Hepatocellular injury in Streptococcus pneumoniae-associated hemolytic uremic syndrome in children. Pediatr Nephrol 1995 Dec;9(6):690-3
Date
12/01/1995Pubmed ID
8747106DOI
10.1007/BF00868713Scopus ID
2-s2.0-0029616224 (requires institutional sign-in at Scopus site) 31 CitationsAbstract
Streptococcus pneumoniae is an uncommon etiological organism in hemolytic uremic syndrome (HUS). Production of neuraminidase by S. pneumoniae results in exposure of red blood cell T-antigen, resulting in hemolysis, thrombocytopenia, and acute renal failure. Hepatic involvement in this form of HUS has not been described in the literature. We report in three children with S. pneumoniae-associated HUS the presence of severely elevated transaminases and conjugated hyperbilirubinemia. Increases in asparagine transaminase ranged from 11 to 46 times normal values and an increase in alanine transaminase ranged from 1.6 to 8 times normal. In all patients the rise in total bilirubin was 7-15 times normal. Biliary tree obstruction and viral causes for liver dysfunction were absent. Hepatocellular injury in S. pneumoniae-associated HUS likely results from mechanisms involved in sepsis and pneumonia-induced jaundice, combined with severely increased bilirubin production following massive hemolysis. The hepatic injury in all three patients resolved within 9, 5, and 10 days. Our experience suggests that an extensive evaluation including liver biopsy is not indicated.
Author List
Pan CG, Leichter HE, Werlin SLAuthor
Cynthia G. Pan MD Adjunct Professor in the Pediatrics department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Alanine TransaminaseAspartate Aminotransferases
Female
Hemolytic-Uremic Syndrome
Humans
Hyperbilirubinemia
Infant
Liver
Male
Pneumococcal Infections
Thrombocytopenia
