DOI: 10.1097/01.inf.0000059965.34065.49
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Issn Print: 0891-3668
Publication Date: 2003/04/01
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Excerpt
Hepatitis A virus is the most frequent causative agent of hepatitis in infancy, but it is rarely responsible for neonatal hepatitis. 1 Hepatitis A infection is usually transmitted by the fecal-oral route, but it can be transmitted by the intrauterine vertical route, by blood transfusions and via nosocomial contamination especially in intensive care units. 2–10 Hepatitis A infection is usually nonicteric in children, and its course is milder than in adults. It has been reported that mothers with nonicteric hepatitis A infection in pregnancy do not transmit the infection to their babies. 1, 11 On the other hand there have been reports of hepatitis A infection transmitted vertically and causing neonatal cholestasis. 3–5, 12
We report a rare case of vertically transmitted hepatitis A infection causing neonatal cholestasis.
Case report. A 1-month-old male baby was admitted to our hospital because of jaundice, darkening of urine color and prolonged bleeding at sites where blood was taken. The patient was born vaginally in the 40th gestational week with a birth weight of 3500 g. He was the third child of the family. He had no problems in the postnatal period, and he was breast-fed by his mother. Jaundice was first noted 15 days previously and increased gradually, the color of the urine became darker and the stool was intermittently acholic.
The infant’s weight was 4500 g (50th to 75th percentile) and height 55 cm (50th to 75 percentile). Icterus was detected in skin and sclera, and the liver was soft and palpable 4 cm below the right costal margin. The spleen was not palpable. Other physical findings were normal. Laboratory examinations showed hemoglobin 10.4 g/dl, hematocrit 30.5%, white blood cell count 12.8 × 103 units/l with a differential count of lymphocytes 68%, polymorphonuclear leukocytes 30% and monocytes 2%. Platelet count was 445 × 103, aspartate aminotransferase 258 units/l, alanine aminotransferase 398 units/l, alkaline phosphatase 150 units/l, gamma-glutamyl transpeptidase 108 units/l, total bilirubin 7.4 mg/dl, direct bilirubin 4.3 mg/dl, total protein 7.5 g/dl, albumin 4.1 g/dl, prothrombin time 24.6 s (activity 34%), internationalized normal ratio 1.8 (N = 0.85 to 1.2) and alpha-1-antitrypsin 260 mg/dl. C-reactive protein was negative. Serum and urine amino acid chromatography were normal.
By abdominal ultrasonography the liver was larger than normal, parenchymal echogenicity was normal and intrahepatic and extrahepatic bile ducts were normal in configuration. Fundoscopic examination was normal. Serologic test results were negative for anti-Toxoplasma IgM, IgG, anti-herpes virus IgM, IgG, anti-HIV-1 and -2, antirubella IgM, anti-cytomegalovirus IgM, hepatitis B surface antigen, anti-hepatitis core antibody IgM and anti-hepatitis surface antibody. Anti-hepatitis A virus (anti-HAV) IgM antibodies were positive by micro-enzyme-linked immunosorbent assay (Bio-Rad).
It was learned that the patient’s father had had acute icteric hepatitis A infection 2 months before the infant’s delivery and that his anti-HAV IgG and anti-HAV IgM were positive. The mother has history of anorexia and generalized malaise 2 weeks before the delivery. On serologic examination of the mother, anti-HAV IgM antibody was positive, and anti-HAV IgG antibody was negative. Other household members did not have symptoms.
Fresh frozen plasma (10 ml/kg) was administered once. Control prothrombin activity was elevated to 87%. Vitamin A, D, E and K support therapy was initiated. Liver biopsy was not performed.
