Re: thyroid and BB old study by excellent group.

[Guest guest]

That's interesting. BB's are stll the initial treatment when hypertyroidism or if it's mean cousin thyrotoxosis rears it's head and even though I had tried BB's before, it always dropped my heart into the 40's on any dose and I felt so tired and depressed . That is until I had the hyperthyroidism too (my mother died at age 38 at 5'4" and 84lbs and she had it). Then the BB was the best thing ever.....for me at that time. I was very healthy when the PA showed up (and the hypokalemia

- years before they found the PA and and my resting HR was 60 anyway - as everything I did was cardio related especially basketball ) and I was talking to my wife today that it may have been as long as 7-8 years ago that PA started! I was generally so healthy and active that BP spikes were just brushed off by my docs and me for years. Yet I know since 2008 the

hyperthyroidism I also had came and went based on my symptoms, but stayed more than it went - seemed to follow a flu and everyone teased me that I "caught everything" and took 6 months to get over it only to start it again, until the H1N1 flu that I got so bad late 2009, then I thought the end of the world had come. Like the BP with my PA, I would go to the ER during the (undiagnosed ) thyroid iissue with a HR 140, BP 170/140, killer headaches and incredible leg cramps and weakness and they would load me with K (EVERY single time I went, and my ER records[we only have one ER in Prescott AZ] show on average I showed up q 2 months in 2009 and 2010), and try to get things down (they would for a few hours...and that only sometimes) so they could get me out. Never checked thyroid. And I was always complaining of a strange anxiety that I would tell them IS NOT depression, nor a real anxiety attack as it was there at 4pm or 4am just the

same. I think I have said insomnia is

indescribable during that period and the headaches beyond description. And by 1/10 my vision started failing me (temporary though due to thyroid) and I developed what I thought was a lid lag, but was really a "retracted" eyelid in one eye common with hyperthyroid, but it made me think stroke of course, and hyperthyroid gives a sort of psychosis untreated and I was getting there by Jan 2010 for certain and already anxious, with daily BP of 160/120-130 and I perseverated that the stroke or MI was any moment. But what can one do....?. Oh AND my heart pounded in my chest so hard I had to get up at night (I didn't sleep anyway) because it bothered me so much to feel it pound. Liek a bomb was going off all the time. I realize we all have our demons with our illnesses, but to me I can only compare hyperthyroidsim (AND the low K, HTN, and PA issues yet to be found) to a disease that must be what hell feels like....well okay...without my

mother-in-law there. Single worse 2 years of my life. My point is really that I was SO texbookt PA AND hyperthyroid it was uncanny. An no one checked thyroid even a TSH. They were colleagues and I simply assumed with my symptoms they would check it. I worked another ER and urgent care and thyroid was always part and parcel of those symptoms that I checked routinely. .I got some of my ER records a few weeks back and I noticed back in 2009, months before I completely collapsed in 4/2010 (when they found the HYPERTHYROID, but not PA yet) one doctor wrote...."patient keeps insisting he has a fever, but he never has one when we check it but he does appear flushed". That doc drew blood but only CBC, d dimer, CMP and cardiac enzymes. Nothing else. I felt hot in the snow and slept all night with the AC on even in Texas panhandle where the day we moved to AZ it was 16 degrees. And I just kept getting misdiagnosed or non diagnosed over

and over . I think they thought I was simply a drug seeker in w/d by the way I was treated by some. But an hour after they gave me a dose of metoprolol that one time they found the hyperthyroidism in 4/10 ...BAMM!!! But I was so close to a near total paralyisis that this time they had to look a bit harder. The BB? it was a Godsend then and there. Ever since the hyperthyroid I had some rate issues with it getting too fast now.So the BB helped tremendously. I also during this period in 2009 was taking vicodin, not for the same reason alot take it (didn't make me tired or high) but I grew to depend on it for the leg cramps. I told the docs that they stopped the cramps. Period. Even when I stopped taking them completely in Summer 2010, I still had the leg issues due to potassium. But...I found a few studies the other day by accident that talked about how hydrocodone "opens the body's potassium" channels! I think this was why it worked so

dramatically for me. Now of course between DASH and spiro I don't need anything like that, but I found it interesting. And I craved pickles, tomatoes, oranges, bananas, all the time. But i sure was textbook PA and hyperthyroid. But no one reads their actual textbooks anymore. 43 yo M with PA and Hyperthyroid Subject: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Grim Clarence" Date: Saturday, March 26, 2011, 10:17 PM

J Clin Endocrinol Metab. 1977 May;44(5):1002-5.Plasma thyroxine, 3,3',5-triiodothyronine and 3,3',5'-triiodothyronine during beta-adrenergic blockade in hyperthyroidism.Verhoeven RP, Visser TJ, Doctor R, Hennemann G, Schalekamp MA.AbstractPlasma thyroxine (T4), 3,3',5-triiodothyronine (T3) and

3,3',5'-triiodothyronine (rT3) were measured in 16 patients with Graves' disease. Patients were studied under the following conditions: first without any treatment, then, during beta-adrenergic blockade with propranolol, and finally after euthyroidism had been attained by carbimazole. During propranolol T3/T4 ratio decreased, whereas T4 remained unchanged. After carbimazole T3/T4 ratio returned to its pretreatment value. rT3/T4 ratio showed opposite changes. These results suggest that peripheral conversion of T4 into T3 and rT3 in hyperthyroidism is, at least partly, dependent on the functional status of the beta-adrenergic system. Suppressed peripheral conversion of T4 into T3 during beta-adrenergic blocking agents may contribute to the beneficial effects of these drugs in thyrotoxicosis.

[Guest guest]

,

so much of your story sounds like mine. 

The only problem is that spiro did nothing for my symptoms.  It lowered my BP but that is all.  My symptoms - anxiety, muscle pain,

paralysis, a little dropsy on one side of my face, fevers, migraines, BP

spikes, chest pounding, (hypo) thyroid, arrhythmias, low K - were all a result

of Lyme disease.  I expect even my PA may

someday resolve.  

Val

From: hyperaldosteronism

[mailto:hyperaldosteronism ] On Behalf Of Bingham

That's interesting. BB's are

stll the initial treatment when hypertyroidism or if it's mean cousin

thyrotoxosis rears it's head and even though I had tried BB's before, it

always dropped my heart into the 40's on any dose and I felt so tired and

depressed . That is until I had the hyperthyroidism too (my mother died at

age 38 at 5'4 " and 84lbs and she had it). Then the BB was the best

thing ever.....for me at that time.

I was very healthy when the PA showed up (and the hypokalemia - years

before they found the PA and and my resting HR was 60 anyway - as

everything I did was cardio related especially basketball ) and I was

talking to my wife today that it may have been as long as 7-8 years

ago that PA started! I was generally so healthy and active that BP

spikes were just brushed off by my docs and me for years.

Yet I know since 2008 the hyperthyroidism I also had came and went

based on my symptoms, but stayed more than it went - seemed to follow a flu

and everyone teased me that I " caught everything " and took 6

months to get over it only to start it again, until the H1N1 flu that I got

so bad late 2009, then I thought the end of the world had come.

Like the BP with my PA, I would go to the ER during the (undiagnosed

) thyroid iissue with a HR 140, BP 170/140, killer headaches and incredible

leg cramps and weakness and they would load me with K (EVERY single time I

went, and my ER records[we only have one ER in Prescott AZ] show on average

I showed up q 2 months in 2009 and 2010), and try to get things down (they

would for a few hours...and that only sometimes) so they could get me out.

