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Cholestatic hepatitis in children infected with the human immunodeficiency virus
D Persaud1, B Bangaru, M A Greco
1Department of Pediatrics, New York University Medical Center/Bellevue Hospital Center, New York 10016.
Insights
Infants with perinatally acquired human immunodeficiency virus 1 infection can develop cholestatic hepatitis. This severe liver condition often presents early and is frequently fatal, with opportunistic infections being common causes of death.
Area of Science:
- Pediatric Hepatology
- Infectious Diseases
- Virology
Background:
- Perinatally acquired human immunodeficiency virus 1 (HIV-1) infection is a significant global health concern in infants.
- Early diagnosis and understanding of HIV-1 manifestations are crucial for timely intervention and improved outcomes.
Observation:
- Seven infants with perinatally acquired HIV-1 infection presented with a distinct clinical syndrome of cholestasis and hepatitis.
- Hepatitis was the initial manifestation in five infants, with a median onset age of 7 months.
- Elevated liver enzymes and bilirubin levels were noted, with a mean CD4 count of 766 cells/mm³ at hepatitis onset.
Findings:
- Six out of seven infants died within 12 weeks of hepatitis onset, primarily due to complications from Pneumocystis carinii pneumonia and cytomegalovirus.
- Liver failure was the direct cause of death in only one infant.
- No specific etiologic agent was identified for the cholestatic hepatitis, and HIV-1 RNA was not detected in liver tissues.
Implications:
- This study highlights a severe, often fatal, hepatic manifestation of vertically transmitted HIV-1 in infants.
- The findings underscore the need for vigilance regarding opportunistic infections and liver disease in HIV-1-infected infants.
- Further research is needed to elucidate the pathogenesis of HIV-1-associated cholestatic hepatitis and identify potential therapeutic targets.
Abstract:
A distinct clinical syndrome of cholestasis and hepatitis occurred during early infancy in seven infants with perinatally acquired human immunodeficiency virus 1 infection. In five infants hepatitis was the first manifestation of human immunodeficiency virus 1 infection. The median age of onset of hepatitis was 7 months (range, 5 to 10 months). The mean total bilirubin concentration at presentation was 7.4 mg/dl (range, 3.9 to 11 mg/dl), the mean aspartate aminotransferase was 1512 IU/liter (range, 782 to 2960 IU/liter) and the mean alanine amino-transferase 512 IU/liter (range, 92 to 1247 IU/liter). The absolute CD4 count at the time of onset of hepatitis ranged from 191 to 2298 cells/mm3 (mean, 766 cells/mm3). Six of the seven children died within 12 weeks of onset of hepatitis, three as a result of complications of Pneumocystis carinii pneumonia, and two died of complications secondary to cytomegalovirus. In only one infant was the cause of death the direct consequence of liver failure. The seventh infant died 17 months after the onset of hepatitis of dilated cardiomyopathy. No specific etiologic agent has been identified as the cause of cholestatic hepatitis in these infants. In situ hybridization studies to detect human immunodeficiency virus 1 messenger RNA was negative in the liver tissue obtained at biopsy and autopsy in five of the samples tested.