Elsevier

The Lancet

Volume 352, Issue 9142, 28 November 1998, Pages 1739-1741
The Lancet

Articles
Acute parvovirus B19 infection associated with fulminant hepatitis of favourable prognosis in young children

https://doi.org/10.1016/S0140-6736(98)06165-0Get rights and content

Summary

Background

The cause of fulminant hepatitis (FH) in children is unexplained in up to 50% of cases. We report parvovirus B19 as an agent associated with FH in children and compare clinical characteristics of these patients with those of age-matched patients with FH of other origin.

Methods

45 patients presented with FH. No cause was apparent in 21 patients. Parvovirus B19 genome was retrospectively sought by PCR in serum collected at admission in 41 patients.

Findings

Parvovirus B19 genome was detected in serum from four of 21 patients with unexplained FH (four of 11 younger than 5 years). No B19 DNA was detected in serum from patients with other types of FH or from 82 patients with biliary atresia. Parvovirus B19 IgM was detected in one of the four patients. Patients with parvovirus B19 infection had significantly lower bilirubin concentrations than age-matched patients with FH due to hepatitis A (nine) or other causes (nine) (poisoning with amanita excluded). All patients with parvovirus B19 survived without orthotopic liver transplantation, with restoration of normal liver function within 17 days.

Interpretation

In patients younger than 5 years with FH of unexplained origin, evidence of acute parvovirus B19 was associated with a distinct clinical pattern. In particular, low bilirubin concentrations and rapid recovery of liver function without transplantation were distinctive features.

Introduction

In a third to half of all children with fulminant hepatitis (FH) no cause is found.1 Once well-known hepatotropic agents and metabolic, toxic, and immunological causes have been excluded, an infectious origin remains a possibility. Opportunistic infections may be the cause of FH in immunocompromised patients.2 Parvovirus B19 DNA has been found in the liver of patients with fulminant hepatic failure associated with bone-marrow aplasia, and in serum of patients with acute, otherwise unexplained, hepatitis.3, 4, 5 Parvovirus B19 is the agent that causes erythema infectiosum (fifth disease). This virus is also associated with an acute aplastic crisis in patients with chronic haemolysis and causes bone-marrow failure in immunocompromised patients and acute or sometimes chronic arthropathies in adults.6, 7, 8, 9

We report a retrospective study of four immunecompetent patients, younger than age 5 years, who developed FH at the time of acute parvovirus B19 infection. The mode of presentation is compared with that of 18 age-matched patients with FH of other causes. To control specificity, parvovirus B19 genome was sought in an additional 37 children with FH and in 82 children who underwent transplantation for biliary atresia during the same period.

Section snippets

Methods

Between 1987 and 1997, 45 children were admitted to our unit with FH. Criteria for the diagnosis of FH were: liver disease of recent onset (less than 8 weeks); encephalopathy diagnosed clinically or by electroencephalography; and deficient hepatic synthetic function, with prothombin time, factor V blood level below 25%, or both.1, 10 All patients with FH were admitted to the intensive-care unit and were registered on the transplant waiting list unless contraindicated. If a patient recovered

Results

The B19 genome was detected in serum taken at the time of FH in four of 11 patients with unexplained FH (table 1). Other causes in this age-group included hepatitis A (nine cases), A phalloides poisoning (two), Epstein-Barr virus infection (one), and hepatitis C virus infection (one). Two of the children positive for parvovirus B19 had been admitted in 1992 and two in 1996. PCR did not detect B19 sequences in any of the other FH patients or any of the 82 age-matched controls with extrahepatic

Discussion

In this retrospective study of 45 children with FH, four cases classified as unknown aetiology were associated with acute parvovirus B19 infection. These four children represented a third of patients younger than 5 years. In one of the four children, an underlying metabolic disorder may have aggravated the liver damage. In three patients, however, parvovirus B19 was the only pathogen detected and no underlying metabolic disorder was identified. No patient with B19-associated FH had a history of

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