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急性胰腺炎时甲状旁腺反应不足。

Inadequate parathyroid response in acute pancreatitis.

作者信息

Robertson G M, Moore E W, Switz D M, Sizemore G W, Estep H L

出版信息

N Engl J Med. 1976 Mar 4;294(10):512-6. doi: 10.1056/NEJM197603042941002.

Abstract

We studied nine consecutive hypocalcemic patients with acute pancreatitis to elucidate the mechanism of hypocalcemia. Mean serum ionized calcium, 0.97 mM, was below the normal mean of 1.16 mM (P less than 0.001). Seven of eight patients tested had normal parathyroid hormone levels. All responded to parenteral parathyroid extract by increasing serum ionized calcium and urinary cyclic AMP, indicating parathyroid-hormone-responsive target organs. Calcitonin and glucagon concentrations were increased above normal in some patients, but there was no relation with serum ionized calcium. Parenteral glucagon had no significant effect on serum ionized calcium or calcitonin concentrations. These findings suggest that neither glucagon nor calcitonin was primarily responsible for the hypocalcemia, which did not produce expected increases in serum parathyroid hormone concentrations. Relative parathyroid insufficiency may account for the persistent hypocalcemia frequently observed in patients with acute pancreatitis.

摘要

我们研究了9例连续性急性胰腺炎伴低钙血症患者,以阐明低钙血症的机制。平均血清离子钙为0.97 mM,低于正常平均值1.16 mM(P<0.001)。8例接受检测的患者中有7例甲状旁腺激素水平正常。所有患者对肠外甲状旁腺提取物均有反应,血清离子钙和尿环磷酸腺苷增加,表明甲状旁腺激素反应性靶器官正常。部分患者降钙素和胰高血糖素浓度高于正常,但与血清离子钙无关。肠外给予胰高血糖素对血清离子钙或降钙素浓度无显著影响。这些发现表明,胰高血糖素和降钙素均不是低钙血症的主要原因,低钙血症并未引起血清甲状旁腺激素浓度的预期升高。相对甲状旁腺功能不全可能是急性胰腺炎患者中经常观察到的持续性低钙血症的原因。

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