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急性胰腺炎中的补体激活与补体调控蛋白

Complement activation and complement control proteins in acute pancreatitis.

作者信息

Whicher J T, Barnes M P, Brown A, Cooper M J, Read R, Walters G, Williamson R C

出版信息

Gut. 1982 Nov;23(11):944-50. doi: 10.1136/gut.23.11.944.

Abstract

Serum levels of the complement proteins C3, C4, C1 inhibitor (C1 INH), factor I (C3b inactivator) and factor H (BIH) and plasma levels of cleavage products of C3 (C3c) and factor B were measured in 26 patients with acute pancreatitis. Breakdown of C3 occurred in 19 patients, as shown by a reduction in C3 level and the presence of C3c. C4 levels, however, did not fall and factor B breakdown products were not detected, thus suggesting that enzymatic cleavage of C3 occurred without significant involvement of either the early classical pathway or the alternative pathway. C1 INH and factor H both showed increases, presumably reflecting an acute phase response. Factor I showed an initial fall followed by a rise. There was no correlation between the presence or extent of C3 breakdown and the clinical condition of the patients. It is concluded that C3 cleavage in pancreatitis probably results from tryptic activity and that the measurement of complement components has no part to play in the management of the disease.

摘要

对26例急性胰腺炎患者测定了补体蛋白C3、C4、C1抑制物(C1 INH)、I因子(C3b灭活剂)和H因子(BIH)的血清水平以及C3裂解产物(C3c)和B因子的血浆水平。19例患者出现C3分解,表现为C3水平降低和C3c的存在。然而,C4水平未下降,且未检测到B因子分解产物,因此提示C3的酶促裂解发生时,早期经典途径或替代途径均未显著参与。C1 INH和H因子均显示升高,推测反映了急性期反应。I因子先下降后上升。C3分解的存在或程度与患者的临床状况之间无相关性。结论是胰腺炎中的C3裂解可能是胰蛋白酶活性所致,补体成分的测定在该疾病的管理中不起作用。

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