Hypothyroidism and excessive sweating
by cris2009, Jul 08, 2009
Hello All,

This is sort of gross but ever since my partial thyroidectomy in September 2007, I have been excessively sweating all the time, especially in my armpits. I have never had a problem with sweating before in my life. I am hypothyroid but seem to have symptoms of both hyper and hypo.
I have tests done and it's not menopause or adrenal issues. I am currently on .50 of Synthroid and I believe my last TSH was 2.9?? ( still confused how all THAT works).

Anyway, has anyone else noticed themselves sweating, a lot?  

Is it the Synthroid? Is it that my levels are not right?

Any info, help, same stories???

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Member Comments (28)
by rdavila, Jul 08, 2009

Me too.  I can just be standing, doing nothing and start sweating.  Moreover, though Im Hypo, I have an intolorance to heat not cold.  I love the cold bc I DONT SWEAT.  It is so emparassing. (pls excuse the spelling...)
by rdavila, Jul 08, 2009
P.S. I don't think that its the synthroid bc I had this prob b4 the meds.
by Terri627, Jul 08, 2009
Hi Cris,

Yes, I have been experiencing this very embarrassing problem since I had my thyroid
removed. In fact, I'm sitting here next the the open door, typing. Must be quite a
workout because I am sweating right now. In the clinic department where I work,
it seems l am hearing people complain all day about how cold it is. Well, they
don't have to work in that department, so I keep it as cold as the a/c will allow.
Sometimes I want to jump into the deep freezer just to cool off. My only coworker
wears long sleeves and a long sleeve lab coat to keep warm. But, there I am
self-conscious, sure I am not the lovely fresh flower I want to be. I am currently
hypo, meds are messed up again, but the cold air is a welcome treat.

So, yes, I am somewhat relieved to know there are people who share my pain.
But, when I'm has to be really cold out...I'm freezing! There doesn't seem
to be a happy medium in there for me at all :(
by cris2009, Jul 14, 2009

Thanks for getting back to me. Well I am glad that I am not alone.

Hmm. If you are saying it is not the actual medication, then what do you attribute it to?
TSH levels not right?
by cris2009, Jul 14, 2009

Thanks for getting back to me.

Sounds like your TSH level is not right either. Could this be the problem? Have you been tested for anything else to rule other reasons out?
by Texas2013, Mar 26, 2011
I am currently a second year medical student and was recently diagnosed with Hoshimoto's thyroiditis (the most common form of primary hypothyroidism) and my hyperhidrosis is what caused me to seek clinical attention -It's embarrassing to do a physical exam on someone and start sweating all over them. The TSH test is the most sensitive test for hypothyroidism and is the best indicator for positive clinical outcome Why this test works is because TSH is secreted under negative feedback via free T3 (which is converted from T4 in the brain) therefore, High TSH means that there is either a pituitary tumor (Very Very RARE and tend to be familial) or primary hypothyroidism (>99%). This can be differentiated by a laboratory measurement of high free T4 (=TUMOR) or Low free T4 (=Primary thyroid dysfunction). To answer your question, the primary hypothyroidisms are clinically diagnosed with a TSH over 10 and low free T4, so your TSH being below 10 seems makes me believe that you are in a euthyroid state on your current replacement therapy. Levothyroxine (Synthroid) is literally a T4 replacement that is made by recombinant bacteria; therefore, since this is analogous to natural T4 it isn't likely to be the problem. However, I feel your pain 100% because my hyperhidrosis is currently the bane of my existence. Theoretically, after prolonged treatment there should be a down regulation of the sweat glands after a prolonged state of euthyroidism however, I am not so lucky as to have experienced this yet! The problem stems from the fact that there is a high stress level on the body which causes excess DHEA-S to be secreted from the adrenal glands (primarily due to an attempt to replace gonadal hormones like testosterone from the low Luteinizing hormone via High TSH) this causes maturation and overstimulation of the sweat glands and other things like male-pattern baldness, enlarging prostate, and thick facial hair (Hirsutism). This process is accelerated if you are overweight and/or a smoker. Hope this answers your question fully and I wish you the best..
by gimel, Mar 26, 2011
am taking the time to write all this because  there are a couple of things that you should be aware of, that you won't hear about during your medical training.  I say this because you made several statements that obviously you have already been taught, that upon close examination just don't hold water.  

