methimazole and Osteoporosis

Topics: Aged; Anticoagulants; Antithyroid Agents; Atrial Fibrillation; Female; Humans; Hyperthyroidism; Methimazole; Osteoporosis; Practice Guidelines as Topic; Risk Factors; Thyroid Function Tests; Thyrotropin; Thyroxine

It is well-know that hyperthyroidism is one of the key causes of secondary osteoporosis. High values of thyroid hormones increase the bone mineral turnover speed by promoting osteoclastic and osteoblastic activities. The aim of our study is to evaluate the increase of bone mineral density (BMD) in osteoporotic and hyperthyroid patients treated with only antithyroid drugs versus patients treated with antithyroid drugs and diphosphonates.. Twenty-six elderly male patients, 65-75 years, were selected. In all these patients, thyroid function (FT3, FT4, TSH, Tg, AbTg, AbTPO) was evaluated at baseline and after 6 and 12 months from the start of medical treatment; the following were evaluated: BMD, calcium serum, phosphorus serum, alkaline phosphatase, PTH and 24 hours urinary calcium, phosphorus and hydroxyprolin. Thirteen patients (group 1) were treated with antithyroid drugs (methimazole 5-20 mg/die/os) and diphosphonates (alendronate 10 mg/die/os). The control group of 13 patients (group 2) was treated with antithyroid drugs only.. After 6 months of treatment, the patients of group 1 showed a mean increase of 2.5% in lumbar spine BMD compared with a mean increase of 0.3% in group 2 (p<0.01). After 12 months, group 1 showed a mean increase of 6.2% in lumbar spine BMD, compared with a mean increase of 2% in group (p<0.001).. The combination of antithyroid and diphosphonates drugs appears to be more efficacious than antithyroid therapy alone for the treatment of osteoporosis in male hyperthyroid patients.

Topics: Aged; Alendronate; Alkaline Phosphatase; Antithyroid Agents; Bone Density; Calcium; Case-Control Studies; Drug Therapy, Combination; Humans; Hyperthyroidism; Male; Methimazole; Osteoporosis; Parathyroid Hormone; Phosphorus; Treatment Outcome

Topics: Aged; Alendronate; Antithyroid Agents; Bone Density; Drug Therapy, Combination; Femur Neck; Humans; Hyperthyroidism; Lumbar Vertebrae; Male; Methimazole; Osteoporosis

Adults with hyperthyroidism have been found to have decreased bone mineral density (BMD) and higher fracture risk. The most typical cause of hyperthyroidism is Graves' disease. However, there are limited studies on how hyperthyroidism affects bone metabolism and fractures in children. We describe a unique instance of a patient who initially displayed a fragility fracture and was ultimately identified with Graves' disease after biochemical evaluations.. A 2-year-8-month-old female presented with fragility fractures three times in only 7 months. A series of examinations were performed to evaluate any possible malformations or abnormalities of bone metabolism. Graves' disease was found, and drug therapies were employed (methimazole, propranolol, calcium carbonate, vitamin D). Since children with Graves' disease and fragility fractures have been uncommonly described in the past, a stringent and thorough long-term follow-up was initiated.. Children with undiagnosed Graves' disease had a higher risk of fractures and osteoporosis. This case suggests that BMD measurement may be necessary for the initial evaluation of Graves' disease in children.

Topics: Adult; Child; Female; Graves Disease; Humans; Hyperthyroidism; Infant; Methimazole; Osteoporosis; Propranolol

The osteoporosis associated with human hyperthyroidism has traditionally been attributed to elevated thyroid hormone levels. There is evidence, however, that thyroid-stimulating hormone (TSH), which is low in most hyperthyroid states, directly affects the skeleton. Importantly, Tshr-knockout mice are osteopenic. In order to determine whether low TSH levels contribute to bone loss in hyperthyroidism, we compared the skeletal phenotypes of wild-type and Tshr-knockout mice that were rendered hyperthyroid. We found that hyperthyroid mice lacking TSHR had greater bone loss and resorption than hyperthyroid wild-type mice, thereby demonstrating that the absence of TSH signaling contributes to bone loss. Further, we identified a TSH-like factor that may confer osteoprotection. These studies suggest that therapeutic suppression of TSH to very low levels may contribute to bone loss in people.

Topics: Animals; Bone Density; Bone Diseases, Metabolic; Bone Resorption; Dose-Response Relationship, Drug; Drug Implants; Hormone Replacement Therapy; Hyperthyroidism; Hypothyroidism; Methimazole; Mice; Mice, Inbred C57BL; Mice, Knockout; Osteoporosis; Phenotype; Receptors, Thyrotropin; Signal Transduction; Thyrotropin; Thyroxine