Abstract

We conducted prospective surveillance of childhood hemolytic uremic syndrome (HUS) from 1997 to 2001 to describe disease incidence and clinical, epidemiologic and microbiologic characteristics. We compared our findings, where possible, with those of a previous study conducted from 1985 to 1988. The average annual incidence of HUS for the United Kingdom and Ireland (0.71/100,000) was unchanged from 1985 to 1988. The overall early mortality had halved, but the reduction in mortality was almost entirely accounted for by improved outcome in patients with diarrhea-associated HUS. The principal infective cause of diarrhea-associated HUS was Shiga toxin-producing Escherichia coli O157 (STEC O157), although in the 1997-2001 survey STEC O157 phage type (PT) 21/28 had replaced STEC O157 PT2 as the predominant PT. The risk of developing diarrhea-associated HUS was significantly higher in children infected with STEC O157 PT 2 and PT 21/28 compared with other PTs. Hypertension as a complication of HUS was greatly reduced in patients with diarrhea-associated HUS.

Highlights

  • We conducted prospective surveillance of childhood hemolytic uremic syndrome (HUS) from 1997 to 2001 to describe disease incidence and clinical, epidemiologic and microbiologic characteristics

  • At least 80% of childhood HUS is attributable to infection with Shiga toxin–producing Escherichia coli (STEC)

  • Diarrhea-associated HUS was defined as disease that immediately followed diarrhea or bloody diarrhea

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Summary

Introduction

We conducted prospective surveillance of childhood hemolytic uremic syndrome (HUS) from 1997 to 2001 to describe disease incidence and clinical, epidemiologic and microbiologic characteristics. The most serious manifestation of infection with Shiga toxin–producing Escherichia coli (STEC) in humans is hemolytic uremic syndrome (HUS). This syndrome comprises a triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure, usually after a prodromal illness of acute gastroenteritis [1]. We conducted prospective surveillance of childhood HUS in the United Kingdom and Ireland from 1997 to 2001 to describe the impact of disease and clinical, epidemiologic, and microbiologic characteristics of the patients. We compared our findings, where possible, with those of a previous study [3,4]

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