First is the belief that "TSH is the most sensitive test for hypothyroidism".  Yes, that is what is taught by most medical schools, but the reality is that TSH is affected by so many variables that it is totally inadequate as the sole diagnostic for thyroid.  TSH even has a circadian rhythm that peaks at around 9 p.m.  and is lowest around 9 a.m..   Studies have shown as much as a 72 % difference from high to low, so the time of day when blood is drawn is important.  I have unsuccessfully searched and searched for supporting data that TSH correlates even adequately with the most important thyroid test, which is free T3.  I say this because FT3 largely regulates metabolism and many other body functions.  Scientific studies have also shown that FT3 correlated best with hypo symptoms, while FT4 and TSH did not correlate.  Here is a link to that study.

The degree of correlation of FT3 to symptoms is amazing when considering that the symptom score was a total of 8 main hypo symptom ratings that were individually rated subjectively by the patients.  If you want to be dismayed further, take a look at the variability inherent in a large group of patients that were screened for thyroid problems and then tested for TSH.    The results are shown in fig. 2 on page 5 of this link.

As far as TSH correlating with T3, that is not supported by this study.
I ran across this link some time ago.  If you look at Fig. 6-7 you will see that for a given individual, TSH correlated very well with FT4.  In fact for each of the three individuals with test data that are plotted, the FT4 accounts for above 85% of the variation in TSH.  This is very good correlation, and leaves little room for any FT3 effect on TSH.

If you look further at the three curved lines, representing three sets of data, you will see that each one is different.  There is great variation from one line to another.  For example if you plotted a horizontal line at about .8 TSH, the corresponding FT4 among the three would vary from about 6, up to about 14.  This huge amount of variation in just three sets of patient data shows conclusively that TSH and FT4 do not correlate well at all for the general population of patients.  The data show that you could establish a very good correlation of TSH to FT4 for a given patient, by running a series of tests and doing statistical analysis of the results.  But the result of that would not justify the bother and the cost.  

Trying to use TSH as a diagnostic is bad enough.  It is even worse when trying to dose a patient by only trying to get the TSH result to fall within the range after medication.  This quote is from the following link to the British Medical Journal, Sept. 1986. 

"We consider that biochemical tests of thyroid function are of
little, if any, value clinically in patients receiving thyroxine
replacement. Most patients are rendered euthyroid by a daily dose
of 100 or 150 mcg of thyroxine. Further adjustments to the dose
should be made according to the patient's clinical response."

So from what I have learned from patients on the Forum and what research I have done, TSH is only an indicator, to be considered along with more important indicators such as symptoms and also levels of the biologically active thyroid hormones, free T3 and free T4.  Symptom relief should be all important, not test results.  

Your eyes might be further opened if you will read through this link.

Another thing you should be aware of is that, contrary to what you might hear at school, FT3 and FT4 results that fall just within the low limit of the reference range are frequently consistent with having hypo symptoms.   This is easily explainable by the fact that the reference ranges have never been corrected like was done for TSH over 8 years ago.  At that time the AACE came to the conclusion that there were far more hypo patients than the 2 1/2%  predicted by their old reference range.  When they went back and purged the data base for suspect hypo patients, and recalculated the limits, the range went from .5 - 5.0 down to .3 - 3.0.  That was a drastic change.  Unfortunately most labs and doctors still cling to the old range, and many hypo patients suffer from it.  

Also unfortunately the data bases for FT3 and FT4 have never been similarly purged of suspect hypo patient data.  With much experience with statistical analysis, I would roughly estimate that if the data bases were purged like done for TSH, that the new ranges would look more like the upper half of the current ranges.  Clearly to me, that is why we hear from so many members with FT3 and FT4  in the lower part of the ranges, yet they still suffer with hypo symptoms.  Many of our members report that symptom relief for them required that FT3 was adjusted into the upper part of its range and FT4 adjusted to at least midpoint of its range.  

