, understanding full well that we may have patients with persistent or recurrent hyperaldosteronism long after unilateral adrenalectomy, hence our ongoing follow-up of these patients.

Abdominal CT is unreliable in correctly identifying the abnormal adrenal gland in patients with PH due to APAs, particularly when both adrenal glands are abnormal. We believe that the liberal use of adjunctive diagnostic studies, such as AVS, is crucial for accurate subtype differentiation in patients with PH. Adrenal vein sampling is accurate and has a low morbidity rate. Laparoscopic adrenalectomy is associated with excellent outcomes in patients with APAs.

AUTHOR INFORMATION

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Correspondence: Fiemu E. Nwariaku, MD, Department of Surgery, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-9156 (fiemu.nwariaku@...

).

Accepted for Publication: December 18, 2005.

Previous Presentation: This paper was presented at the 113th Scientific Session of the Western Surgical Association; November 8, 2005; Rancho Mirage, Calif; and is published after peer review and revision. The discussions that follow this article are based on the originally submitted manuscript and not the revised manuscript.

Author Affiliations: Departments of Surgery (Drs Nwariaku, , Holt, Livingston, and Snyder), Medicine (Drs Auchus, Nesbitt, Vongpatanasin, and Victor), Radiology (Drs Watumull and Dolmatch), and Pathology (Dr Wians), University of Texas Southwestern Medical Center, Dallas.

REFERENCES

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1. Loh KC, Koay ES, Khaw MC, Emmanuel SC, Young WF Jr. Prevalence of primary aldosteronism among Asian hypertensive patients in Singapore. J Clin Endocrinol Metab. 2000;85:2854-2859. FREE FULL TEXT

2. Rossi E, Regolisti G, Negro A, Sani C, Davoli S, Perazzoli F. High prevalence of primary aldosteronism using postcaptopril plasma aldosterone to renin ratio as a screening test among Italian hypertensives. Am J Hypertens. 2002;15:896-902. FULL TEXT | WEB OF SCIENCE | PUBMED

3. Fardella CE, Mosso L, Gomez- C, et al. Primary hyperaldosteronism in essential hypertensives: prevalence, biochemical profile, and molecular biology. J Clin Endocrinol Metab. 2000;85:1863-1867. FREE FULL TEXT

4. Young WF Jr. Minireview: primary aldosteronism–changing concepts in diagnosis and treatment. Endocrinology. 2003;144:2208-2213. FREE FULL TEXT

5. White EA, Schambelan M, Rost CR, Biglieri EG, Moss AA, Korobkin M. Use of computed tomography in diagnosing the cause of primary aldosteronism. N Engl J Med. 1980;303:1503-1507. WEB OF SCIENCE | PUBMED

6. Nwariaku FE, Champine J, Kim LT, Burkey S, O'keefe G, Snyder WH III. Radiologic characterization of adrenal masses: the role of computed tomography–derived attenuation values. Surgery. 2001;130:1068-1071. FULL TEXT | WEB OF SCIENCE | PUBMED

7. Korobkin M. CT characterization of adrenal masses: the time has come. Radiology. 2000;217:629-632. FREE FULL TEXT

8. Boland GW, Lee MJ, Gazelle GS, Halpern EF, Mc MM, Mueller PR. Characterization of adrenal masses using unenhanced CT: an analysis of the CT literature. AJR Am J Roentgenol. 1998;171:201-204. FREE FULL TEXT

9. Francis IR, Korobkin M. Incidentally discovered adrenal masses. Magn Reson Imaging Clin N Am. 1997;5:147-164. PUBMED

10. Bastounis EA, Karayiannakis AJ, Anapliotou ML, Nakopoulou L, Makri GG, Papalambros EL. Incidentalomas of the adrenal gland: diagnostic and therapeutic implications. Am Surg. 1997;63:356-360. WEB OF SCIENCE | PUBMED

11. Ganguly A. Primary aldosteronism. N Engl J Med. 1998;339:1828-1834. FULL TEXT | WEB OF SCIENCE | PUBMED

12. Nomura K, Kusakabe K, Maki M, Ito Y, Aiba M, Demura H. Iodomethylnorcholesterol uptake in an aldosteronoma shown by dexamethasone-suppression scintigraphy: relationship to adenoma size and functional activity. J Clin Endocrinol Metab. 1990;71:825-830. FREE FULL TEXT

13. Rossi GP, Chiesura-Corona M, Tregnaghi A, et al. Imaging of aldosterone-secreting adenomas: a prospective comparison of computed tomography and magnetic resonance imaging in 27 patients with suspected primary aldosteronism. J Hum Hypertens. 1993;7:357-363. WEB OF SCIENCE | PUBMED

