Abstract

Introduction: Hepatitis E virus (HEV) infection in pregnancy results in high rates of preterm labour, antepartum haemorrhage, poor fetal outcomes, intrauterine fetal deaths and maternal mortality. Case: A 32 year old G1/P0 HIV-positive Nigerian woman presented at the 27th week of gestation with abdominal pain and jaundice. The ultrasonographic evaluation showed a normal sized fetus, normal umbilical and cerebral Doppler values, but an oligohydramnios. The fetal heart rate showed a decreased variability. Blood pressure and urine test was normal. The initial labs showed normal platelets but signs of beginning liver failure (ALT 1683 U/l [10–35 U/l], total bilirubin 43mg/dl [0–1.2mg/dl] and haemolysis (haptoglobin <5mg/dl [30–200mg/dl], figure 1). The patient was hospitalised with the diagnosis of beginning liver failure of unknown origin and anti-HIV treatment was stopped. HEV RNA, initially negative, seroconverted on day 17. Betamethasone i.m. 2×12mg was given. Due to an increased HIV load of 106 copies/ml antiviral therapy was restarted and NFV was exchanged for tenofovir (TDF). With this regimen liver enzymes and haemolysis normalized. A scheduled caesarean section for prevention of vertical transmission of HIV infection was performed at week 36. The fetal outcome was excellent (Apgar-Score 9/10/10, pH: 7.31, total bilirubin level: 7.9mg/dl). Now, 9 months after birth, the child is still developing normal. HIV and hepatitis serologies are negative. Discussion: The unexpected good perinatal outcome underlines in our view the clinical importance of the placenta as an efficient barrier to even high conjugated bilirubin levels. Interdisciplinary team-work was crucial in the management of this case.

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