Sub-clinical thyroid disease

By definition sub-clinical diseases only come to our attention as a result of screening. In my evaluation of patients referred for osteoporosis I screen for hyperthyroidism in almost all.

The patient that prompts today’s blog is a 55-year-old woman who had her first bone density study in 1999 when she was still premenopausal. She did not recall why the study had been ordered but the result was OK. By the time she had her first follow up study in 2003 she had become menopausal and there was the expected early postmenopause rapid drop in bone density. She took alendronate for a year before stopping due to gastro-intestinal adverse effects. She had a further decline in 2005 and 2008 but the changes were quite small.

Somewhere in this time frame she had an episode of “thyroiditis,” which resolved aside from persistent tachycardia for which she is taking propranolol 20 mg once or twice a day. She also had a history of kidney stone, which raises the possibility of hypercalciuria. Physical examination was normal and in particular she had no overt manifestations of thyroid disease. Her 24 hour urine calcium was normal.

Free T4 was at the upper limit of normal at 1.46 ng/dL (reference 0.50 to 1.50) but TSH was low at 0.03 mIU/L (reference (0.34 to 5.60). To go along with this, serum C-telopeptide (CTX), a marker of bone resorption, was also at the upper end of the normal range at 650 pg/mL (reference 242 to 696), a value consistent with the thyroid studies.

There would be nothing wrong with re-starting her on a bisphosphonate since these drugs work by inhibiting bone resorption. However, with a treatable secondary cause of osteoporosis, albeit “sub-clinical,” it would be more appropriate to treat the secondary cause first. Confirmation of a cause and effect relationship between her thyroid disease and her ongoing bone loss will come when I re-check the CTX in three months. If my approach in this case is correct the CTX should be lower as thyroid function improves.