14. Geisinger MA, Zelch MG, Bravo EL, Risius BF, O'Donovan PB, Borkowski GP. Primary hyperaldosteronism: comparison of CT, adrenal venography, and venous sampling. AJR Am J Roentgenol. 1983;141:299-302. FREE FULL TEXT

15. Young WF, Stanson AW, GB, Grant CS, Farley DR, van Heerden JA. Role for adrenal venous sampling in primary aldosteronism. Surgery. 2004;136:1227-1235. FULL TEXT | WEB OF SCIENCE | PUBMED

16. Rossi GP, Sacchetto A, Chiesura-Corona M, et al. Identification of the etiology of primary aldosteronism with adrenal vein sampling in patients with equivocal computed tomography and magnetic resonance findings: results in 104 consecutive cases. J Clin Endocrinol Metab. 2001;86:1083-1090. FREE FULL TEXT

17. Magill SB, Raff H, Shaker JL, et al. Comparison of adrenal vein sampling and computed tomography in the differentiation of primary aldosteronism. J Clin Endocrinol Metab. 2001;86:1066-1071. FREE FULL TEXT

18. Doppman JL, Gill JR Jr, DL, et al. Distinction between hyperaldosteronism due to bilateral hyperplasia and unilateral aldosteronoma: reliability of CT. Radiology. 1992;184:677-682. FREE FULL TEXT

19. Young WF Jr, Klee GG. Primary aldosteronism: diagnostic evaluation. Endocrinol Metab Clin North Am. 1988;17:367-395. WEB OF SCIENCE | PUBMED

20. Young WF Jr, Stanson AW, Grant CS, GB, van Heerden JA. Primary aldosteronism: adrenal venous sampling. Surgery. 1996;120:913-919. FULL TEXT | WEB OF SCIENCE | PUBMED

21. Doppman JL, Gill JR Jr. Hyperaldosteronism: sampling the adrenal veins. Radiology. 1996;198:309-312. FREE FULL TEXT

22. Rossi GP, Sacchetto A, Visentin P, et al. Changes in left ventricular anatomy and function in hypertension and primary aldosteronism. Hypertension. 1996;27:1039-1045. FREE FULL TEXT

23. Sawka AM, Young WF, GB, et al. Primary aldosteronism: factors associated with normalization of blood pressure after surgery. Ann Intern Med. 2001;135:258-261. FREE FULL TEXT

24. Celen O, O'Brien MJ, Melby JC, Beazley RM. Factors influencing outcome of surgery for primary aldosteronism. Arch Surg. 1996;131:646-650. FREE FULL TEXT

25. Rocha R, -Berger CL, Yang P, Scherrer R, Delyani J, McMahon E. Selective aldosterone blockade prevents angiotensin II/salt-induced vascular inflammation in the rat heart. Endocrinology. 2002;143:4828-4836. FREE FULL TEXT

26. Rocha R, Rudolph AE, Frierdich GE, et al. Aldosterone induces a vascular inflammatory phenotype in the rat heart. Am J Physiol Heart Circ Physiol. 2002;283:H1802-H1810. FREE FULL TEXT

27. Rocha R, Funder JW. The pathophysiology of aldosterone in the cardiovascular system. Ann N Y Acad Sci. 2002;970:89-100. WEB OF SCIENCE | PUBMED

28. Rocha R, GH. Rationale for the use of aldosterone antagonists in congestive heart failure. Drugs. 2002;62:723-731. FULL TEXT | WEB OF SCIENCE | PUBMED

29. Stier CT Jr, Chander PN, Rocha R. Aldosterone as a mediator in cardiovascular injury. Cardiol Rev. 2002;10:97-107. FULL TEXT | PUBMED

30. ez DV, Rocha R, Matsumura M, et al. Cardiac damage prevention by eplerenone: comparison with low sodium diet or potassium loading. Hypertension. 2002;39:614-618. FREE FULL TEXT

31. Ghose RP, Hall PM, Bravo EL. Medical management of aldosterone-producing adenomas. Ann Intern Med. 1999;131:105-108. FREE FULL TEXT

32. Bravo EL. Medical management of primary hyperaldosteronism. Curr Hypertens Rep. 2001;3:406-409. PUBMED

33. Sywak M, Pasieka JL. Long-term follow-up and cost benefit of adrenalectomy in patients with primary hyperaldosteronism. Br J Surg. 2002;89:1587-1593. FULL TEXT | WEB OF SCIENCE | PUBMED

Discussion

s, MD, San , Tex: The diagnosis and treatment of PH really has become quite a challenge and more complicated since Conn's initial description back in 1955. The multiple subtypes, as Dr Nwariaku had showed you, have really necessitated screening tests with aldosterone-renin ratios in conjunction with an aldosterone suppression test. Once confirmed, the patient is typically followed with an imaging study to localize the adenoma. The decision to proceed with AVS is controversial. Dr Nwariaku and his colleagues have done an excellent job presenting results that suggest that this study should be performed in all patients. Their manuscript differed slightly from their abstract by including 50% more patients who underwent adrenalectomy and excluding the patients who had aldosterone-renin ratios that were less than 20. It is from these data that I have a few questions.