Never checked thyroid. And I was always complaining of a strange anxiety

that I would tell them IS NOT depression, nor a real anxiety attack as it

was there at 4pm or 4am just the same. I think I have said insomnia is

indescribable during that period and the headaches beyond description.

And by 1/10 my vision started failing me (temporary though due to thyroid)

and I developed what I thought was a lid lag, but was really a

" retracted " eyelid in one eye common with hyperthyroid, but it

made me think stroke of course, and hyperthyroid gives a sort of psychosis

untreated and I was getting there by Jan 2010 for certain and already

anxious, with daily BP of 160/120-130 and I perseverated that the stroke or

MI was any moment. But what can one do....?. Oh AND my heart pounded in my

chest so hard I had to get up at night (I didn't sleep anyway) because it

bothered me so much to feel it pound. Liek a bomb was going off all the time.

I realize we all have our demons with our illnesses, but to me I can only

compare hyperthyroidsim (AND the low K, HTN, and PA issues yet to be found)

to a disease that must be what hell feels like....well okay...without my

mother-in-law there. Single worse 2 years of my life. My point is

really that I was SO texbookt PA AND hyperthyroid it was uncanny. An

no one checked thyroid even a TSH. They were colleagues and I simply

assumed with my symptoms they would check it. I worked another ER and

urgent care and thyroid was always part and parcel of those symptoms that I

checked routinely. .

I got some of my ER records a few weeks back and I noticed back in 2009,

months before I completely collapsed in 4/2010 (when they found the

HYPERTHYROID, but not PA yet) one doctor wrote.... " patient keeps

insisting he has a fever, but he never has one when we check it but he does

appear flushed " . That doc drew blood but only CBC, d dimer, CMP and

cardiac enzymes. Nothing else. I felt hot in the snow and slept all night

with the AC on even in Texas panhandle where the day we moved to AZ it was

16 degrees.

And I just kept getting misdiagnosed or non diagnosed over and over .

I think they thought I was simply a drug seeker in w/d by the way I was

treated by some. But an hour after they gave me a dose of metoprolol that

one time they found the hyperthyroidism in 4/10 ...BAMM!!! But I was so

close to a near total paralyisis that this time they had to look a bit

harder. The BB? it was a Godsend then and there. Ever since the

hyperthyroid I had some rate issues with it getting too fast now.

So the BB helped tremendously. I also during this period in 2009 was

taking vicodin, not for the same reason alot take it (didn't make me tired

or high) but I grew to depend on it for the leg cramps. I told the docs

that they stopped the cramps. Period. Even when I stopped taking them

completely in Summer 2010, I still had the leg issues due to potassium.

But...I found a few studies the other day by accident that talked about how

hydrocodone " opens the body's potassium " channels! I think this

was why it worked so dramatically for me. Now of course between DASH and

spiro I don't need anything like that, but I found it interesting. And I

craved pickles, tomatoes, oranges, bananas, all the time.

But i sure was textbook PA and hyperthyroid. But no one reads their

actual textbooks anymore.

43 yo M with PA and Hyperthyroid

Subject: thyroid and BB old study by excellent group.

To: hyperaldosteronism

Cc: " Grim Clarence "

Date: Saturday, March 26, 2011, 10:17 PM

J Clin Endocrinol Metab. 1977

May;44(5):1002-5.

Plasma thyroxine, 3,3',5-triiodothyronine and

3,3',5'-triiodothyronine during beta-adrenergic blockade in

hyperthyroidism.

Verhoeven RP, Visser TJ, Doctor R, Hennemann G, Schalekamp MA.

Abstract

Plasma thyroxine (T4),

3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) were

measured in 16 patients with Graves' disease. Patients were studied under

the following conditions: first without any treatment, then, during

beta-adrenergic blockade with propranolol, and finally after euthyroidism had

been attained by carbimazole. During propranolol T3/T4 ratio decreased,

whereas T4 remained unchanged. After carbimazole T3/T4 ratio returned to

its pretreatment value. rT3/T4 ratio showed opposite changes. These results

suggest that peripheral conversion of T4 into T3 and rT3 in hyperthyroidism

is, at least partly, dependent on the functional status of the

beta-adrenergic system. Suppressed peripheral conversion of T4 into T3

during beta-adrenergic blocking agents may contribute to the beneficial

effects of these drugs in thyrotoxicosis.

[Guest guest]

I just looked at a for NPs and PAs that pays $ for diagonsitc challenges. Which you certainly seem to fit at least from the ERs perspective. I will write for details or can give you info. How was the HyperT picked up?BB only work to control heart rate and I assume you have had I131 or PTU of you had thyroiditis that has now burned out.Was your Mom in Costa Rica as well?And I assume you were working in US earl on?That's interesting. BB's are stll the initial treatment when hypertyroidism or if it's mean cousin thyrotoxosis rears it's head and even though I had tried BB's before, it always dropped my heart into the 40's on any dose and I felt so tired and depressed . That is until I had the hyperthyroidism too (my mother died at age 38 at 5'4" and 84lbs and she had it). Then the BB was the best thing ever.....for me at that time. I was very healthy when the PA showed up (and the hypokalemia - years before they found the PA and and my resting HR was 60 anyway - as everything I did was cardio related especially basketball ) and I was talking to my wife today that it may have been as long as 7-8 years ago that PA started! I was generally so healthy and active that BP spikes were just brushed off by my docs and me for years. Yet I know since 2008 the hyperthyroidism I also had came and went based on my symptoms, but stayed more than it went - seemed to follow a flu and everyone teased me that I "caught everything" and took 6 months to get over it only to start it again, until the H1N1 flu that I got so bad late 2009, then I thought the end of the world had come. Like the BP with my PA, I would go to the ER during the (undiagnosed ) thyroid iissue with a HR 140, BP 170/140, killer headaches and incredible leg cramps and weakness and they would load me with K (EVERY single time I went, and my ER records[we only have one ER in Prescott AZ] show on average I showed up q 2 months in 2009 and 2010), and try to get things down (they would for a few hours...and that only sometimes) so they could get me out. Never checked thyroid. And I was always complaining of a strange anxiety that I would tell them IS NOT depression, nor a real anxiety attack as it was there at 4pm or 4am just the same. I think I have said insomnia is indescribable during that period and the headaches beyond description. And by 1/10 my vision started failing me (temporary though due to thyroid) and I developed what I thought was a lid lag, but was really a "retracted" eyelid in one eye common with hyperthyroid, but it made me think stroke of course, and hyperthyroid gives a sort of psychosis untreated and I was getting there by Jan 2010 for certain and already anxious, with daily BP of 160/120-130 and I perseverated that the stroke or MI was any moment. But what can one do....?. Oh AND my heart pounded in my chest so hard I had to get up at night (I didn't sleep anyway) because it bothered me so much to feel it pound. Liek a bomb was going off all the time. I realize we all have our demons with our illnesses, but to me I can only compare hyperthyroidsim (AND the low K, HTN, and PA issues yet to be found) to a disease that must be what hell feels like....well okay...without my mother-in-law there. Single worse 2 years of my life. My point is really that I was SO texbookt PA AND hyperthyroid it was uncanny. An no one checked thyroid even a TSH. They were colleagues and I simply assumed with my symptoms they would check it. I worked another ER and urgent care and thyroid was always part and parcel of those symptoms that I checked routinely. .I got some of my ER records a few weeks back and I noticed back in 2009, months before I completely collapsed in 4/2010 (when they found the HYPERTHYROID, but not PA yet) one doctor wrote...."patient keeps insisting he has a fever, but he never has one when we check it but he does appear flushed". That doc drew blood but only CBC, d dimer, CMP and cardiac enzymes. Nothing else. I felt hot in the snow and slept all night with the AC on even in Texas panhandle where the day we moved to AZ it was 16 degrees. And I just kept getting misdiagnosed or non diagnosed over and over . I think they thought I was simply a drug seeker in w/d by the way I was treated by some. But an hour after they gave me a dose of metoprolol that one time they found the hyperthyroidism in 4/10 ...BAMM!!! But I was so close to a near total paralyisis that this time they had to look a bit harder. The BB? it was a Godsend then and there. Ever since the hyperthyroid I had some rate issues with it getting too fast now.So the BB helped tremendously. I also during this period in 2009 was taking vicodin, not for the same reason alot take it (didn't make me tired or high) but I grew to depend on it for the leg cramps. I told the docs that they stopped the cramps. Period. Even when I stopped taking them completely in Summer 2010, I still had the leg issues due to potassium. But...I found a few studies the other day by accident that talked about how hydrocodone "opens the body's potassium" channels! I think this was why it worked so dramatically for me. Now of course between DASH and spiro I don't need anything like that, but I found it interesting. And I craved pickles, tomatoes, oranges, bananas, all the time. But i sure was textbook PA and hyperthyroid. But no one reads their actual textbooks anymore. 43 yo M with PA and Hyperthyroid Subject: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Grim Clarence" Date: Saturday, March 26, 2011, 10:17 PM J Clin Endocrinol Metab. 1977 May;44(5):1002-5.Plasma thyroxine, 3,3',5-triiodothyronine and 3,3',5'-triiodothyronine during beta-adrenergic blockade in hyperthyroidism.Verhoeven RP, Visser TJ, Doctor R, Hennemann G, Schalekamp MA.AbstractPlasma thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) were measured in 16 patients with Graves' disease. Patients were studied under the following conditions: first without any treatment, then, during beta-adrenergic blockade with propranolol, and finally after euthyroidism had been attained by carbimazole. During propranolol T3/T4 ratio decreased, whereas T4 remained unchanged. After carbimazole T3/T4 ratio returned to its pretreatment value. rT3/T4 ratio showed opposite changes. These results suggest that peripheral conversion of T4 into T3 and rT3 in hyperthyroidism is, at least partly, dependent on the functional status of the beta-adrenergic system. Suppressed peripheral conversion of T4 into T3 during beta-adrenergic blocking agents may contribute to the beneficial effects of these drugs in thyrotoxicosis.

