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Nine children with acute typical post-diarrhea hemolytic uremic syndrome (HUS) were treated with intravenous gammaglobulin (IVIG). These children were compared to nine children with HUS who did not receive IVIG. The use of IVIG did not appear to have a beneficial effect on eight of the nine treated children. There were no significant differences found in the duration of hemorrhagic colitis, thrombocytopenia, elevation of the white blood count (WBC), anuria, dialysis, or hospitalization, or the presence of a central nervous system complication or pancreatitis. Although no significant difference was found in the duration of thrombocytopenia, there was a trend towards a longer duration of thrombocytopenia in children treated with IVIG (P = 0.13). One child demonstrated both an increase in her platelet count and a decrease in her WBC count within 24 h of receiving her first dose of IVIG.

A retrospective study of 76 children with hemolytic uremic syndrome (HUS) who were admitted to the Alberta Children's Hospital in Calgary. Alberta between January 1982 and December 1988 was undertaken to explore the gastrointestinal manifestations of the syndrome. The children (mean age of 4.0 +/- 3.1 years) presented primarily during the summer months with a microangiopathic hemolytic anemia (Hgb 94 +/- 26 g/L), thrombocytopenia (platelets 87 +/- 83 X 10(9)/L), and acute renal failure (oligoanuria with a BUN of 26 +/- 15 mmol/L, and a creatinine of 294 +/- 90 mumol/L). Forty-three children required dialysis for 10 +/- 17 days. The duration of hospitalization was 17 +/- 17 days. Four children died of complications attributable to HUS. The following symptoms and gastrointestinal manifestations of HUS were noted: fever (33%), vomiting (80%), abdominal discomfort/tenderness (59%), diarrhea (100%), hemorrhagic colitis (79%), rectal prolapse (13%), colonic stricture (3%), colonic perforation (1%), intussusception (1%), indirect hyperbilirubinemia (49%), and elevated hepatocellular enzymes (58%). Of the last 29 children studied, 19 (66%) had elevated levels of amylase and lipase in the presence of acute renal failure, and six (21%) had a marked elevation of lipase (more than four times normal) with additional supportive evidence of pancreatitis. The additional supportive evidence included persistent elevation of lipase after the resolution of acute renal failure in four children, a marked increment in lipase in association with abdominal pain and an abnormal ultrasound of the pancreas after the initiation of oral feeding in a fifth child, and pancreatic exocrine and endocrine necrosis at autopsy in a sixth child.(ABSTRACT TRUNCATED AT 250 WORDS)