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Although some studies
suggest differently, it is generally accepted that bone mass is
reduced in thyrotoxicosis, and overt osteoporosis occurs in
long-standing hyperthyroidism. For this reason, many incorporate
measurements of thyroid hormones or thyroid-stimulating hormone
(TSH) in the evaluation of elderly subjects with osteoporosis. It
has been reported that the negative effect of thyroid hormone on
bone occurs more frequently in female patients.
The effects on bone mass appears to be reversible after effective treatment of the thyroid disease. Normalisation of the thyroid function tests, leads to a substantial increase in bone mineral density measured both at the lumbar spine and proximal femur. Grant et al reported however, that previous hyperthyroidism remained a risk factor for osteoporosis in patients who were treated with radio-active iodine and who were currently euthyroid. Whether "subclinical" hyperthyroidism, i.e. a decreased TSH with normal values for thyroid hormones, has any effect on bone mass is still matter of debate. Subjects with subclinical hyperthyroidism have a slight increase in bone turnover and might have a reduced bone mass. Faber et al found that bone density decreased by approximately 2% per year in postmenopausal women with subclinical hyperthyroidism who were untreated. Treatment with radio-active iodine, resulting in normalisation of TSH, prevented this bone loss at a faster rate. Similar results were reported by Mudde et al, who found that in postmenopausal women with endogenous subclinical hyperthyroidism, treatment with methimazol prevented excessive bone loss. On the other hand, in a study by Folder et al, there was no difference in bone mass in premenopausal women with subclinical hyperthyroidism compared to an euthyroid control group, although they did find a slight and not statistically significant lower bone mass in postmenopausal women with subclinical hyperthyroidism. The results of the various studies on this matter, suggest that bone loss in subclinical hyperthyroidism is primarily a problem in postmenopausal women. The difference between pre- and postmenopausal women might be explained by the fact that bone turnover is already increased in the latter. High levels of thyroid hormone accelerate this process further with subsequently an increase in the rate of bone loss. Although on theoretical grounds (see above), one would expect that in hypothyroidism, bone mass might be elevated, it appears to be similar to that of euthyroid subjects. Subsequent treatment of hypothyroidism with thyroid hormone has been reported to decrease or to have no effect on bone mineral density. For instance, in a study by Hanna et al, there was no effect on bone mass by adequate thyroid replacement therapy. Schneider et al, found that a replacement dose of thyroxin of 1.6 µg/kg or less, had no effect on bone mass, whereas higher doses led to a decrease in bone mineral density. In order to suppress TSH-secretion, subjects with thyroid carcinoma and nontoxic goitre, receive supraphysiologic doses of thyroid hormone. In a meta-analysis, Raber et al examined the effect of supraphysiologic doses of thyroid hormone on bone mass. After on average 8.5 years, subjects had 2.67% lower bone mass than controls. However, Franklyn et al found no effect of suppressive doses of thyroid hormone on bone density in subjects who had undergone thyroidectomy for differentiated thyroid cancer, despite long-term thyroxin therapy. As with subclinical hyperthyroidism, it has been suggested that supraphysiologic doses of thyroid hormone leads to bone loss primarily in postmenopausal women, and not in premenopausal women or in men. However, the size of the studies addressing this matter are too small to draw definite conclusions. Several studies have shown that the negative effects of thyroid hormone on bone can be negated by either bisphosphonates or (in women) maybe by estrogen replacement therapy. Calcitonin has not proven to be effective. Few studies have addressed the question whether thyroid disease increases fracture risk and the results of these studies are inconsistent. In a retrospective study, Solomon et al found no enhanced prevalence of hip, vertebral or forearm fractures in subjects with thyroid disease. However, they did observe a propensity for fractures to occur earlier in women with a history of hyperthyroidism. Leese et al observed no excess of fractures in patients on thyroxin treatment even when TSH was suppressed. In contrast, Franklyn et al recently reported an excess mortality (standardised mortality ratio 2.9) as a consequence of hip fractures in a large group of women treated with radioactive iodine for hyperthyroidism. |
