# More research on subclinical exogenous hyperthyroid risks



## artms (Jul 23, 2011)

Turns out the research from Society for Endocrinology
British Endocrine Societies was a breakthrough big deal especially for us who feel better in low range with adequate Frees. I feel much better about it. Enjoy the excerpts and go to the links for abstracts.\

http://www.australianprescriber.com/magazine/22/6/132/4
Risk of osteoporosis
There has been some concern that thyroxine given in doses that suppress serum TSH to undetectable concentrations might promote osteoporosis. Meta-analyses of various controlled studies in which thyroxine therapy has been (in some patients) excessive are difficult to interpret because of the heterogeneity of patients studied.12,13 One meta-analysis suggests that postmenopausal women with serum TSH concentration suppressed to below the reference range have a higher annual bone loss than healthy individuals not given thyroxine12; another suggests that thyroxine therapy, even when adjusted to give a TSH value within the range, is associated with bone loss in premenopausal women.13 However, a study of 1180 women (largely postmenopausal) on thyroxine for over 1 year found no increased rate of fracture when serum TSH concentration was suppressed to below 0.05 mU/L compared with those with a serum TSH concentration in the range 
0.05-4 mU/L.14 
It is likely that patients most at risk of developing osteoporosis from thyroxine therapy are those whose hypothyroidism has resulted from treatment of hyperthyroidism that might already have reduced bone mass. This view is supported by the results of a case-control study involving 148 women that examined the effect of previous thyroid history and thyroxine therapy on bone mineral density: thyroxine therapy alone did not represent a significant risk factor for loss of bone mineral density, but there was an increased risk of bone lost in postmenopausal (but not premenopausal) women with a previous history of thyrotoxicosis treated with radioiodine.15 The risk of osteoporosis from thyroid replacement therapy has probably been overestimated.

http://www.ncbi.nlm.nih.gov/pubmed/8770627?dopt=Abstract

Our study suggests that slightly suppressive L-thyroxine administration in nontoxic goitre can activate bone turnover but constitutes neither an actual risk factor for bone loss nor, consequently, for osteoporotic fractures.

http://www.ncbi.nlm.nih.gov/pubmed/8772604?dopt=Abstract
T4-suppressive therapy was associated with bone loss in postmenopausal women, which could be prevented by either calcium supplementation or intranasal calcitonin, although the latter did not provide additional benefit compared to calcium alone. However, careful titration of T4 dosage to maintain biochemical euthyroidism is a better way to avoid the adverse effect of T4 on bone.

http://hormones.gr/preview.php?c_id=171

In conclusion, the etiology of subclinical hyperthyroidism possibly affects BMD in postmenopausal women. Postmenopausal women with endogenous subclinical hyperthyroidism have significantly lower BMD, mainly at the distal and proximal cortical bone,versus healthy postmenopausal women. Therefore, endogenous subclinical hyperthyroidism (both of autoimmune and non autoimmune etiology) might be considered as an additional risk factor for oseoporosis in postmenopausal women. On the other hand, exogenous subclinical hyperthyroidism has no effect on BMD. Postmenopausal women with subclinical hyperthyroidism have a higher bone turnover rate in comparison with the control group, though they do not differ in biochemical parameters of calcium and phosphorous metabolism. 
http://www.ccjm.org/content/77/11/803.full

http://hormones.gr/preview.php?c_id=144

The management of exogenous SubHyper relies on appropriate adjustment of T4 dosage taking into consideration a) individual requirements in T4, sex, age and the presence of cardiovascular disease or other co-morbidity, b) the recognition that small changes in serum FT4 have a logarithmic effect on TSH, c) the variability of FT4-TSH interactions between individuals, d) the instability of T4 preparations and its bioavailability, and e) the values of serum FT4 and FT3 that accompany a suppressed TSH. This last parameter is of importance since it is the free thyroid hormones values in the serum that generate and reflect the thyroid metabolic state of the organism rather than the degree of TSH suppression.

http://hormones.gr/preview.php?c_id=171
The etiology of subclinical hyperthyroidism influences B MD in postmenopausal women. Endogenous subclinical hyperthyroidism might be considered as an additional risk factor for osteoporosis in postmenopausal women, especially for cortical bone, whereas exogenous subclinical hyperthyroidism has no effect on BMD.

Studies examining the effects of exogenous subclinical hyperthyroidism on bone density have been inconsistent. The results of two meta-analyses (1994 and 1996) showed significant bone loss in postmenopausal women on LT4 suppressive therapy versus the control group.21,22 However, two recent systematic reviews of the literature showed that BMD changes in postmenopausal women on LT4 suppressive therapy remain unclear and require further evaluation.19,20

However, in our study only women with endogenous subclinical hyperthyroidism had significantly lower BMD versus the control group, whereas there were no significant differences in BMD between patients with exogenous subclinical hyperthyroidism and the control group. Therefore, it is likely that not only low TSH level but also the etiology of subclinical hyperthyroidism affect BMD.

