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• W4237672022 abstract "A 1-month-old baby became icteric after 15 days of age. The father had acute icteric hepatitis A infection 2 months before the baby was born. In serum from the mother anti-hepatitis A virus (anti-HAV) IgM antibody was positive and anti-HAV IgG antibody was negative. The neonate had hepatitis A infection by clinical symptoms, laboratory results and detection of anti-HAV IgM antibodies. 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. In the monthly follow-up examinations, a gradual decrease in abnormal liver function tests was observed. Laboratory findings of the baby, mother and father are summarized in Table 1.TABLE 1: Laboratory findings of baby, mother and fatherThe patient is now 13 months old with normal growth and development. The aspartate aminotransferase value is 25 units/l, and the alanine aminotransferase value is 32 units/l. Anti-HAV IgM antibodies are negative, and anti-HAV IgG antibodies are positive. Discussion. In our patient the liver function tests were elevated, stool color was acholic, gallbladder and bile ducts were visualized and considered normal and anti-HAV IgM antibody was positive. Our patient had not received blood or blood products before hospitalization. The mother did not have a history of icterus; however, 2 weeks before delivery she had anorexia and malaise which was attributed to pregnancy but which might have been caused by hepatitis A infection given that subsequent tests showed that anti-HAV IgM antibody was positive and anti-HAV IgG antibody was negative. We believe that she had acute nonicteric hepatitis A just before the delivery because her anti-HAV IgG was still negative. Other causes for neonatal cholestasis in our patient were ruled out by appropriate tests. The viremic phase of hepatitis A infection is very short, occurring ∼7 days before the icteric phase. Peak shedding of the virus in the stool occurs during the clinical prodrome and before biochemical evidence of hepatitis. Because the incubation period of hepatitis A infection is 10 to 50 days and anti-HAV IgM antibody in the mother was positive, we believe that the baby was infected by intrauterine transmission or during the birth process by contact with stool. Hepatitis A infection prevalence is 92% in the 25- to 29-year age group in Turkey. 12 In conclusion hepatitis A infection should be considered in the differential diagnosis of neonatal cholestasis, especially in areas where the prevalence of this infection is high." @default.
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• W4237672022 date "2003-04-01" @default.
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