I hope that this small sampling of the type of info that is available will make you stop and ask questions before you become yet another doctor that does not listen to symptoms, and diagnoses by only TSH, or if FT3 and FT4 are tested  and results fall within the very low area of the ranges, then conclude firmly that "everything is normal" and nothing further is needed,  "Your symptoms must be due to something else."

I would have no problem with the current ranges if they were used as guidelines within which to adjust FT3 and fT4 as necessary to relieve symptoms.  Instead the ranges are used as pass/fail.  Where is the logic to that when the ranges are so broad?  How can a test result at the very low limit possibly be equally as good for the patient as one toward the high limit of the range?

But I should warn you that bringing up these questions will not make you popular with your professors.  It might even adversely affect your grades.  Only in a few medical schools that we have learned about are they teaching that TSH is old hat and that FT3 and FT4 are the most important tests.  Even in those schools I am not sure that they are yet teaching that the clinical approach is the best.

I know you don't have a lot of spare time, but I suggest that you spend a few minutes occasionally on the Forum.  You'll find out a lot about reality in the world of hypothyroidism, as opposed to the theories you are being taught.  I hope that you will pop in once in a while and let us know how these thoughts were received in school.   LOL
by Texas2013, Mar 27, 2011
First off I would like to say I am a student doctor; I don’t claim to be a licensed physician.  Also, gimel I commend you for doing ample research on the topic and you seem quite knowledgeable about the topic.  However, for this patient I stated that serum FT4 would indicate the actual manner of their thyroid dysfunction and is always an indicated test for hypothyroidism. Furthermore, I have multiple problems with your argument and have stated them below.

First off, in addressing the paper you cited regarding the FT3 as the best indicator for therapeutic outcome, If you read the study design they used the old RIA for laboratory TSH. The new RIA-TSH  has a much greater accuracy and precision rating which correlates better with a positive predictive value than the test available between May 1984 and July 1997. Furthermore, in regards to this resource I have to side with the current American Thyroid Association Guidelines for Detection of Thyroid Dysfunction as of 2000 which states:
"Serum TSH measurement is the single most reliable test to diagnose all common forms of hypothyroidism and hyperthyroidism, particularly in the ambulatory setting. An elevated serum TSH concentration is present in both overt and mild hypothyroidism. In the latter, the serum FT4 concentration is, by definition, normal. While serum TSH measurement confirms or excludes the diagnosis in all patients with primary hypothyroidism, it will not reliably identify patients with central (secondary) hypothyroidism, in whom serum TSH concentrations may be low, normal, or mildly elevated. When there is suspicion of pituitary or hypothalamic disease, the serum FT4 concentration should be measured in addition to the serum TSH concentration."

In addressing the topic of TSH secretion and  the circadian rhythm (which is present in all hypothalamic-pituitary hormone secretion except prolactin) in disease processes the cyclic pattern of hypothalamic release is not upheld; the fact is, that TSH secretion is both stimulated by TRH from the hypothalamus (causing the circadian rhythm) and suppressed by hypothalamic dopamine, hypothalamic and free somatostatin, and free T4 (FT4). In the absence of FT4, the lack of suppression (negative feedback) is great enough that hypothalamic TRH stimulation is not needed in order to stimulate TSH secretion. For this reason, prolonged and severe hypothyroidism can induce a TSH secreting pituitary adenoma