[Guest guest]

And I was very fortunate that after just 2 doses of 25mg spiro I was already down to 120/80 ( back then 6/2010) I saw my endo for the hyperthyroidism, and first visit I had a BP somewhere in the 160/130 range, he told me to go see a cardiologist. I did, then the cardio put me on the spiro, I went back to an endo appt and he got mad that I never "told HIM" about the BP issues....ugh....go figure. I reminded him HE sent me to the cardiologist.....what a world sometimes ). If I keep away from the salt, and spiro, then it's fine. It's the hidden salt in things, seems to bring it up immediately, but only temporary.

Subject: thyroid and BB old study by excellent group.

To: hyperaldosteronism

Cc: "Grim Clarence"

Date: Saturday, March 26, 2011, 10:17 PM

J Clin Endocrinol Metab. 1977

May;44(5):1002-5.

Plasma thyroxine, 3,3',5-triiodothyronine and

3,3',5'-triiodothyronine during beta-adrenergic blockade in

hyperthyroidism.

Verhoeven RP, Visser TJ, Doctor R, Hennemann G, Schalekamp

MA.

Abstract

Plasma thyroxine (T4),

3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) were

measured in 16 patients with Graves' disease. Patients were studied under

the following conditions: first without any treatment, then, during

beta-adrenergic blockade with propranolol, and finally after euthyroidism had

been attained by carbimazole. During propranolol T3/T4 ratio decreased,

whereas T4 remained unchanged. After carbimazole T3/T4 ratio returned to

its pretreatment value. rT3/T4 ratio showed opposite changes. These results

suggest that peripheral conversion of T4 into T3 and rT3 in hyperthyroidism

is, at least partly, dependent on the functional status of the

beta-adrenergic system. Suppressed peripheral conversion of T4 into T3

during beta-adrenergic blocking agents may contribute to the beneficial

effects of these drugs in thyrotoxicosis.

[Guest guest]

Same ER I had been going to, but a new doc was working PT that weekend (it was a Sunday) and as they told him "I always come in" I just looked at him and told him that "SOMETHING is seriously wrong!" and he agreed. He ran some tests, tanked me up with K, put me on BB and walked in and said, "did you know you have hyperthyroidism" and I WANTED to say "No #@%!!!, but I didn't. Just glad he listened. After that I went to endo. I did come back to the ER 3 times, and one 5 days stay for malignant HTN on 5 meds last Sept/Oct and they did a 24 hour urine, and other blood work, but did not take me off lisinopril, BB's or clonodine to do anything. She suspected Pheo possiblity, but only did a renal bedside U/S and told me I was fine, and never used spiro there. It was a couple weeks later that the cardio suspected Conn's. Was never mentioned in

the hospital. Now the endo since dx has me with Conn's (and he already about it as he called it by name before I did) based on HX and response to spiro, but like I said we are doing some more scans and MIBG scan, but I had so many scans with dye I want to wait a while. There are no after hours care here and I personally actually worked in the Phoenix proper 2 hours away normally, but was not going down there to Phoenix that day. Oh yeah, my thyroid tests were all fine. Had all the scans, blood work etc. and it resolved without the meds, which me and endo had talked about I not being a candidate for surgery or the medicine at that time, due to the BP issue.And....I am as American as they come - never left the states - Danish and English 2nd generation from Long Beach Ca. It's actually Dale, but middle name is and they called me from day one I got first breath....just funny....it's not ""...but

I am just laughing in a nice way.....my mother was the whitest woman with red hair you'd ever meet outside of albinoism from Detroit Mi. She was Connie, not Consuela...never been to Puerto Rico, just lived in the countries of Oklahoma, Texas, went to the University of Utah for PA, and now Prescott AZ.....I prefer the midwest most of all and would go back to OK tomorrow if we didn't have 6 kids and one getting ready to graduate HS. Maybe next year. Prescott is nice, but not a big AZ fan. Subject: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Grim Clarence" Date: Saturday, March 26, 2011, 10:17 PM J Clin Endocrinol Metab. 1977 May;44(5):1002-5.Plasma thyroxine, 3,3',5-triiodothyronine and 3,3',5'-triiodothyronine during beta-adrenergic blockade in hyperthyroidism.Verhoeven RP, Visser TJ, Doctor R, Hennemann G, Schalekamp MA.AbstractPlasma thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) were measured in 16 patients with Graves' disease. Patients were studied under the following conditions: first without any treatment, then, during beta-adrenergic blockade with propranolol, and finally after euthyroidism had been attained by carbimazole. During propranolol T3/T4 ratio decreased, whereas T4 remained unchanged. After carbimazole T3/T4 ratio returned to its pretreatment value. rT3/T4 ratio showed opposite changes. These results suggest that peripheral conversion of T4 into T3 and rT3 in hyperthyroidism is, at least partly, dependent

on the functional status of the beta-adrenergic system. Suppressed peripheral conversion of T4 into T3 during beta-adrenergic blocking agents may contribute to the beneficial effects of these drugs in thyrotoxicosis.