On the other hand, exogenous subclinical hyperthyroidism has no effect on BMD. Postmenopausal women with subclinical hyperthyroidism have a higher bone turnover rate in comparison with the control group, though they do not differ in biochemical parameters of calcium and phosphorous metabolism.

http://www.ncbi.nlm.nih.gov/pubmed/17324919
CONCLUSION:
The etiology of subclinical hyperthyroidism influences B MD in postmenopausal women. Endogenous subclinical hyperthyroidism might be considered as an additional risk factor for osteoporosis in postmenopausal women, especially for cortical bone, whereas exogenous subclinical hyperthyroidism has no effect on BMD.

http://endocrinetoday.com/view.aspx?rid=62295
"Our findings confirm that it may be safe for patients with hypothyroidism to take marginally higher doses of thyroxine than our currently recommended," Leese said in the release. "However, careful monitoring of these patients would still be required. We now need other studies to confirm our findings before any changes are made to routine clinical care." low, 0.04 mU/L-0.4 mU/L. 
http://www.endocrine-abstracts.org/ea/0021/ea0021oc5.6.htm
Society for Endocrinology BES 2010
Manchester, UK
15 March 2010 - 18 March 2010
Society for Endocrinology
British Endocrine Societies

http://www.imt.ie/news/uncategorized/2010/03/thyroxine-safe-with-low-tsh-levels.html

http://elaine-moore.suite101.com/uk-study-shows-that-low-tsh-doesn-a264769


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## Andros (Aug 26, 2009)

artms said:


> Turns out the research from Society for Endocrinology
> British Endocrine Societies was a breakthrough big deal especially for us who feel better in low range with adequate Frees. I feel much better about it. Enjoy the excerpts and go to the links for abstracts.\
> 
> http://www.australianprescriber.com/magazine/22/6/132/4
> ...


What a wealth of information; how can we ever thank you? You have been very very busy.

It's what I have always said; "Whatever it takes to get the patient to the euthyroid state; that is the place to be"

Hyper or hypo; neither bodes well for the body. This is true for animals as well.

It will take forever to read through the links but I am going to pursue it.

Thanks again!


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## artms (Jul 23, 2011)

I really wanted to sort out reliable research from the fringys. I think these are pretty good.

endogenous etiology refers to physiologic hyperthyroid
exogenous etiology stems from thyroxin replacement
subclinical is low range TSH before suppression .04-.4

So basically those who have exogenous subclinical hyperthyroid status due to T4 replacement do not suffer from increased fractures, low bone density or cardiomyopathy as opposed to those who are endogenously subclinical hyperthyroid on their way to frank hyperthyroid.
Bone density treatment with supplements and drugs which reduce fractures work with those who have drug related exogenous subclinical hyperthyroid.

I also ran into a lot of research that had a safe cut off of .1 That sounds a little too slick and arbitrary to me but who knows?It's still better than 1. for many folks. Many heads are better than one so if any of you find more in these or other links please post. Another thing I ran across was the benefit of Calcitonin which, BTW is in dessicated thyroid. Another plus.And to think the Endo I fired wanted me ill with a TSH of 1. We shouldn't have to work so hard, it's their job to keep up on this stuff.


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## Octavia (Aug 1, 2011)

artms, thanks for posting.

Regarding this part:

However, a study of 1180 women (largely postmenopausal) on thyroxine for over 1 year found no increased rate of fracture when serum TSH concentration was suppressed to below 0.05 mU/L compared with those with a serum TSH concentration in the range 
0.05-4 mU/L.14 

If I'm reading the post correctly, this study does not appear to examine very long-term effects...is that how you're reading it, too? Have you found other studies that look at the long-term effects of TSH suppression? I've never looked for these types of studies, so it would be interesting to know.


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## artms (Jul 23, 2011)

The latest was the real breakthrough, this one
http://endocrinetoday.com/view.aspx?rid=62295

http://www.mombu.com/medicine/medicine/t-study-osteoporosis-2235988.html

A large meta-analysis of patients with exogenous subclinical hyperthyroidism
showed that bone loss was greater among postmenopausal women with this
condition than among those without it.17 However, the validity of these
results is questionable, since the study also found increased bone loss in
premenopausal women who were receiving levothyroxine replacement therapy and
who had normal serum thyrotropin concentrations. Furthermore, the increased
risk of fracture reported in older women taking thyroid hormones disappears
when those with a history of hyperthyroidism are excluded.18 The evidence
that exogenous subclinical hyperthyroidism is a risk factor for osteoporosis
is therefore inconclusive.19,20 "

http://www.dr-bob.org/tips/split/Thyroid-replacement.html


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## artms (Jul 23, 2011)

The latest was the real breakthrough, this one
http://endocrinetoday.com/view.aspx?rid=62295

http://www.mombu.com/medicine/medicine/t-study-osteoporosis-2235988.html

A large meta-analysis of patients with exogenous subclinical hyperthyroidism
showed that bone loss was greater among postmenopausal women with this
condition than among those without it.17 However, the validity of these
results is questionable, since the study also found increased bone loss in
premenopausal women who were receiving levothyroxine replacement therapy and
who had normal serum thyrotropin concentrations. Furthermore, the increased
risk of fracture reported in older women taking thyroid hormones disappears
when those with a history of hyperthyroidism are excluded.18 The evidence
that exogenous subclinical hyperthyroidism is a risk factor for osteoporosis
is therefore inconclusive.19,20 "

http://www.dr-bob.org/tips/split/Thyroid-replacement.html


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