Sudden Blindness in Acute Pancreatitis: Possible Role of Complement-Induced Retinal Leukoembolization

Harry S Jacob, Ira M. Goldstein, Irving Shapiro, Philip R. Craddock, Dale E Hammerschmidt, Gerald Weissmann

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74 Scopus citations


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 of 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.

Original languageEnglish (US)
Pages (from-to)134-136
Number of pages3
JournalArchives of Internal Medicine
Issue number1
StatePublished - Jan 1981

Bibliographical note

Funding Information:
18531, AM-11949, HL-19721, and GM-23211 from the National Institutes of Health,bygrantsfromtheNationalFoundation-MarchofDimes,The andbyafromtheNationalScienceFoundation (grantCo.76-05621),TheWhitehallFoundation,


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