TY - JOUR
T1 - Sudden Blindness in Acute Pancreatitis
T2 - Possible Role of Complement-Induced Retinal Leukoembolization
AU - Jacob, Harry S
AU - Goldstein, Ira M.
AU - Shapiro, Irving
AU - Craddock, Philip R.
AU - Hammerschmidt, Dale E
AU - Weissmann, Gerald
N1 - Funding Information:
18531, AM-11949, HL-19721, and GM-23211 from the National Institutes of Health,bygrantsfromtheNationalFoundation-MarchofDimes,The andbyafromtheNationalScienceFoundation (grantCo.76-05621),TheWhitehallFoundation,
PY - 1981/1
Y1 - 1981/1
N2 - 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.
AB - 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.
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U2 - 10.1001/archinte.1981.00340010126025
DO - 10.1001/archinte.1981.00340010126025
M3 - Article
C2 - 7447575
AN - SCOPUS:0019424109
SN - 0003-9926
VL - 141
SP - 134
EP - 136
JO - Archives of Internal Medicine
JF - Archives of Internal Medicine
IS - 1
ER -