In addressing the source, I have a few things to say regarding the figure you are looking at is regarding suppression of TSH with levothyroxine supplementation. They are comparing FT4 with TSH to show the negative feedback control of hypothalamic suppression. If one were trying to correlate disease state with therapeutic outcome you would need to use total T4 (TT4). The serum concentration of TT4 as a result of TBG abnormalities, or drugs competing with T4 binding to TBG, have no effect on the level of serum TSH and serial evaluations and thus serves as a better independent indicator of actual therapeutic levels (in fact, when a physician order T4 the results reported are TT4)  Furthermore, I believe that you are misinterpreting the figure and are making gross assumptions based upon a sample size of 3 people.  They state a coefficient of determination (r^2) ranging between 0.875-0.902, this correlates to a negative correlation coefficient (r) of 0.935-0.949 (93.5%-94.9%) which is not large enough to be considered statistically different considering n=3 and thus CANNOT be extrapolated to as a reference for the general population (especially since this is not a population wide study). This being said, the data means that there is practically a 1:1 inverse relationship between plasma [TSH] and [FT4] even in this relatively small population in which co-morbidities are not known (i.e., we don’t get better tests in medicine!)

Also, it should be noted that FT3 is measured in the urine and is directly dependent upon hepatic and renal Type I iodothyronine deiodinase, but biological activity is dependent upon Type 2 iodothyronine deiodinase found in the CNS, heart, fat, muscle, skin, heart, etc.. Therefore, any hepatic disease, renal disease, or 199 of the top 200 prescribed drugs in America, which may affect the liver or kidneys, can alter the power of this test. (N.B. >99% of all drugs are metabolized by the liver &/or kidneys and thus affect them in one way or another.)

Before I begin on my review of your citation of British Medical Journal, Sept. 1986,.which is based upon 2nd generation TSH testing, I want to state that higher doses of T4 (>150 mcg/day) carries a significant risk of cardiac arrhythmias and atrial fibrillation which cause thromboembolic strokes in 30% of all a-fib patients. The quote that you cite is no longer the valid as it is outdated. The current belief is that the sensitive thyrotropin (TSH) test is the preferred method to monitor therapy because it agrees with physiologic measures of thyroid hormone EFFECT. Among clinically euthyroid patients who take 100 to 150 micrograms/d of levothyroxine, the probability that the sensitive thyrotropin will be undetectable is close to 50% (i.e., 50/100 with hypothyroidism will not have detectable TSH) . These patients are most likely to benefit from testing. Patients who take over 250 micrograms/d are almost certain to have undetectable sensitive thyrotropin levels; in these patients, the dose may be lowered without testing.. Ann Intern Med. 1990 Sep 15;113(6):450-4.

To be frank, the vast majority of patients’ that have continued symptomatology (greater than 3 months) despite clinical euthyroidism are dealing with low level depression or anxiety and actually benefit from prolonged SSRI therapy rather than increased T4, especially in light of the fact that at higher doses of T4 there is a serious risk of side effects. So in the case of hypothyroidism, the goal is not necessarily symptom relief as it is correction of [TSH] since the vast majority of residual symptoms tend to be psychosomatic if they are persistent for 2-3 months after treatment. According to an article in Psychiatry Investig. 2010 Dec;7(4):264-9 “There was a significant association between lower (hyperthyroid) serum TSH levels (<0.5 mIU/L) and cognitive impairment after adjustment [odds ratio 7.12 (95% confidence interval 1.35-37.5)]. However, no association was found between TSH levels and depression.” Therefore, depression and anxiety symptoms (sweating, fatigue, sadness, guilt, palpitations, tremor, fear, etc...) are better treated with antidepressant/antipsychotic drugs rather than dangerously high doses of levothyroxine. In fact, one of the best things a hypothyroid patient can do reverse the ‘residual’ symptoms is to exercise (which causes endorphin release and relieves stress!)

In regards to your reference to, the opinion of one person that does not show data supporting his claim cannot be taken at face value. The multiple problems associated with the full hearted belief that one man’s feelings about an issue is indeed fact, even when that belief is in gross opposition with the concurrent consensus found in multiple peer reviewed journals and multinational health organizations is very dangerous. For example, who knows how many children have died due to preventable disease when one man, Dr. Andrew Wakefield, misrepresented or altered the medical histories of all 12 of the patients whose cases formed the basis of the 1998 study linking the use of childhood vaccines with autism. The fact is simple, without data to support your claims; a claim is just an opinion NOT fact