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Severe viral hepatitis type B in infancy;
Insights
Severe hepatitis B virus infection can occur in infants, sometimes leading to death. Maternal transmission and neonatal blood exposure are significant risk factors for infant hepatitis B.
Area of Science:
- Hepatology
- Virology
- Pediatrics
Background:
- Infants can develop severe acute viral hepatitis, presenting as fulminant liver failure.
- Hepatitis B virus (HBV) infection is a significant concern in neonatal populations.
- Risk factors include neonatal blood product exposure and maternal carriage of hepatitis B surface antigen (HBSAg).
Purpose of the Study:
- To investigate the clinical presentation and outcomes of acute viral hepatitis in infants.
- To determine the association of hepatitis B virus with severe hepatitis in infants.
- To identify potential routes of transmission, including maternal contamination.
Main Methods:
- Analysis of clinical data from fourteen infants with acute viral hepatitis.
- Assessment of liver function tests (prothrombin time, serum glutamic pyruvic transaminase, bilirubin).
- Hepatitis B virus markers (hepatitis B surface antigen [HBSAg] and antibody [HBSAb]) detection using passive haemagglutination and radioimmunoassay.
- Liver biopsy in cases of liver failure.
- Review of neonatal transfusion history and maternal HBSAg carrier status.
Main Results:
- Eleven out of fourteen infants had evidence of hepatitis B virus infection (HBSAg and/or rising HBSAb).
- Liver biopsies in eight infants showed widespread necrosis without inflammation.
- Eight infants had received neonatal blood derivatives; five had mothers who were chronic HBSAg carriers.
- Eight out of fourteen infants died despite intensive supportive care, including exchange transfusions and anti-HBS gamma-globulins.
Conclusions:
- Severe and fulminant hepatitis B can occur in infants.
- Infants are capable of eliminating the hepatitis B virus.
- Maternal contamination is a likely source of severe hepatitis in infants.
- Early identification and management of hepatitis B in infants are crucial.
Abstract:
Fourteen infants aged from 2 to 5 months were admitted to hospital with acute viral hepatitis. Their clinical presentation ranged from severe disease to fulminant hepatitis. In all patients the prothrombin-time was 10% or less of normal and serum glutamic pyruvic transaminase and bilirubin were increased. In eight cases liver-biopsy specimens were obtained during liver failure and showed a widespread necrosis without inflammatory cells. Hepatitis-B-surface antigen (HBSAg) and antibody (HBSAb) were sought by several techniques, including passive haemagglutination and radioimmunoassay. Hepatitis was associated with hepatitis-B virus in eleven out of fourteen patients as judged by the detection of HBSAg and/or a secondary rise in HBSAb. In eight cases, the infants had received blood-derivatives in the neonatal period. The mothers of five of the remaining cases were found to be chronic carriers of HBSAg. Despite intensive supportive therapy, including repeated exchange transfusions and administration of anti-HBS gamma-globulins (six cases), eight patients died. These cases demonstrate that severe or fulminant type-B hepatitis can develop in infants, who are capable of completely eliminating the hepatitis-B virus. They also suggest that severe hepatitis can result from maternal contamination.