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Hepatic Injury in the Toxic Epidemic Syndrome Caused by Ingestion of Adulterated Cooking Oil (Spain, 1981)
Author(s) -
SolisHerruzo JosÉ A.,
Castellano Gregorio,
Colina Francisco,
Morillas Juan Diego,
TeresamuñozYagüe Maria,
Coca Maria Del Carmen,
Jelavic Dusko
Publication year - 1984
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840040123
Subject(s) - cholestasis , medicine , jaundice , gastroenterology , liver injury , toxic hepatitis , ingestion , lesion , hepatitis , bilirubin , pathology , asymptomatic
Abstract We describe the clinico‐pathological characteristics of hepatic injury associated with the toxic‐epidemic syndrome caused by the consumption of adulterated rapeseed oil. Of 842 toxic‐epidemic syndrome patients admitted to our hospital between May, 1981, and January, 1982, 24.1% showed signs of liver involvement which was more frequent in women and in the fourth decade of life. No statistical significance was found in relation to alcohol consumption, treatment with potentially hepatotoxic antibiotics, or adult respiratory distress syndrome. Most (91.6%) patients with hepatic injury were asymptomatic; jaundice or abdominal pain was rarely noted. One patient died of acute liver failure following Budd‐Chiari syndrome. Serum 7‐glutamyl transpeptidase activity was raised in all cases, alkaline phosphatase in 94.6%, and less frequently lactate dehydrogenase (80%), SGPT (84.7%), and SGOT (76%). Serum total bilirubin was usually normal (89.2%). The histologic lesion was similar to drug‐induced cholestatic hepatitis. Lamellar inclusions, canalicular injury, giant mitochondria, and hyperplasia of the smooth endoplasmic reticulum were seen by electron microscopy. Ultrastructural signs of cholestasis were common (78.9%). The pathogenesis of this lesion is unknown; however, because of similarities with chlorpromazine‐induced cholestatic hepatitis, we suggest that a combination of hypersensitivity and intrinsic hepatotoxicity is a possible mechanism.