My first question relates to the patient cohort that did not undergo AVS. In this study, 86% (6/7) of these patients who underwent adrenalectomy with CT imaging alone had improvement in the management of their hypertension. This compares with only 60% (15/25) of the patients who had improvement following AVS and subsequent adrenalectomy. The excellent results in the patients who had CT alone suggests that the 54% concordance rate in the patients with both CT and AVS did not apply to these patients. There appears to be a selection bias. How were the patients selected to undergo adrenalectomy with CT alone, and which factors may have contributed to the increased success rate in these patients? Could the specificity of the aldosterone-renin ratio elevated to amount "X" in conjunction with a dominant nodule on CT of greater than a size "Y" be high enough to proceed directly to surgery?

Second, the negative effects of hyperaldosteronism on the cardiovascular system have recently come to the forefront in the medical literature. As we know, adrenalectomy in PH is very successful in leading to the resolution of the hypokalemia, with 100% success rates in those studies. It now may have the added effect of improving cardiac morbidity. Do you have follow-up aldosterone levels in your patients?

My final question is really a difficult one to ask as an endocrine surgeon. Eplerenone, a selective aldosterone receptor antagonist, does not have the side effects that spironolactone did. In essence, the patients don't have the gynecomastia or the vaginal bleeding. It is well tolerated. It costs approximately $100 a month. Comparing this to the cost of AVS in conjunction with laparoscopic adrenalectomy, at least in my institution, it is more expensive to get the venous sampling than to do the adrenalectomy. It would probably take about 12 to 15 years to break even. Do you think that PH will become a medical disease?

Dr Nwariaku: Thank you, Dr s, for your thoughtful questions. In response to the question about the outcomes of patients who underwent surgery without AVS, those patients were patients we enrolled early on, at the beginning of the study, and, interestingly, they demonstrated more severe hyperaldosteronism. Their nodule sizes were significantly larger, over 2 cm. They had more severe hypertension, profound hypokalemia, and required more antihypertensive drugs. So these patients were included in the surgical group but did not undergo AVS because of their unequivocal severe hyperaldosteronism.

In response to your question about eplerenone, there has been interest by some to treat patients with APAs medically, with good results. And now with eplerenone, which has a more favorable side effect profile, there is more enthusiasm to do that. The question becomes one of cost. And that is one of the limitations of our study. There are no data looking at the cost of long-term use of eplerenone compared with surgery. There is a study I think by Dr Pasieka and colleagues from several years ago which examines the medical management with spironolactone vs surgery, and they demonstrated cost benefit for surgical patients who underwent adrenalectomy. This question probably needs to be examined in the future.

Clive S. Grant, MD, Rochester, Minn: We agree entirely that AVS is an excellent and vitally important technique, but not necessarily for every patient. Have you found a subgroup of patients for whom you might be able to rely on CT, for example, a younger patient with more severe disease, with a single nodule in 1 adrenal gland and the contralateral adrenal that is well visualized and normal? Second, if guided by AVS, how often have you identified unilateral hyperplasia as the pathology after adrenalectomy, and what has been the outcome of those patients?

Dr Nwariaku: The findings with AVS are similar to those presented by your group. Currently, we offer AVS to all our patients. Part of the reason is that we see patients with abdominal CT obtained from outside radiologists, and many of these are either inadequately performed or improperly interpreted. So we are either repeating them or sending them to AVS.

The subgroup of patients that I would anticipate would not require AVS would be patients such as those I just described, the patient with more severe hyperaldosteronism, more severe hypokalemia, and larger nodules. And if you examine the older data, when CT was used and found to be accurate, those nodules were usually 2 and 2.5 cm, and the other adrenal gland was normal. So such patients may benefit from adrenalectomy without AVS.

Quan-Yang Duh, MD, San Francisco, Calif: Of the 20 patients who had unilateral disease by CT scan, 14 had a concordant study and 6 had a discordant study. Were there any differences in the size of the tumors in the concordant vs the discordant ones? We all agree that if the CT scan shows bilateral normal or bilateral abnormal glands, you need venous sampling. But the discordant percentage of 30% seems high.

The second question is, after a positive venous sampling finding high secretion on one side only, have you ever had a failed operation? We have at least 1 failure after a positive venous sampling. You would expect selected venous catheterization to be 100% accurate, if positive, but it is not.

