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DOI 10.1016/s0026-0495(96)90203-6

Медицинская библиотека · Metabolism: clinical and experimental · 1996

Decreased cortical and increased cancellous bone in two children with primary hyperparathyroidism.

Boechat M I, Westra S J, Van Dop C, Kaufman F, Gilsanz V, Roe T F

Клинический случайСравнительное исследованиеСтатьяПоддержка службы здравоохранения СШАПеревод пока не подготовлен

Аннотация

The basis for this study is two children with primary hyperparathyroidism (PHPT) who radiographically manifested both marked subperiosteal resorption and prominent osteosclerosis. We hypothesize that the parathyroid hormone (PTH) elevation not only increased osteoclastic resorption of cortical bone but also simultaneously enhanced cancellous bone formation, giving rise to osteosclerosis. In this report, we describe the changes in trabecular and cortical bone density, as measured by quantitative computed tomography (QCT), in these two young patients with severe PHPT, before and after removal of a parathyroid adenoma. Before surgery, the radiographic findings of subperiosteal resorption and osteosclerosis were associated with low cortical and high cancellous bone density values in both children. Within 1 week of surgery, both cortical and cancellous bone density values increased and serum concentrations of calcium and, to a lesser degree, phosphorus decreased due to the "hungry bone syndrome." Twelve weeks after parathyroidectomy, QCT bone density values and skeletal radiographs were normal in both patients. The findings suggest that in patients with severe PHPT, the catabolic effect of PTH on cortical bone may be associated with a simultaneous anabolic effect on cancellous bone, and PTH may cause a significant redistribution of bone mineral from cortical to cancellous bone.

Для цитирования: Boechat M I, Westra S J, Van Dop C, Kaufman F, Gilsanz V, Roe T F. Decreased cortical and increased cancellous bone in two children with primary hyperparathyroidism.. Metabolism: clinical and experimental. 1996. DOI: 10.1016/s0026-0495(96)90203-6.

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