[Guest guest]

I don't understand how you were diagnosised with HThy but you blood tests were all normal?CE Grim MDSame ER I had been going to, but a new doc was working PT that weekend (it was a Sunday) and as they told him "I always come in" I just looked at him and told him that "SOMETHING is seriously wrong!" and he agreed. He ran some tests, tanked me up with K, put me on BB and walked in and said, "did you know you have hyperthyroidism" and I WANTED to say "No #@%!!!, but I didn't. Just glad he listened. After that I went to endo. I did come back to the ER 3 times, and one 5 days stay for malignant HTN on 5 meds last Sept/Oct and they did a 24 hour urine, and other blood work, but did not take me off lisinopril, BB's or clonodine to do anything. She suspected Pheo possiblity, but only did a renal bedside U/S and told me I was fine, and never used spiro there. It was a couple weeks later that the cardio suspected Conn's. Was never mentioned in the hospital. Now the endo since dx has me with Conn's (and he already about it as he called it by name before I did) based on HX and response to spiro, but like I said we are doing some more scans and MIBG scan, but I had so many scans with dye I want to wait a while. There are no after hours care here and I personally actually worked in the Phoenix proper 2 hours away normally, but was not going down there to Phoenix that day. Oh yeah, my thyroid tests were all fine. Had all the scans, blood work etc. and it resolved without the meds, which me and endo had talked about I not being a candidate for surgery or the medicine at that time, due to the BP issue.And....I am as American as they come - never left the states - Danish and English 2nd generation from Long Beach Ca. It's actually Dale, but middle name is and they called me from day one I got first breath....just funny....it's not ""...but I am just laughing in a nice way.....my mother was the whitest woman with red hair you'd ever meet outside of albinoism from Detroit Mi. She was Connie, not Consuela...never been to Puerto Rico, just lived in the countries of Oklahoma, Texas, went to the University of Utah for PA, and now Prescott AZ.....I prefer the midwest most of all and would go back to OK tomorrow if we didn't have 6 kids and one getting ready to graduate HS. Maybe next year. Prescott is nice, but not a big AZ fan. Subject: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Grim Clarence" Date: Saturday, March 26, 2011, 10:17 PM J Clin Endocrinol Metab. 1977 May;44(5):1002-5.Plasma thyroxine, 3,3',5-triiodothyronine and 3,3',5'-triiodothyronine during beta-adrenergic blockade in hyperthyroidism.Verhoeven RP, Visser TJ, Doctor R, Hennemann G, Schalekamp MA.AbstractPlasma thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) were measured in 16 patients with Graves' disease. Patients were studied under the following conditions: first without any treatment, then, during beta-adrenergic blockade with propranolol, and finally after euthyroidism had been attained by carbimazole. During propranolol T3/T4 ratio decreased, whereas T4 remained unchanged. After carbimazole T3/T4 ratio returned to its pretreatment value. rT3/T4 ratio showed opposite changes. These results suggest that peripheral conversion of T4 into T3 and rT3 in hyperthyroidism is, at least partly, dependent on the functional status of the beta-adrenergic system. Suppressed peripheral conversion of T4 into T3 during beta-adrenergic blocking agents may contribute to the beneficial effects of these drugs in thyrotoxicosis.

[Guest guest]

TSH was very low 0.11. Everything else thyroid was ok or just above the cut-off. Scans were all normal. Subject: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Grim Clarence" Date: Saturday, March 26, 2011, 10:17 PM J Clin Endocrinol Metab. 1977 May;44(5):1002-5.Plasma thyroxine, 3,3',5-triiodothyronine and 3,3',5'-triiodothyronine during beta-adrenergic blockade in hyperthyroidism.Verhoeven RP, Visser TJ, Doctor R, Hennemann G, Schalekamp MA.AbstractPlasma thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) were measured in 16 patients with Graves' disease. Patients were studied under the following conditions: first without any treatment, then, during beta-adrenergic blockade with propranolol, and finally after euthyroidism had been attained by carbimazole. During propranolol T3/T4 ratio decreased, whereas T4 remained unchanged. After carbimazole T3/T4 ratio returned to its pretreatment value. rT3/T4 ratio showed opposite changes. These results suggest that peripheral conversion of T4 into T3 and rT3 in hyperthyroidism is, at least partly, dependent on the functional status of the beta-adrenergic system. Suppressed peripheral conversion of T4 into T3 during beta-adrenergic blocking agents may contribute to the beneficial effects of these drugs in

thyrotoxicosis.

[Guest guest]

So they thought you had burned out thyroiditis? I don't understand the physiology of how one can have hyperthyroidism without being hyperthryoid. TSH alone does not make the Dx.Also u said you were hosp with malignant HTN. Very rare in PA. The Dx requires hemorrhages and exudates in the fundi. With out that it is not mailig. BP alone does not make the Dx. CE Grim MDTSH was very low 0.11. Everything else thyroid was ok or just above the cut-off. Scans were all normal. Subject: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Grim Clarence" Date: Saturday, March 26, 2011, 10:17 PM J Clin Endocrinol Metab. 1977 May;44(5):1002-5.Plasma thyroxine, 3,3',5-triiodothyronine and 3,3',5'-triiodothyronine during beta-adrenergic blockade in hyperthyroidism.Verhoeven RP, Visser TJ, Doctor R, Hennemann G, Schalekamp MA.AbstractPlasma thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) were measured in 16 patients with Graves' disease. Patients were studied under the following conditions: first without any treatment, then, during beta-adrenergic blockade with propranolol, and finally after euthyroidism had been attained by carbimazole. During propranolol T3/T4 ratio decreased, whereas T4 remained unchanged. After carbimazole T3/T4 ratio returned to its pretreatment value. rT3/T4 ratio showed opposite changes. These results suggest that peripheral conversion of T4 into T3 and rT3 in hyperthyroidism is, at least partly, dependent on the functional status of the beta-adrenergic system. Suppressed peripheral conversion of T4 into T3 during beta-adrenergic blocking agents may contribute to the beneficial effects of these drugs in thyrotoxicosis.

[Guest guest]

The thought was it was really the hypokalemia that got me into the ER that am, but the HR, HTN, the long s/s of the severe insomnia, anxiety, and the other stuff going on was driven by the hyperT. I may have been on a recovery side of the hyperT, thus only my TSH was still messed up then. I didn't get to see the endo until nearly 2 months after that ER visit. By then TSH still low, but a t3's, t4's, antibodies all WNL. Still, even though i was there AGAIN at that ER with low K, severe HTN, he looked through my old records and never looked for, nor mentioned PA. I even went back to the ER between that day and seeing the endo for the first time because the BP was so out-of-control and it was blamed on the hyperT. Saw my primary care doc too twice in between and he did order a 24 hr urine and some others, but never stopped any meds. The

BB though was finally well tolerated by me and at minimum slowed the pounding heart and the rate. Only need it occasionally now when the rate gets out of control (which unless it is a SE of the spiro we don't know why), but was able to stop it about July/August last year when I finally got a normal TSH and s/s of the hyperT dissipated. I can almost recall the very day waking up and thinking that weird anxiety is gone, the pounding heart is gone, the vision is fine...and so on. It was an incredible ride until then......except the PA was there and BP never changed even after normal thyroid.. Subject: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Grim Clarence" Date: Saturday, March 26, 2011, 10:17 PM J Clin Endocrinol Metab. 1977 May;44(5):1002-5.Plasma thyroxine, 3,3',5-triiodothyronine and 3,3',5'-triiodothyronine during beta-adrenergic blockade in hyperthyroidism.Verhoeven RP, Visser TJ, Doctor R, Hennemann G, Schalekamp MA.AbstractPlasma thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) were measured in 16 patients with Graves' disease. Patients were studied under the following conditions: first without any treatment, then, during beta-adrenergic blockade with propranolol, and finally after euthyroidism had been attained by carbimazole. During propranolol T3/T4 ratio decreased, whereas T4 remained unchanged. After carbimazole T3/T4 ratio returned to its pretreatment value. rT3/T4 ratio showed opposite changes. These results suggest that peripheral conversion of T4 into T3 and rT3 in hyperthyroidism is, at least partly, dependent on the functional status of the beta-adrenergic system. Suppressed peripheral conversion of T4 into T3 during beta-adrenergic blocking agents may contribute to the beneficial effects of these drugs in

thyrotoxicosis.

