The effects of subclinical hyperthyroidism on bone mineral density (BMD) induced by thyroid-stimulating hormone (TSH) suppression therapy in patients with differentiated thyroid cancer (DTC) remains unclear. We conducted a meta-analysis to determine the influence of TSH suppression therapy on BMD.
We performed a systematic search to identify studies which included BMD measurement of femoral neck, total hip or lumbar spine in patients on TSH suppression therapy for DTC. Main outcome measures were difference of BMD of femoral neck, total hip or lumbar spine measured by dual energy X-ray absorptiometry between patients and controls.
A systematic search yielded a total of 11 published controlled cross-sectional studies (including about 571 patients and 836 controls). TSH suppression therapy was associated with the lower BMD of total hip (weighted mean difference [WMD], −0.023; 95% confidence interval [CI], −0.047 to 0.000;
Although the included studies were limited by small numbers, results suggested possible association between chronic TSH suppression therapy and the lower BMD of spine and total hip in postmenopausal women (but not in premenopausal women and men) with DTC. A large, well-designed study with long-term follow-up would provide further insight into the influence of TSH suppression therapy and loss of BMD.
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Patients with gastrointestinal disease (GI) are at risk for osteopenia or osteoporosis, which can lead to fractures. Although these patients may be at risk from a young age, gastroenterologists often overlook this fact in practice. There are well-known GI diseases associated with osteopenia and osteoporosis, such as the post-gastrectomy state, inflammatory bowel disease (IBD), and celiac disease. As there is an increase in the prevalence of IBD patients, newly diagnosed celiac disease in adulthood, and gastric cancer survivors following gastrectomy, bone disease in these patients becomes an important issue. Here, we have discussed osteoporosis and fractures in GI disease, especially in the post-gastrectomy state, IBD, and celiac disease. Although the pathogenesis of bone loss in each disease has not been fully identified, we have confirmed that the prevalence of osteoporosis and fractures in each of these diseases is high. There are scarce studies comparing the prevalence of osteoporosis or osteoporotic fractures in GI disease patients with studies in postmenopausal women, and specific guidelines for their management in each disease have not been established. Intensive surveillance and management are needed to ensure that these patients attain peak bone mass for age and sex to prevent fractures.
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