Accelerated bone loss in hypothyroid patients overtreated with L-thyroxine

Article Abstract:

Thyroid hormones are important for proper cell growth and development, but an excess of thyroid hormones may lead to the accelerated breakdown of bone in the body (osteoporosis), a process that makes the bones brittle. Osteoporosis can affect any bone in the body, but most frequently affects the vertebrae, the units that make up the spine. This condition is most common in postmenopausal women, and frequently leads to debilitating hip and leg fractures. This study assessed the rates of bone loss from the spine, forearm, and leg in 10 women who had low thyroid hormone levels (hypothyroidism) and who were overtreated with thyroid hormones, meaning they were inadvertently given doses that were too high for them. Also, approximately 240 women with no disease of the thyroid gland were studied as a control group; the number of controls varied slightly depending on the specific bones evaluated. All patients were receiving calcium supplementation at the time of the study. Women with hypothyroidism who were overtreated with thyroid hormones had a greater rate of bone loss from the spine, and exhibited similar losses in the forearm and leg, as compared with control women. These results suggest that women with hypothyroidism who are overtreated with an excess of thyroid hormones may lose bone more rapidly and develop osteoporosis more readily than women with no known thyroid disease. The results also suggest that women being treated with thyroid supplements should be carefully followed for signs of osteoporosis. (Consumer Summary produced by Reliance Medical Information, Inc.)

Complications and side effects, Physiological aspects, Drug therapy, Hypothyroidism, Thyroid hormones, Aged women, Elderly women, Thyroid diseases

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Glucocorticoid-induced osteoporosis: pathogenesis and management

Article Abstract:

Glucocorticoids, hormones released from the adrenal cortex, are involved in the regulation of carbohydrate and protein metabolism. These hormones have also been shown to cause osteoporosis or bone loss, and patients receiving long-term glucocorticoid therapy have developed fractures of the vertebrae or spine. The clinical findings, pathogenesis, and treatment of glucocorticoid-induced osteoporosis are discussed. Results of studies suggest that glucocorticoids have direct effects on the bone, specifically by preventing bone formation and increasing bone breakdown. These hormones also decrease the absorption of calcium in the intestine and promote calcium elimination by the kidneys. Osteoporosis develops in 50 percent of persons on long-term glucocorticoid therapy. The use of low-dose forms that can be eliminated rapidly from the body may help prevent glucocorticoid-induced osteoporosis. Other measures to prevent or treat bone loss due to glucocorticoid therapy include maintaining physical activity, sufficient calcium and vitamin D intake, sodium restriction, use of thiazide diuretics which increase water elimination from the body, and therapy to replace gonadal hormones such as estrogen and testosterone. In conclusion, osteoporosis is a common adverse effect of long-term therapy with glucocorticoids. (Consumer Summary produced by Reliance Medical Information, Inc.)

Corticosteroids, Adrenocortical hormones

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Secondary osteoporosis: the potential relevance of leptin and low body weight

Article Abstract:

The hormone leptin may explain the link between body mass and osteoporosis. Leptin deficiency has been linked to high bone mass, which could explain why obesity protects against osteoporosis, and why girls with anorexia have a higher risk of osteoporosis. Leptin is a hormone that controls body weight.

Editorial, Leptin, Body weight

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