[Guest guest]

My guess is that the BB effect had nothing to do with Thyroid. It helped block the hyperaldo increased SNS activity. HyperThy usually causes systolic HTN and diastolic hypotension due to the profound vasodlating effects and the increase in CO.I suspect the TSH assay was somehow wrong. Some how I was thinking you were in Costa Rica but must be another Phys Assis? The thought was it was really the hypokalemia that got me into the ER that am, but the HR, HTN, the long s/s of the severe insomnia, anxiety, and the other stuff going on was driven by the hyperT. I may have been on a recovery side of the hyperT, thus only my TSH was still messed up then. I didn't get to see the endo until nearly 2 months after that ER visit. By then TSH still low, but a t3's, t4's, antibodies all WNL. Still, even though i was there AGAIN at that ER with low K, severe HTN, he looked through my old records and never looked for, nor mentioned PA. I even went back to the ER between that day and seeing the endo for the first time because the BP was so out-of-control and it was blamed on the hyperT. Saw my primary care doc too twice in between and he did order a 24 hr urine and some others, but never stopped any meds. The BB though was finally well tolerated by me and at minimum slowed the pounding heart and the rate. Only need it occasionally now when the rate gets out of control (which unless it is a SE of the spiro we don't know why), but was able to stop it about July/August last year when I finally got a normal TSH and s/s of the hyperT dissipated. I can almost recall the very day waking up and thinking that weird anxiety is gone, the pounding heart is gone, the vision is fine...and so on. It was an incredible ride until then......except the PA was there and BP never changed even after normal thyroid.. Subject: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Grim Clarence" Date: Saturday, March 26, 2011, 10:17 PM J Clin Endocrinol Metab. 1977 May;44(5):1002-5.Plasma thyroxine, 3,3',5-triiodothyronine and 3,3',5'-triiodothyronine during beta-adrenergic blockade in hyperthyroidism.Verhoeven RP, Visser TJ, Doctor R, Hennemann G, Schalekamp MA.AbstractPlasma thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) were measured in 16 patients with Graves' disease. Patients were studied under the following conditions: first without any treatment, then, during beta-adrenergic blockade with propranolol, and finally after euthyroidism had been attained by carbimazole. During propranolol T3/T4 ratio decreased, whereas T4 remained unchanged. After carbimazole T3/T4 ratio returned to its pretreatment value. rT3/T4 ratio showed opposite changes. These results suggest that peripheral conversion of T4 into T3 and rT3 in hyperthyroidism is, at least partly, dependent on the functional status of the beta-adrenergic system. Suppressed peripheral conversion of T4 into T3 during beta-adrenergic blocking agents may contribute to the beneficial effects of these drugs in thyrotoxicosis.

[Guest guest]

Just the low TSH. T4 was just inside the upper limit of Lab Corps norm - at the edge of "high" as was the T3. No explanation unless all the meds I was on, including the hydrocodone and occasional various muscle relaxers (they were trying to MAKE me sleep - didn't work) like soma, flexeril, threw them into normal range. I am trying to recall if I was on prednisone near that time too, but I am not sure as that can slew them. They put me on it occasionally because I was always sick with cold like symptoms too (I know now most likely due to the clonidine, but I was pretty confused toward the latter stages and just went with the flow)Subject: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Grim Clarence" Date: Saturday, March 26, 2011, 10:17 PM J Clin Endocrinol Metab. 1977 May;44(5):1002-5.Plasma thyroxine, 3,3',5-triiodothyronine and 3,3',5'-triiodothyronine during beta-adrenergic blockade in hyperthyroidism.Verhoeven RP, Visser TJ, Doctor R, Hennemann G, Schalekamp MA.AbstractPlasma thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) were measured in 16 patients with Graves' disease. Patients were studied under the following conditions: first without any treatment, then, during beta-adrenergic blockade with propranolol, and finally after euthyroidism had been attained by carbimazole. During propranolol T3/T4 ratio decreased, whereas

T4 remained unchanged. After carbimazole T3/T4 ratio returned to its pretreatment value. rT3/T4 ratio showed opposite changes. These results suggest that peripheral conversion of T4 into T3 and rT3 in hyperthyroidism is, at least partly, dependent on the functional status of the beta-adrenergic system. Suppressed peripheral conversion of T4 into T3 during beta-adrenergic blocking agents may contribute to the beneficial effects of these drugs in thyrotoxicosis.

[Guest guest]

I never had any rate issues before, but it starting getting into the 130's 140's during the thyroid period. BP never wavered until I got the spiro and that was late 2010. Was always high no matter what med. But the forceness of the heartbeat and the rate improved dramatically after I went back on BB in 4/10. Had no effect on BP. I do know I was able to stop (except rarely) the BB after the first normal TSH when the symptoms were gone and this was long before spiro or PA dx. TSH normal since and I have had no return of the hyperT symptomsJust a weird one.....Subject: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Grim Clarence" Date:

Saturday, March 26, 2011, 10:17 PM J Clin Endocrinol Metab. 1977 May;44(5):1002-5.Plasma thyroxine, 3,3',5-triiodothyronine and 3,3',5'-triiodothyronine during beta-adrenergic blockade in hyperthyroidism.Verhoeven RP, Visser TJ, Doctor R, Hennemann G, Schalekamp MA.AbstractPlasma thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) were measured in 16 patients with Graves' disease. Patients were studied under the following conditions: first without any treatment, then, during beta-adrenergic blockade with propranolol, and finally after euthyroidism had been attained by carbimazole. During propranolol T3/T4 ratio decreased, whereas T4 remained unchanged. After carbimazole T3/T4 ratio returned to its pretreatment value. rT3/T4 ratio showed opposite changes. These results suggest that peripheral conversion of T4 into T3 and rT3 in hyperthyroidism is, at least partly, dependent on the functional status of the beta-adrenergic system. Suppressed peripheral conversion of T4 into T3 during beta-adrenergic blocking agents may contribute to the beneficial effects of these drugs in

thyrotoxicosis.