Dr Nwariaku: There were no differences in the sizes of the nodules in the concordant or discordant lesions. Part of that may just be that this subgroup is a highly selected group and has really small tumors, so I am not sure that we would find those differences.

Now, regarding the question of failed AVS, this is a small group of patients, but we haven't had that problem. Now, the Mayo Clinic reports about a 1% incidence of primary unilateral adrenal hyperplasia. Obviously, the long-term follow-up is where the answer to that question will lie. It is possible that there are patients who have bilateral hyperaldosteronism which starts off on one side and eventually develop hypersecretion on the other side, or this could be pure primary unilateral hyperplasia.

Snyder, MD, Temple, Tex: Here is not an uncommon clinical problem that we might face. Adrenal vein sampling (as you pointed out) of the right adrenal vein is difficult to sometimes access, but we get results from the left adrenal vein in the patient with bilateral adrenal nodules. The left adrenal vein aldosterone is increased, but we have no values from the right. How do you manage that patient?

Dr Nwariaku: I think there are 2 patients in this series where we had that problem. And we cheated a little bit. If we can demonstrate that the samples from the area of the right adrenal vein, even if we are not absolutely sure of right vein cannulation, are suppressed compared with the IVC samples, and if the ratio is high, that is, 10:1, for instance, instead of 4:1, we have considered that successful and operated on those 2 patients and they did just well. So that is one possibility. The other way would be to put the patient on eplerenone. Another option is to repeat the AVS procedure. As I showed, 2 patients required a repeat sampling study to obtain the correct numbers.

Cord Sturgeon, MD, Chicago, Ill: My comments are directed toward the data in your abstract. You stated in the abstract that 20 patients had undergone successful adrenalectomy. By looking at the data, I assume that this group of 20 is composed of 12 patients with unilateral CT scan findings and concordant lateralization with AVS and 8 patients with bilateral nodules which then lateralized on AVS, making the 20.

What about those 5 or 6 patients who had a unilateral nodule on the CT scan but discordant lateralization by AVS? Since we know that aldosteronomas are almost always very small, 0.5 to maybe 2 cm, and in many cases they are smaller than the limit of resolution of the imaging studies that are used, shouldn't we be resecting all of those adrenal glands that lateralized to even the normal-appearing side? What did you do in those cases?

Dr Nwariaku: My short answer would be, yes, if they have biochemically confirmed PH using fairly stringent criteria, then they have the disease. And if the lesion is not visible on CT scan but the adrenal venous sampling studies are clear, we would perform adrenalectomy on the localized side.

Dr Sturgeon: But nevertheless, if you had a nodule on one side and your AVS showed the secretion was contralateral, you would take out the normal-looking adrenal gland?

Dr Nwariaku: Yes, we would resect the normal-appearing gland.

Biehl, MD, Seattle, Wash: I know it wasn't part of your study, but I am curious to know if the norcholesterol analogue nuclear medicine study NP-59 [6--(131I)iodomethyl-19-norcholesterol] has been useful at all in your institution and in what setting.

Dr Nwariaku: We have not used the norcholesterol or NP-59. Actually, I don't think that this disease is one where it has much benefit, the reason being that about 20% of patients with PH have tumors that are usually less than 1.5 cm, which is below the limits of resolution for NP-59 scintigraphy. So we haven't used it. In addition to that, it is a 3- to 5-day test and you have to obtain the isotope from outside institutions.

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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Adrenal Venous Sampling: Evaluation of the German Conn's RegistryVonend et al.Hypertension 2011;57:990-995.ABSTRACT | FULL TEXT Use of Excel Spreadsheets to Create Interpretive Reports for Laboratory Tests Requiring Complex CalculationsWiansLab Med 2009;40:5-12.FULL TEXT Adrenal incidentaloma: evaluation and managementSingh and BuchJ. Clin. Pathol. 2008;61:1168-1173.ABSTRACT | FULL TEXT Case Detection, Diagnosis, and Treatment of Patients with Primary Aldosteronism: An Endocrine Society Clinical Practice GuidelineFunder et al.J. Clin. Endocrinol. Metab. 2008;93:3266-3281.ABSTRACT | FULL TEXT Will the Lessons From Primary Aldosteronism Change the Treatment of Hypertension and Left Ventricular Hypertrophy?Auchus and DraznerHypertension 2007;50:837-839.FULL TEXT Is There an Unrecognized Epidemic of Primary Aldosteronism? (Pro)Calhoun and KaplanHypertension 2007;50:447-453.FULL TEXT Is There an Unrecognized Epidemic of Primary Aldosteronism? (Con)Kaplan and CalhounHypertension 2007;50:454-458.FULL TEXT Measurement of 18-Hydroxycorticosterone during Adrenal Vein Sampling for Primary AldosteronismAuchus et al.J. Clin. Endocrinol. Metab. 2007;92:2648-2651.ABSTRACT | FULL TEXT

CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP

> > > > > > > > > > > > > > > > > > > >> > > > > > > > > > > > > > > > > > > > > The other question was about> > > adrenalectomies. The> > > > > > > > > > > > > > > > > > > endocrinologist at> > > > > > > > > > > > > > > > > > > > > Dartmouth as well as the one here in> > > Maine that I see think I> > > > > > > > > > > > > > > > > > > should> > > > > > > > > > > > > > > > > > > > > have an adrenalectomy. One suggests> > > a general sugeon at> > > > > > > > > > > > > > > > > > > Dartmouth by> > > > > > > > > > > > > > > > > > > > > the name of Laycock and the> > > other is suggesting a Maine> > > > > > > > > > > > > > > > > > > > > Oncology surgeon (I'veheard a lot of> > > good about the oncology> > > > > > > > > > > > > > > > > > > > > surgeon) by the name of MacGilvary.> > > My question is what type of> > > > > > > > > > > > > > > > > > > > > surgeon should I be seeing ? I would> > > rather not go back to> > > > > > > > > > > > > > > > > > > Dartmouth> > > > > > > > > > > > > > > > > > > > > for several reasons but someof you> > > told me before that my local> > > > > > > > > > > > > > > > > > > endo> > > > > > > > > > > > > > > > > > > > > was foolish for sending me to the> > > oncology surgeon. The endo is> > > > > > > > > > > > > > > > > > > only> > > > > > > > > > > > > > > > > > > > > sending me to him because she> > > believes he is a good surgeon.Any> > > > > > > > > > > > > > > > > > > > > input would be helpful at thgis> > > point. I apreciate it.> > > > > > > > > > > > > > > > > > > > > Lettie PA in ton Maine> > > > > > > > > > > > > > > > > > > > >> > > > > > > > > > > > > > > > > > > > >> > > > > > > > > > > > > > > > > > > > >> > > > > > > > > > > > > > > > > > > >> > > > > > > > > > > > > > > > > > >> > > > > > > > > > > > > > > > > > >> > > > > > > > > > > > > > > > > > >> > > > > > > > > > > > > > > > > >> > > > > > > > > > > > > > > > >> > > > > > > > > > > > > > > >> > > > > > > > > > > > > > > >> > > > > > > > > > > > > > >> > > > > > > > > > > > > >> > > > > > > > > > > > >> > > > > > > > > > > >> > > > > > > > > > >> > > > > > > > > >> > > > > > > > >> > > > > > > >> > > > > > >> > > > > >> > > > >> > > >> > >> >>

June 1, 2011

We all know Dr. Grim's position. There are also many other specialists who

advocate something else. Is one more right than the other? Depends on who you

ask I guess. That's why they get theybucks! big Each one of us know ourselves

also and ultimately have to make the decision that best fits our own situation.

We know if we will be able to stay with Dash, low salt and Spiro. Afterall some

are probably still smoking, have failed dozens of diets, etc. What's the old

saying, " The road to Hell is paved with good intentions! " I'm happy at 50 mg of

Spiro and low salt which by the way is the same as always since I've always been

low salt.

Did you really want to recommend the Baylor U. position in the following post?

Go to the summary and look at figure 8. Do you see AVS anywhere? Looks like

they are advocating surgery if the testing is positive, wonder if they have

changed that in the last 8 years!

- 64 yo morb. ob. male - 12mm X 13mm rt. a.adnoma with previous rt. flank &

testicle pain. I have decided against an adrenalectomy at this time since

Meds. are working so well. Current BP ave. 112/60.

Other Issues/Opportunities: COPD w/ft Oxygen, OSA w Bi-Pap settings 13/19, Type

II Diab. and PTSD

Meds: Duloxetine hcl 80 MG, Mirtazapine 15 MG, Liothyronine 5MCG, Methadone 15

MG(titrating off S-L-O-W-L-Y) , Metoprolol Tartrate 200 MG, Metformin 2000MG,

Lisinopril 2.5MG and Spironolactone 50 MG.

