Cg. Pan et al., HEPATOCELLULAR INJURY IN STREPTOCOCCUS PNUMONIAE-ASSOCIATED HEMOLYTIC-UREMIC SYNDROME IN CHILDREN, Pediatric nephrology, 9(6), 1995, pp. 690-693
Streptococcus pneumoniae is an uncommon etiological organism in hemoly
tic uremic syndrome (HUS). Production of neuraminidase by S. pneumonia
e results in exposure of red blood cell T-antigen,resulting in hemolys
is, thrombocytopenia, and acute renal failure. Hepatic involvement in
this form of HUS has not been described in the literature. We report i
n three children with S. pneumoniae-associated HUS the presence of sev
erely elevated transaminases and conjugated hyperbilirubinemia. Increa
ses in asparagine transaminase ranged from 11 to 46 times normal value
s and an increase in alanine transaminase ranged from 1.6 to 8 times n
ormal. In all patients the rise in total bilirubin was 7-15 times norm
al. Biliary tree obstruction and viral causes for liver dysfunction we
re absent. Hepatocellular injury in S, pneumoniae-associated HUS likel
y results from mechanisms involved in sepsis and pneumonia-induced jau
ndice, 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 ev
aluation including liver biopsy is not indicated.