[Guest guest]

Was this in the days before supersensitive TSH measurements?CE Grim MDJust the low TSH. T4 was just inside the upper limit of Lab Corps norm - at the edge of "high" as was the T3. No explanation unless all the meds I was on, including the hydrocodone and occasional various muscle relaxers (they were trying to MAKE me sleep - didn't work) like soma, flexeril, threw them into normal range. I am trying to recall if I was on prednisone near that time too, but I am not sure as that can slew them. They put me on it occasionally because I was always sick with cold like symptoms too (I know now most likely due to the clonidine, but I was pretty confused toward the latter stages and just went with the flow)Subject: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Grim Clarence" Date: Saturday, March 26, 2011, 10:17 PM J Clin Endocrinol Metab. 1977 May;44(5):1002-5.Plasma thyroxine, 3,3',5-triiodothyronine and 3,3',5'-triiodothyronine during beta-adrenergic blockade in hyperthyroidism.Verhoeven RP, Visser TJ, Doctor R, Hennemann G, Schalekamp MA.AbstractPlasma thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) were measured in 16 patients with Graves' disease. Patients were studied under the following conditions: first without any treatment, then, during beta-adrenergic blockade with propranolol, and finally after euthyroidism had been attained by carbimazole. During propranolol T3/T4 ratio decreased, whereas T4 remained unchanged. After carbimazole T3/T4 ratio returned to its pretreatment value. rT3/T4 ratio showed opposite changes. These results suggest that peripheral conversion of T4 into T3 and rT3 in hyperthyroidism is, at least partly, dependent on the functional status of the beta-adrenergic system. Suppressed peripheral conversion of T4 into T3 during beta-adrenergic blocking agents may contribute to the beneficial effects of these drugs in thyrotoxicosis.

[Guest guest]

I would suggest a red herring but have not pubmeded HThy AND HTN.I never had any rate issues before, but it starting getting into the 130's 140's during the thyroid period. BP never wavered until I got the spiro and that was late 2010. Was always high no matter what med. But the forceness of the heartbeat and the rate improved dramatically after I went back on BB in 4/10. Had no effect on BP. I do know I was able to stop (except rarely) the BB after the first normal TSH when the symptoms were gone and this was long before spiro or PA dx. TSH normal since and I have had no return of the hyperT symptomsJust a weird one.....Subject: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Grim Clarence" Date: Saturday, March 26, 2011, 10:17 PM J Clin Endocrinol Metab. 1977 May;44(5):1002-5.Plasma thyroxine, 3,3',5-triiodothyronine and 3,3',5'-triiodothyronine during beta-adrenergic blockade in hyperthyroidism.Verhoeven RP, Visser TJ, Doctor R, Hennemann G, Schalekamp MA.AbstractPlasma thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) were measured in 16 patients with Graves' disease. Patients were studied under the following conditions: first without any treatment, then, during beta-adrenergic blockade with propranolol, and finally after euthyroidism had been attained by carbimazole. During propranolol T3/T4 ratio decreased, whereas T4 remained unchanged. After carbimazole T3/T4 ratio returned to its pretreatment value. rT3/T4 ratio showed opposite changes. These results suggest that peripheral conversion of T4 into T3 and rT3 in hyperthyroidism is, at least partly, dependent on the functional status of the beta-adrenergic system. Suppressed peripheral conversion of T4 into T3 during beta-adrenergic blocking agents may contribute to the beneficial effects of these drugs in thyrotoxicosis.

[Guest guest]

Last yearSubject: thyroid and BB old study by excellent

group.To: hyperaldosteronism Cc: "Grim Clarence" Date: Saturday, March 26, 2011, 10:17 PM J Clin Endocrinol Metab. 1977 May;44(5):1002-5.Plasma thyroxine, 3,3',5-triiodothyronine and 3,3',5'-triiodothyronine during beta-adrenergic blockade in hyperthyroidism.Verhoeven RP, Visser TJ, Doctor R, Hennemann G, Schalekamp MA.AbstractPlasma thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) were measured in 16 patients with Graves' disease. Patients were studied under the following conditions: first without any treatment, then, during beta-adrenergic blockade with propranolol, and finally after euthyroidism had been attained by carbimazole. During propranolol T3/T4 ratio decreased, whereas T4 remained unchanged. After carbimazole T3/T4 ratio returned to its pretreatment value. rT3/T4 ratio showed opposite changes. These results suggest that peripheral conversion of T4 into

T3 and rT3 in hyperthyroidism is, at least partly, dependent on the functional status of the beta-adrenergic system. Suppressed peripheral conversion of T4 into T3 during beta-adrenergic blocking agents may contribute to the beneficial effects of these drugs in thyrotoxicosis.

[Guest guest]

They claimed they saw papilldema on admission, CTsays no, optometry now says no. That was Admitting dx as was also hypokalemia. Been hospitalized x 3 for HTN since 9/2008 and never with a normal K . After tsh became normal vision changes were gone completely. The worse symptoms all left as soon as the tsh normalized on lab. I also had this past year Low T, low cortisol, and high calcium. Only the T was very dramatically low. They r/o, as they told me, parathyroid issues.. And had pituitary scan. Told it was normal. As far as an explanation for the BP being so high all the time - and I would often hit 180/140 but never was the sytsolic getting higher than 180, but then I was always on BP meds and they very easily target systolic HTN and not so good with diastolic HTN. My diastolic is the one I never could even bring down a little with

anything but spiro. As for a normal ft4, ft3, etc with a low tsh....subclinical supposedly - but I was not subclinical by any means with the s/s. Was not taking anything that would mimic it, like a serotonin syndrome. Like I have said I have a suspicion it has come and gone. In 2008 when I was in a Lubbock hospital (admitted for HTN and Hypopkalemia) the on call PA came by one evening and told me to talk to Dr so and so in the AM as my TSH was very low, hyperthyroid. He told me he had it, it messed him up for a awhile and he got his out, he was fine. So I brought it up with the cardiologist and he said, "Oh that's not it!" Presumably due to a normal t3 t4 but I do not really know. I trust him and dropped it. Have had a rough time getting those records. I left with no real dx except LVH and HTN and new meds but not spiro and had the HTN ever since until spiro and DASH. There's seems to be plenty of cases of s/s with low

TSH and normal other parameters. So I don't know. S/S were classic hyperT. http://jcem.endojournals.org/cgi/content/abstract/87/3/1068http://www.internationaljournalofcardiology.com/article/S0167-5273%2808%2900475-0/abstract--- Subject: Re: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Clarence Grim" Date: Sunday, March 27, 2011, 11:11 AM

So they thought you had burned out thyroiditis? I don't understand the physiology of how one can have hyperthyroidism without being hyperthryoid. TSH alone does not make the Dx.Also u said you were hosp with malignant HTN. Very rare in PA. The Dx requires hemorrhages and exudates in the fundi. With out that it is not mailig. BP alone does not make the Dx. CE Grim MDTSH was very low 0.11. Everything else thyroid was ok or just above the cut-off. Scans were all normal. Subject: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Grim Clarence" Date: Saturday, March 26, 2011, 10:17 PM J Clin Endocrinol Metab. 1977 May;44(5):1002-5.Plasma thyroxine, 3,3',5-triiodothyronine and 3,3',5'-triiodothyronine during beta-adrenergic blockade in hyperthyroidism.Verhoeven RP, Visser TJ, Doctor R, Hennemann G, Schalekamp MA.AbstractPlasma thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) were measured in 16 patients with Graves' disease. Patients were studied under the following conditions: first without any treatment, then, during beta-adrenergic blockade with propranolol, and finally after euthyroidism had been attained by carbimazole. During propranolol T3/T4 ratio decreased, whereas

T4 remained unchanged. After carbimazole T3/T4 ratio returned to its pretreatment value. rT3/T4 ratio showed opposite changes. These results suggest that peripheral conversion of T4 into T3 and rT3 in hyperthyroidism is, at least partly, dependent on the functional status of the beta-adrenergic system. Suppressed peripheral conversion of T4 into T3 during beta-adrenergic blocking agents may contribute to the beneficial effects of these drugs in thyrotoxicosis.