> > > > > > > > > > > > > >

> > > > > > > > > > > > > > > The other question was about adrenalectomies. The

> > > > > > > > > > > > > endocrinologist at

> > > > > > > > > > > > > > > Dartmouth as well as the one here in Maine that I

see think I

> > > > > > > > > > > > > should

> > > > > > > > > > > > > > > have an adrenalectomy. One suggests a general

sugeon at

> > > > > > > > > > > > > Dartmouth by

> > > > > > > > > > > > > > > the name of Laycock and the other is

suggesting a Maine

> > > > > > > > > > > > > > > Oncology surgeon (I'veheard a lot of good about

the oncology

> > > > > > > > > > > > > > > surgeon) by the name of MacGilvary. My question is

what type of

> > > > > > > > > > > > > > > surgeon should I be seeing ? I would rather not go

back to

> > > > > > > > > > > > > Dartmouth

> > > > > > > > > > > > > > > for several reasons but someof you told me before

that my local

> > > > > > > > > > > > > endo

> > > > > > > > > > > > > > > was foolish for sending me to the oncology

surgeon. The endo is

> > > > > > > > > > > > > only

> > > > > > > > > > > > > > > sending me to him because she believes he is a

good surgeon.Any

> > > > > > > > > > > > > > > input would be helpful at thgis point. I apreciate

it.

> > > > > > > > > > > > > > > Lettie PA in ton Maine

> > > > > > > > > > > > > > >

> > > > > > > > > > > > > >

> > > > > > > > > > > > >

> > > > > > > > > > > >

> > > > > > > > > > >

> > > > > > > > > >

> > > > > > > > >

> > > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > >

> > >

> >

>

June 2, 2011

But it is also the recommendation of my doctors and I have no reason to

disbelieve them - I have found nothing in my reading to show that their advice

is misplaced. I recently posted a paper that was presented at the European

conference of the Association of Endocrinologists (or whatever their official

title is) and that also contained the same guidelines so it's not just the

American surgeons.

I'm sure the cut-off is arbitrary and I questioned it myself when I first came

on this site but the general message is if you're young, you have a recent

problem and you have a clear growth on one side and absolutely nothing unusual

with the other, you chances of success at surgery are high and while it is a

risk to skip AVS, it's good odds.

I know you're concerned but the worst possible case scenario (beyond the risks

of surgery) is that it is actually the right side adrenal that is a problem and

then I'd have to take Spiro for life. So I'd have missed my chance to be drug

free but given that the main philosophy of this site is to take drugs for as

long as possible, I'd have thought that wouldn't be such a terrible thought for

most.

H

> > > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > > > > > The other question was about

> > > adrenalectomies. The

> > > > > > > > > > > > > > > > > > > endocrinologist at

> > > > > > > > > > > > > > > > > > > > > Dartmouth as well as the one here in

> > > Maine that I see think I

> > > > > > > > > > > > > > > > > > > should

> > > > > > > > > > > > > > > > > > > > > have an adrenalectomy. One suggests

> > > a general sugeon at

> > > > > > > > > > > > > > > > > > > Dartmouth by

> > > > > > > > > > > > > > > > > > > > > the name of Laycock and the

> > > other is suggesting a Maine

> > > > > > > > > > > > > > > > > > > > > Oncology surgeon (I'veheard a lot of

> > > good about the oncology

> > > > > > > > > > > > > > > > > > > > > surgeon) by the name of MacGilvary.

> > > My question is what type of

> > > > > > > > > > > > > > > > > > > > > surgeon should I be seeing ? I would

> > > rather not go back to

> > > > > > > > > > > > > > > > > > > Dartmouth

> > > > > > > > > > > > > > > > > > > > > for several reasons but someof you

> > > told me before that my local

> > > > > > > > > > > > > > > > > > > endo

> > > > > > > > > > > > > > > > > > > > > was foolish for sending me to the

> > > oncology surgeon. The endo is

> > > > > > > > > > > > > > > > > > > only

> > > > > > > > > > > > > > > > > > > > > sending me to him because she

> > > believes he is a good surgeon.Any

> > > > > > > > > > > > > > > > > > > > > input would be helpful at thgis

> > > point. I apreciate it.

> > > > > > > > > > > > > > > > > > > > > Lettie PA in ton Maine

> > > > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > >

> > > > > > > > > > > > > >

> > > > > > > > > > > > >

> > > > > > > > > > > >

> > > > > > > > > > >

> > > > > > > > > >

> > > > > > > > >

> > > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > >

> > >

> >

>

June 2, 2011

Thank you for the information. I am actually waiting for a call back from the

endocrinologist at Dartmouth . We have been playing a bit of phone tag. I asked

some questions in regards to why they sent me home (hotel room really)when my K

was at 2.3 and i was vomitting only to come to the Dartmouth ER the next morning

because I couldn't lift my arms or head. In a voicemail she apologized for this

and said she will keep trying to call me. I guess I just want some answers. Am

not feeling very confident with Dartmouth at this point.

