Jacob H S, Goldstein I M, Shapiro I, Craddock P R, Hammerschmidt D E, Weissmann G
Arch Intern Med. 1981 Jan;141(1):134-6.
During an episode of acute alcoholic pancreatitis, severe visual loss and the funduscopic appearance of Purtscher's retinopathy-a syndrome thought to be caused by posterior retinal microembolization-developed in a patient. We propose that emboli in this case may have consisted of aggregated granulocytes since plasma samples from eight to 12 patients with subsequently studied acute pancreatitis caused granulocyte aggregation in vitro. The aggregant was demonstrated to be an activated fragment of the complement system, derived from C5. Since we could generate identical granulocyte aggregating activity by treating serum or purified C5 with trypsin, we suggest that proteases released from an inflamed pancreas might have produced a C5-derived aggregant in this case, as well as in three other previously reported cases of acute pancreatitis and Purtscher's retinopathy. We conclude that complement-induced leukoembolization may be a previously unsuspected cause of vital-tissue damage.
在一例急性酒精性胰腺炎发作期间，一名患者出现了严重的视力丧失以及普尔夏视网膜病变的眼底表现（一种被认为由视网膜后微栓塞引起的综合征）。我们提出，该病例中的栓子可能由聚集的粒细胞组成，因为对随后研究的8至12例急性胰腺炎患者的血浆样本进行体外研究时发现，这些样本会导致粒细胞聚集。已证实聚集剂是补体系统的一种活化片段，源自C5。由于我们通过用胰蛋白酶处理血清或纯化的C5能够产生相同的粒细胞聚集活性，我们认为，在该病例以及其他先前报道的三例急性胰腺炎和普尔夏视网膜病变病例中，发炎胰腺释放的蛋白酶可能产生了一种源自C5的聚集剂。我们得出结论，补体诱导的白细胞栓塞可能是一种此前未被怀疑的重要组织损伤原因。