[Guest guest]

can you do a pubmed on PA and hyperthyroid? I know very low T can cause hyperaldo.CE Grim MDLast yearSubject: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Grim Clarence" Date: Saturday, March 26, 2011, 10:17 PM J Clin Endocrinol Metab. 1977 May;44(5):1002-5.Plasma thyroxine, 3,3',5-triiodothyronine and 3,3',5'-triiodothyronine during beta-adrenergic blockade in hyperthyroidism.Verhoeven RP, Visser TJ, Doctor R, Hennemann G, Schalekamp MA.AbstractPlasma thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) were measured in 16 patients with Graves' disease. Patients were studied under the following conditions: first without any treatment, then, during beta-adrenergic blockade with propranolol, and finally after euthyroidism had been attained by carbimazole. During propranolol T3/T4 ratio decreased, whereas T4 remained unchanged. After carbimazole T3/T4 ratio returned to its pretreatment value. rT3/T4 ratio showed opposite changes. These results suggest that peripheral conversion of T4 into T3 and rT3 in hyperthyroidism is, at least partly, dependent on the functional status of the beta-adrenergic system. Suppressed peripheral conversion of T4 into T3 during beta-adrenergic blocking agents may contribute to the beneficial effects of these drugs in thyrotoxicosis.

[Guest guest]

Papilledema is not enough to Dx malignant phase in my experience and definition and teaching. As you can see it is not an easy sign to Dx. Rarely seen these days used to be very common with H and E when I first started training. I only rely on hemorrhages and exudates. So was not malignant HTN then.They claimed they saw papilldema on admission, CTsays no, optometry now says no. That was Admitting dx as was also hypokalemia. Been hospitalized x 3 for HTN since 9/2008 and never with a normal K . After tsh became normal vision changes were gone completely. The worse symptoms all left as soon as the tsh normalized on lab. I also had this past year Low T, low cortisol, and high calcium. Only the T was very dramatically low. They r/o, as they told me, parathyroid issues.. And had pituitary scan. Told it was normal. As far as an explanation for the BP being so high all the time - and I would often hit 180/140 but never was the sytsolic getting higher than 180, but then I was always on BP meds and they very easily target systolic HTN and not so good with diastolic HTN. My diastolic is the one I never could even bring down a little with anything but spiro. As for a normal ft4, ft3, etc with a low tsh....subclinical supposedly - but I was not subclinical by any means with the s/s. Was not taking anything that would mimic it, like a serotonin syndrome. Like I have said I have a suspicion it has come and gone. In 2008 when I was in a Lubbock hospital (admitted for HTN and Hypopkalemia) the on call PA came by one evening and told me to talk to Dr so and so in the AM as my TSH was very low, hyperthyroid. He told me he had it, it messed him up for a awhile and he got his out, he was fine. So I brought it up with the cardiologist and he said, "Oh that's not it!" Presumably due to a normal t3 t4 but I do not really know. I trust him and dropped it. Have had a rough time getting those records. I left with no real dx except LVH and HTN and new meds but not spiro and had the HTN ever since until spiro and DASH. There's seems to be plenty of cases of s/s with low TSH and normal other parameters. So I don't know. S/S were classic hyperT. http://jcem.endojournals.org/cgi/content/abstract/87/3/1068http://www.internationaljournalofcardiology.com/article/S0167-5273%2808%2900475-0/abstract--- Subject: Re: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Clarence Grim" Date: Sunday, March 27, 2011, 11:11 AM So they thought you had burned out thyroiditis? I don't understand the physiology of how one can have hyperthyroidism without being hyperthryoid. TSH alone does not make the Dx.Also u said you were hosp with malignant HTN. Very rare in PA. The Dx requires hemorrhages and exudates in the fundi. With out that it is not mailig. BP alone does not make the Dx. CE Grim MDTSH was very low 0.11. Everything else thyroid was ok or just above the cut-off. Scans were all normal. Subject: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Grim Clarence" Date: Saturday, March 26, 2011, 10:17 PM J Clin Endocrinol Metab. 1977 May;44(5):1002-5.Plasma thyroxine, 3,3',5-triiodothyronine and 3,3',5'-triiodothyronine during beta-adrenergic blockade in hyperthyroidism.Verhoeven RP, Visser TJ, Doctor R, Hennemann G, Schalekamp MA.AbstractPlasma thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) were measured in 16 patients with Graves' disease. Patients were studied under the following conditions: first without any treatment, then, during beta-adrenergic blockade with propranolol, and finally after euthyroidism had been attained by carbimazole. During propranolol T3/T4 ratio decreased, whereas T4 remained unchanged. After carbimazole T3/T4 ratio returned to its pretreatment value. rT3/T4 ratio showed opposite changes. These results suggest that peripheral conversion of T4 into T3 and rT3 in hyperthyroidism is, at least partly, dependent on the functional status of the beta-adrenergic system. Suppressed peripheral conversion of T4 into T3 during beta-adrenergic blocking agents may contribute to the beneficial effects of these drugs in thyrotoxicosis.

[Guest guest]

gotchyaSubject: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Grim Clarence" Date: Saturday, March 26, 2011, 10:17 PM J Clin Endocrinol Metab. 1977 May;44(5):1002-5.Plasma thyroxine, 3,3',5-triiodothyronine and 3,3',5'-triiodothyronine during beta-adrenergic blockade in hyperthyroidism.Verhoeven RP, Visser TJ, Doctor R, Hennemann G, Schalekamp MA.AbstractPlasma thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3)

were measured in 16 patients with Graves' disease. Patients were studied under the following conditions: first without any treatment, then, during beta-adrenergic blockade with propranolol, and finally after euthyroidism had been attained by carbimazole. During propranolol T3/T4 ratio decreased, whereas T4 remained unchanged. After carbimazole T3/T4 ratio returned to its pretreatment value. rT3/T4 ratio showed opposite changes. These results suggest that peripheral conversion of T4 into T3 and rT3 in hyperthyroidism is, at least partly, dependent on the functional status of the beta-adrenergic system. Suppressed peripheral conversion of T4 into T3 during beta-adrenergic blocking agents may contribute to the beneficial effects of these drugs in thyrotoxicosis.

[Guest guest]

Prensa Med Mex. 1978 May-Jun;43(5-6):177-81.[secondary

arterial hypertension and hyperaldosteronism caused by adrenal adenoma

and subsequently by hyperthyroidism. Case report]. [Article in Spanish] Zamora M, Ortíz Quezada F, García R.PMID: 748913 [PubMed - indexed for MEDLINE]Probl Endokrinol (Mosk). 1975 Sep-Oct;21(5):26-9.[Hyperaldosteronism in thyrotoxicosis]. [Article in Russian]Bezverkhaia TP.AbstractIn

30 patients with a moderately severe and severe form of thyrotoxicosis

a study was made of urinary aldosterone excretion following acid

hydrolysis, by thin-layer chromatography. During decompensation the

majority of the patients displayed an increased aldosterone excretion.

Medicinal compesation of the disease did no lead to normalization of

the mineralocorticoid function of the adrenal glands, whereas

aldosterone excretion remained high in many of the patients. To

ascertain the mechanisms of increase of aldosterone excretion in

thyrotoxicosis a correlative analysis was carried out of associations

between the aldosterone excretion and the circulating blood and plasma

volume, potassium blood plasma content, catecholamine and

17-oxycorticoid excretion. On the basis of the results obtained and

literature data it was supposed that intensified beta-adrenergic

activity of the nervous system and increased catecholamine production

participated in increase in the mineralocorticoid function of the

adrenal glands during thyrotoxicosis.PMID: 1228748 [PubMed - indexed for MEDLINE]Subject: Re: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Clarence Grim" Date: Sunday, March 27, 2011, 5:59 PM

can you do a pubmed on PA and hyperthyroid? I know very low T can cause hyperaldo.CE Grim MD

[Guest guest]

Heres a more recent one:

Endocrine Abstracts (2009) 20

P307

Coincidence of primary hyperaldosteronism with

thyrotoxic nodular goiter presenting as hypokalemic periodic paralysis:

complicating or mimicking one another?