> > >

> > > The other question was about adrenalectomies. The endocrinologist

> > at Dartmouth as well as the one here in Maine that I see think I

> > should have an adrenalectomy. One suggests a general sugeon at

> > Dartmouth by the name of Laycock and the other is suggesting a

> > Maine Oncology surgeon (I'veheard a lot of good about the oncology

> > surgeon) by the name of MacGilvary. My question is what type of

> > surgeon should I be seeing ? I would rather not go back to Dartmouth

> > for several reasons but someof you told me before that my local endo

> > was foolish for sending me to the oncology surgeon. The endo is only

> > sending me to him because she believes he is a good surgeon.Any

> > input would be helpful at thgis point. I apreciate it.

> > > Lettie PA in ton Maine

> > >

> >

>

June 2, 2011

Thank you

>

> > The other question was about adrenalectomies. The endocrinologist at

> > Dartmouth as well as the one here in Maine that I see think I should

> > have an adrenalectomy. One suggests a general sugeon at Dartmouth by

> > the name of Laycock and the other is suggesting a Maine

> > Oncology surgeon (I'veheard a lot of good about the oncology

> > surgeon) by the name of MacGilvary. My question is what type of

> > surgeon should I be seeing ? I would rather not go back to Dartmouth

> > for several reasons but someof you told me before that my local endo

> > was foolish for sending me to the oncology surgeon. The endo is only

> > sending me to him because she believes he is a good surgeon.Any

> > input would be helpful at thgis point. I apreciate it.

> > Lettie PA in ton Maine

> >

>

June 2, 2011

You say he " recommends med Rx for MOST " (emphasis is mine) I am particularly

interested in the ones he did NOT recommend Rx for. Start with " how old were

they? " and finish with " what was the exact reason that he deviated from his

norm? "

By the way, Who in he_ _ is Dr. Bravo and why should I trust him any more than

" Dr. Bill " or Dr. Spock for that matter! (Maybe I'm originally from Mo. also!)

> > > > > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > > > > > > > The other question was about

> > > > > adrenalectomies. The

> > > > > > > > > > > > > > > > > > > > > endocrinologist at

> > > > > > > > > > > > > > > > > > > > > > > Dartmouth as well as the one here

in

> > > > > Maine that I see think I

> > > > > > > > > > > > > > > > > > > > > should

> > > > > > > > > > > > > > > > > > > > > > > have an adrenalectomy. One

suggests

> > > > > a general sugeon at

> > > > > > > > > > > > > > > > > > > > > Dartmouth by

> > > > > > > > > > > > > > > > > > > > > > > the name of Laycock and the

> > > > > other is suggesting a Maine

> > > > > > > > > > > > > > > > > > > > > > > Oncology surgeon (I'veheard a lot

of

> > > > > good about the oncology

> > > > > > > > > > > > > > > > > > > > > > > surgeon) by the name of

MacGilvary.

> > > > > My question is what type of

> > > > > > > > > > > > > > > > > > > > > > > surgeon should I be seeing ? I

would

> > > > > rather not go back to

> > > > > > > > > > > > > > > > > > > > > Dartmouth

> > > > > > > > > > > > > > > > > > > > > > > for several reasons but someof you

> > > > > told me before that my local

> > > > > > > > > > > > > > > > > > > > > endo

> > > > > > > > > > > > > > > > > > > > > > > was foolish for sending me to the

> > > > > oncology surgeon. The endo is

> > > > > > > > > > > > > > > > > > > > > only

> > > > > > > > > > > > > > > > > > > > > > > sending me to him because she

> > > > > believes he is a good surgeon.Any

> > > > > > > > > > > > > > > > > > > > > > > input would be helpful at thgis

> > > > > point. I apreciate it.

> > > > > > > > > > > > > > > > > > > > > > > Lettie PA in ton Maine

> > > > > > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > >

> > > > > > > > > > > > > >

> > > > > > > > > > > > >

> > > > > > > > > > > >

> > > > > > > > > > >

> > > > > > > > > >

> > > > > > > > >

> > > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > >

> > >

> >

>

June 2, 2011

I'd be interested in hearing about this too. Additionally, has Dr. Bravo tracked

quality of life issues in those patients who have been on meds for 30+ years? By

that I mean what kinds of side effects are they living with in exchange for

getting a normal BP and K reading. Gynecomastia? Obesity? Depression? Body odor?

> > > > > > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > > > > > > > > The other question was about

> > > > > > adrenalectomies. The

> > > > > > > > > > > > > > > > > > > > > > endocrinologist at

> > > > > > > > > > > > > > > > > > > > > > > > Dartmouth as well as the one

here in

> > > > > > Maine that I see think I

> > > > > > > > > > > > > > > > > > > > > > should

> > > > > > > > > > > > > > > > > > > > > > > > have an adrenalectomy. One

suggests

> > > > > > a general sugeon at

> > > > > > > > > > > > > > > > > > > > > > Dartmouth by

> > > > > > > > > > > > > > > > > > > > > > > > the name of Laycock and the

> > > > > > other is suggesting a Maine

> > > > > > > > > > > > > > > > > > > > > > > > Oncology surgeon (I'veheard a

lot of

> > > > > > good about the oncology

> > > > > > > > > > > > > > > > > > > > > > > > surgeon) by the name of

MacGilvary.

