Goldstein I M, Cala D, Radin A, Kaplan H B, Horn J, Ranson J
Am J Med Sci. 1978 May-Jun;275(3):257-64. doi: 10.1097/00000441-197805000-00003.
Active proteolytic enzymes are released into the gland parenchyma and surrounding tissues during episodes of acute pancreatitis. Since complement components are potential substrates for active proteases and may be the source of biologically active peptides capable of mediating tissue injury, we have examined sera obtained from 12 patients during 13 episodes of acute pancreatitis for evidence of complement catabolism. In 8 of 13 acute phase sera, there were decreased levels of CH50, C3, C4, or some combination thereof as well as degradation products of C3 (revealed by crossed immunoelectrophoresis). In convalescent sera, levels of complement components were normal or elevated. Measurements of alpha1-antitrypsin, alpha2-macroglobulin, and trypsin inhibitory capacity failed to reveal evidence of protease-antiprotease imbalance. These findings provide evidence of complement catabolism in acute pancreatitis and suggest the possibility that activated complement components may play a role in the pathogenesis of some systemic pathologic changes which occur in this disease.
在急性胰腺炎发作期间,活性蛋白水解酶被释放到腺实质和周围组织中。由于补体成分是活性蛋白酶的潜在底物,并且可能是能够介导组织损伤的生物活性肽的来源,我们检查了13次急性胰腺炎发作期间从12名患者获得的血清,以寻找补体分解代谢的证据。在13份急性期血清中的8份中,CH50、C3、C4或它们的某种组合水平降低,以及C3的降解产物(通过交叉免疫电泳显示)。在恢复期血清中,补体成分水平正常或升高。α1-抗胰蛋白酶、α2-巨球蛋白和胰蛋白酶抑制能力的测量未能揭示蛋白酶-抗蛋白酶失衡的证据。这些发现提供了急性胰腺炎中补体分解代谢的证据,并提示活化的补体成分可能在该疾病发生的一些全身病理变化的发病机制中起作用的可能性。