Zaloga G P, Chernow B
Ann Intern Med. 1987 Jul;107(1):36-41. doi: 10.7326/0003-4819-107-1-36.
To learn about the pathogenesis of sepsis-associated hypocalcemia, we measured serum ionized calcium concentrations in 60 critically ill patients with bacterial sepsis; 12 (20%) had hypocalcemia. The mortality rate in the hypocalcemic patients with sepsis (50%) was higher than that in the normocalcemic patients with sepsis (29%). Only patients with gram-negative sepsis became hypocalcemic, and hypocalcemia contributed to hypotension in 7 of the 12 hypocalcemic patients. Serum calcium concentrations returned to normal in each of those patients with sepsis who survived. Hypocalcemia during sepsis occurred in previously normocalcemic patients and was multifactorial in origin, resulting from acquired parathyroid gland insufficiency, renal 1 alpha-hydroxylase insufficiency, vitamin D deficiency, and acquired calcitriol resistance. We conclude that the hypocalcemia of sepsis is associated with a high mortality rate and usually occurs in previously normocalcemic patients who acquire a defect in the parathyroid-vitamin D axis.
为了解脓毒症相关低钙血症的发病机制,我们测定了60例重症细菌性脓毒症患者的血清离子钙浓度;其中12例(20%)出现低钙血症。脓毒症低钙血症患者的死亡率(50%)高于脓毒症血钙正常患者(29%)。仅革兰阴性菌脓毒症患者出现低钙血症,12例低钙血症患者中有7例的低钙血症导致了低血压。存活的脓毒症患者血清钙浓度均恢复正常。脓毒症期间的低钙血症发生于既往血钙正常的患者,其病因是多因素的,由获得性甲状旁腺功能不全、肾1α-羟化酶功能不全、维生素D缺乏以及获得性骨化三醇抵抗所致。我们得出结论,脓毒症低钙血症与高死亡率相关,且通常发生于既往血钙正常但甲状旁腺-维生素D轴出现缺陷的患者。