> > > > > > My question is what type of

> > > > > > > > > > > > > > > > > > > > > > > > surgeon should I be seeing ? I

would

> > > > > > rather not go back to

> > > > > > > > > > > > > > > > > > > > > > Dartmouth

> > > > > > > > > > > > > > > > > > > > > > > > for several reasons but someof

you

> > > > > > told me before that my local

> > > > > > > > > > > > > > > > > > > > > > endo

> > > > > > > > > > > > > > > > > > > > > > > > was foolish for sending me to

the

> > > > > > oncology surgeon. The endo is

> > > > > > > > > > > > > > > > > > > > > > only

> > > > > > > > > > > > > > > > > > > > > > > > sending me to him because she

> > > > > > believes he is a good surgeon.Any

> > > > > > > > > > > > > > > > > > > > > > > > input would be helpful at thgis

> > > > > > point. I apreciate it.

> > > > > > > > > > > > > > > > > > > > > > > > Lettie PA in ton Maine

> > > > > > > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > >

> > > > > > > > > > > > > >

> > > > > > > > > > > > >

> > > > > > > > > > > >

> > > > > > > > > > >

> > > > > > > > > >

> > > > > > > > >

> > > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > >

> > >

> >

>

June 2, 2011

Or you live somewhere where healthcare is not funded or bonused the same way ;-)

> > > > > > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > > > > > > > > The other question was about

> > > > > > adrenalectomies. The

> > > > > > > > > > > > > > > > > > > > > > endocrinologist at

> > > > > > > > > > > > > > > > > > > > > > > > Dartmouth as well as the one

here in

> > > > > > Maine that I see think I

> > > > > > > > > > > > > > > > > > > > > > should

> > > > > > > > > > > > > > > > > > > > > > > > have an adrenalectomy. One

suggests

> > > > > > a general sugeon at

> > > > > > > > > > > > > > > > > > > > > > Dartmouth by

> > > > > > > > > > > > > > > > > > > > > > > > the name of Laycock and the

> > > > > > other is suggesting a Maine

> > > > > > > > > > > > > > > > > > > > > > > > Oncology surgeon (I'veheard a

lot of

> > > > > > good about the oncology

> > > > > > > > > > > > > > > > > > > > > > > > surgeon) by the name of

MacGilvary.

> > > > > > My question is what type of

> > > > > > > > > > > > > > > > > > > > > > > > surgeon should I be seeing ? I

would

> > > > > > rather not go back to

> > > > > > > > > > > > > > > > > > > > > > Dartmouth

> > > > > > > > > > > > > > > > > > > > > > > > for several reasons but someof

you

> > > > > > told me before that my local

> > > > > > > > > > > > > > > > > > > > > > endo

> > > > > > > > > > > > > > > > > > > > > > > > was foolish for sending me to

the

> > > > > > oncology surgeon. The endo is

> > > > > > > > > > > > > > > > > > > > > > only

> > > > > > > > > > > > > > > > > > > > > > > > sending me to him because she

> > > > > > believes he is a good surgeon.Any

> > > > > > > > > > > > > > > > > > > > > > > > input would be helpful at thgis

> > > > > > point. I apreciate it.

> > > > > > > > > > > > > > > > > > > > > > > > Lettie PA in ton Maine

> > > > > > > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > > >

> > > > > > > > > > > > > > >

> > > > > > > > > > > > > >

> > > > > > > > > > > > >

> > > > > > > > > > > >

> > > > > > > > > > >

> > > > > > > > > >

> > > > > > > > >

> > > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > >

> > >

> >

>

June 2, 2011

There are some very good Dr at Dartmouth but also some not very good ones.

> > >

> > > The other question was about adrenalectomies. The endocrinologist at

Dartmouth as well as the one here in Maine that I see think I should have an

adrenalectomy. One suggests a general sugeon at Dartmouth by the name of

Laycock and the other is suggesting a Maine Oncology surgeon (I'veheard a lot of

good about the oncology surgeon) by the name of MacGilvary. My question is what

type of surgeon should I be seeing ? I would rather not go back to Dartmouth for

several reasons but someof you told me before that my local endo was foolish for

sending me to the oncology surgeon. The endo is only sending me to him because

she believes he is a good surgeon.Any input would be helpful at thgis point. I

apreciate it.

> > > Lettie PA in ton Maine

> > >

> >

>

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Re: Ooops forgot the 2nd question

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