摘要
骨頭飢餓症候群是一種成功的切除副甲狀腺後因骨頭過度再礦化造成低血鈣和低血磷。需要補充大量的鈣質來矯正。本文是描述一位原發性副甲狀腺機能亢進的病患因作副甲狀腺切除引發骨頭飢餓症候群。我們給予病患補充大量的鈣克康注射劑(calcium gluconate)和氫氧化維生素D(dihydroxy-vitamin D3)，病患低血鈣的情形在持續33天後才得到改善。有些學者認為在切除副甲狀腺手術前給予補充氫氧化維生素D可以預防此症候群的發生。但臨床的觀察顯示此做法的效果是可疑的。有些個案研究顯示在開刀前給予雙磷酸鹽類可預防骨頭飢餓症候群的發生。詳細的機轉並不清楚。但雙磷酸鹽除了暫時性抑制骨質再礦化外，也可以抑制蝕骨細胞的作用。目前對於骨頭飢餓症候群仍有許多未知之處，我們需要對此作更深入的研究。
關鍵字
無資料並列摘要
Hungry bone syndrome (HBS) is a syndrome of persistent hypocalcemia and hypophosphatemia resulting from extensive bone remineralization after successful parathyroidectomy. Large amounts of calcium are needed to correct it. We describe a patient with primary hyperparathyroidism who developed HBS after parathyroidectomy. She received copious amounts of calcium infusion and calcitriol before her serum calcium level returned to normal range. Some authors believed preoperative treatment with dihydroxy-vitamin D3 may prevent this syndrome. But its effect is variable. A few case reports suggested that preoperative administration of bisphosphonates prohibits hungry bone syndrome. Though the exact mechanism is not known, bisphosphonates are known to have potent inhibitory effect on osteoclastic activity in addition to transient inhibitory effect on mineralization. Much more research on HBS is needed.
延伸閱讀
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