Re: Dash vs Surgery vs Dr. Grim vs challenging accepted medical opinion

[Guest guest]

Alison, I'm having a little trouble understanding what you are looking for. I

tried to access your articles and 2 of them require I pay ~$4o each to read so

that might be alot of the problem. If you are looking for someone who is

apparently doing well on meds and DASH I probably fit that bill. Part of the

problem is identifying when meds take full effect. I think Stowasser et al

alluded to that and suggested testing:

Laboratory Assessment During Medical Treatment

For patients demonstrating bilateral aldosterone production on AVS, treatment

with aldosterone antagonists usually brings about marked improvement in

hypertension control.5,34,39 Only small doses (for example, 12.5–50 mg daily of

spironolactone and/or 2.5–20 mg daily of amiloride) are usually required for

optimal antihypertensive effect. In countries where eplerenone, a modified form

of spironolactone with negligible blockade of the androgen receptor, is

available, it can be used as a preferred alternative. Its widespread usage will

depend on pricing. It is a little more than half as effective as spironolactone,

mg for mg, so that higher doses are required. However, its greater selectivity

permits this increase to adequate dosage, evidenced by renin rising into the

mid-normal range, without pro-oestrogenic side-effects. At present in Australia,

it is available under favourable pricing arrangements only for patients with

heart failure following recent myocardial infarction.

Patience is required as the full effect of each dose level takes weeks or months

to be achieved. These medications correct hypokalaemia quickly in all but the

most severe cases of PA, and potassium supplements should therefore usually be

ceased when they are commenced, and, if not ceased, then progressively reduced

(watching potassium levels) as the aldosterone antagonist has its full effect.

Overtreatment with these agents can cause volume contraction with pre-renal

failure, rising creatinine concentrations and potentially life-threatening

hyperkalaemia.34 They should therefore be used with great caution in patients

with existing renal impairment, and electrolytes and creatinine should be

regularly checked.

The extent to which renin levels become `unsuppressed' is a useful indication of

the degree of blockade of aldosterone effect induced by any given treatment

dose. While normalisation of potassium and blood pressure levels have been

traditionally regarded as evidence of adequate treatment, it could be argued

(given that aldosterone excess is now known to induce adverse cardiovascular

effects independently of its effects on blood pressure) that the goal should be

`complete' reversal of excessive aldosterone action. In this way, normalisation

of renin levels may be more reassuring than simply correcting hypertension and

hyperkalaemia since it indicates that the dose of mineralocorticoid antagonist

is adequate to correct the sodium/volume expansion. Given that adverse

cardiovascular effects of aldosterone excess appear to be dependent on sodium

balance, normal renin levels would imply correction of sodium overload as well.

In some patients, however, the degree to which doses can be increased in order

to achieve normalisation of renin levels will be limited by tolerability. Even

at spironolactone doses of 12.5–25 mg daily, side effects (such as gynaecomastia

in males and menstrual irregularity in females) are not uncommon. As with the

risk of hyperkalaemia and uraemia, these side effects are dose-dependent.

Assessment of renin levels is also helpful in guiding changes in management for

patients in whom hypertension has not yet become optimally controlled following

introduction of mineralocorticoid antagonist treatment. If renin levels have

already become `unsuppressed', for example, persisting hypertension is best

treated by adding in or increasing the dose of other antihypertensive

medications. It must be remembered that renin suppression can persist for long

periods after `cure' of unilateral PA by adrenalectomy, if PA was longstanding.

It may therefore also take some time for `complete' blockade of the

mineralocorticoid receptor to result in renin becoming `unsuppressed'.

I copied the part I will be attempting to watch and intend to talk with my PCP

Monday but I'm not sure how " willing " she will be to participate in a Trial

Study. Renin and aldo tests appear to be sent out to Quest Labs by the VA so

there is an expense. Most other tests are done inhouse so while there is an

expense it is probably less.

I am already planning to ask her to check the status of LVH regression and a PFT

to see changes in my lungs beside " normal " blood work.

Did you look at that article and does it cover any of what you are asking? When

I saw this " (given that aldosterone excess is now known to induce adverse

cardiovascular effects independently of its effects on blood pressure) " I

thought there might be more in the main part of the article. (I still haven't

studied rhe article, my printer ran out of ink and I can't read w/o a

highlighter!)

If you missed it, it is at:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874431/pdf/cbr_31_2_39.pdf

- 65 yo super ob. male - 12mm X 13mm rt. a.adnoma with previous rt. flank

pain. Treating with Meds. And DASH. . Current BP(last week ave): 125/73

Other Issues/Opportunities: OSA w Bi-Pap settings 13/19, DM2, and PTSD.

Meds: Duloxetine hcl 80 MG, Mirtazapine 7.5 MG, Metoprolol Tartrate 200 MG,

81mg asprin, Metformin 2000MG and Spironolactone 50 MG.

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> > > > >> Doesnt Dr. Grim have alot of insight as to how best to deal

> > > with this disease? I mean, who else has spent their career studying

> > > it? Seriously, is there anyone else?

> > > > >> If his recommendations are based on his lifes work, can we

> > > really argue it?

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