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Possible Role of Complement-Induced Retinal Leukoembolization

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

Arch Intern Med. 1981;141(1):134-136.

Abstract
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.

(Arch Intern Med 141:134-136, 1981)

Author Affiliations
From the Departments of Medicine (Drs Jacob, Craddock, and Hammerschmidt) and Ophthalmology (Dr Shapiro), University of Minnesota Medical School, Minneapolis; and the Department of Medicine, New York University Medical School, New York (Drs Goldstein and Weissmann).

Footnotes
Accepted for publication Feb 25, 1980.

Reprint requests to University of Minnesota Hospitals, Box 480 Mayo Memorial Bldg, Minneapolis, MN 55455 (Dr Jacob).

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