Inan Anaforoglu & Ekrem Algün

Department of Endocrinology; Trabzon Numune Training and Research Hospital, Trabzon, Turkey.

Thyrotoxicosis and primary hyperaldosteronism both

cause hypokalemic periodic paralysis. A 51-year-old woman, with a

history of 3 episodes of transient muscle weakness, was admitted to the

emergency unit with complaint of the weakness of legs. Her medical

history included hypertension for 10 years. A nodule approximately 3 cm

in diameter was palpated in the left anterior neck. Decreased strength

(2/5) and deep tendon reflexes in lower extremities symmetrically with

normal sensory examination were detected. Initial laboratory findings

were significant for a potassium of 1.5 mEq/l and sodium of 148 mmol/l.

Thyroid function tests were compatible with primary hyperthyroidism

with a hyperactive nodule in scintigraphy. The patient was prescribed

propylthiouracil. Her potassium was replaced. She completely regained

muscle strength. A diagnosis of thyrotoxic hypokalemic periodic

paralysis was supposed. Nevertheless, a decrease in potassium level was

observed in each time, immediately when replacement of potassium was

stopped. A high level of aldosterone 51.6 ng/dl with supressed renin

0.2 ng/ml per hour, and the high ratio of aldosterone to renin (258)

were compatible with the diagnosis of primary hyperaldosteronism.

Plasma aldosteron was found to be 66.8 ng/dl after saline infusion

test. Imaging of surrenal glands showed an adrenal mass on the left

side. The diagnosis of hyperaldosteronism was supposed. Spironolactone,

200 mg/day, was started gradually. On the second week of therapy the

patient became normokalemic without support of oral potassium

perchloride. Spironolactone 200 mg/day and amlodipin 10 mg/day was

enough to control her blood pressure. Whether thyrotoxicosis or

hyperaldosteronism triggered hypokalemic periodic paralysis in this

patient is a matter of debate. Two cases of thyrotoxicosis and primary

aldosteronism complicating with hypokalemic periodic paralysis have

been introduced to literature to date. In conclusion, adrenal function

should be considered in a patient with hypertension and hypokalemia

whatever the presentation of cases are.Subject: Re: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Clarence Grim" Date: Sunday, March 27, 2011, 5:59 PM

can you do a pubmed on PA and hyperthyroid? I know very low T can cause hyperaldo.CE Grim MD

[Guest guest]

This pt had a thyroid nodule which helps helps the DXSO WE NOW have 3 IIn the world lit would expect more than that by chance as both are fairly common but T causing paralysis is rare bTiped sad Send form miiPhone ;-)May your pressure be low!CE Grim MDSpecializing in DifficultHypertension

Heres a more recent one:

Endocrine Abstracts (2009) 20

P307

Coincidence of primary hyperaldosteronism with

thyrotoxic nodular goiter presenting as hypokalemic periodic paralysis:

complicating or mimicking one another?

Inan Anaforoglu & Ekrem Algün

Department of Endocrinology; Trabzon Numune Training and Research Hospital, Trabzon, Turkey.

Thyrotoxicosis and primary hyperaldosteronism both

cause hypokalemic periodic paralysis. A 51-year-old woman, with a

history of 3 episodes of transient muscle weakness, was admitted to the

emergency unit with complaint of the weakness of legs. Her medical

history included hypertension for 10 years. A nodule approximately 3 cm

in diameter was palpated in the left anterior neck. Decreased strength

(2/5) and deep tendon reflexes in lower extremities symmetrically with

normal sensory examination were detected. Initial laboratory findings

were significant for a potassium of 1.5 mEq/l and sodium of 148 mmol/l.

Thyroid function tests were compatible with primary hyperthyroidism

with a hyperactive nodule in scintigraphy. The patient was prescribed

propylthiouracil. Her potassium was replaced. She completely regained

muscle strength. A diagnosis of thyrotoxic hypokalemic periodic

paralysis was supposed. Nevertheless, a decrease in potassium level was

observed in each time, immediately when replacement of potassium was

stopped. A high level of aldosterone 51.6 ng/dl with supressed renin

0.2 ng/ml per hour, and the high ratio of aldosterone to renin (258)

were compatible with the diagnosis of primary hyperaldosteronism.

Plasma aldosteron was found to be 66.8 ng/dl after saline infusion

test. Imaging of surrenal glands showed an adrenal mass on the left

side. The diagnosis of hyperaldosteronism was supposed. Spironolactone,

200 mg/day, was started gradually. On the second week of therapy the

patient became normokalemic without support of oral potassium

perchloride. Spironolactone 200 mg/day and amlodipin 10 mg/day was

enough to control her blood pressure. Whether thyrotoxicosis or

hyperaldosteronism triggered hypokalemic periodic paralysis in this

patient is a matter of debate. Two cases of thyrotoxicosis and primary

aldosteronism complicating with hypokalemic periodic paralysis have

been introduced to literature to date. In conclusion, adrenal function

should be considered in a patient with hypertension and hypokalemia

whatever the presentation of cases are.Subject: Re: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Clarence Grim" Date: Sunday, March 27, 2011, 5:59 PM

can you do a pubmed on PA and hyperthyroid? I know very low T can cause hyperaldo.CE Grim MD

[Guest guest]

did they measure renin as well it should have been high?CE Grim MDPrensa Med Mex. 1978 May-Jun;43(5-6):177-81.[secondary arterial hypertension and hyperaldosteronism caused by adrenal adenoma and subsequently by hyperthyroidism. Case report].[Article in Spanish] Zamora M, Ortíz Quezada F, García R.PMID: 748913 [PubMed - indexed for MEDLINE]Probl Endokrinol (Mosk). 1975 Sep-Oct;21(5):26-9.[Hyperaldosteronism in thyrotoxicosis].[Article in Russian]Bezverkhaia TP.AbstractIn 30 patients with a moderately severe and severe form of thyrotoxicosis a study was made of urinary aldosterone excretion following acid hydrolysis, by thin-layer chromatography. During decompensation the majority of the patients displayed an increased aldosterone excretion. Medicinal compesation of the disease did no lead to normalization of the mineralocorticoid function of the adrenal glands, whereas aldosterone excretion remained high in many of the patients. To ascertain the mechanisms of increase of aldosterone excretion in thyrotoxicosis a correlative analysis was carried out of associations between the aldosterone excretion and the circulating blood and plasma volume, potassium blood plasma content, catecholamine and 17-oxycorticoid excretion. On the basis of the results obtained and literature data it was supposed that intensified beta-adrenergic activity of the nervous system and increased catecholamine production participated in increase in the mineralocorticoid function of the adrenal glands during thyrotoxicosis.PMID: 1228748 [PubMed - indexed for MEDLINE]Subject: Re: thyroid and BB old study by excellent group.To: hyperaldosteronism Cc: "Clarence Grim" Date: Sunday, March 27, 2011, 5:59 PM can you do a pubmed on PA and hyperthyroid? I know very low T can cause hyperaldo.CE Grim MD