Antiretrovirals
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Hepatitis, lactic acidosis and secondary non-immune hydrops fetalis: case report A female fetus developed hepatitis, lactic acidosis and secondary non-immune hydrops fetalis (NIHF) following in-utero exposure to dolutegravir, emtricitabine, tenofovir and zidovudine for maternal human immunodeficiency virus (HIV) infection and intrapartum HIV prophylaxis. Following birth, she received zidovudine, nevirapine and lamivudine as prophylaxis against HIV infection, which also contributed in the hepatitis, lactic acidosis and secondary NIHF [not all routes stated; dosages not stated]. The mother of the fetus was diagnosed with HIV infection during second trimester and started receiving tenofovir, dolutegravir and emtricitabine. Subsequently, a fetal ultrasound revealed reversed end-diastolic flow on Doppler with category III fetal heart tracings, growth restriction at the 5th percentile, pericardial effusion and ascites. Therefore, delivery was scheduled. The woman was also administered intrapartum zidovudine for prophylaxis. The female neonate was delivered via urgent cesarean section at 34 4/7 weeks of gestation and weighed 1760g. Apgar scores were 1, 4, 6, and 7 at 1, 5, 10, and 15 minutes, respectively. Physical examination revealed respiratory distress and generalised oedema, notably over the extremities and abdominal wall. The girl underwent intubation at delivery. Her initial laboratory tests revealed thrombocytopenia, elevated transaminases and significant lactic acidosis. The girl was treated with platelet transfusion and total parenteral nutrition. She started receiving nevirapine, lamivudine and zidovudine. She also received ampicillin and gentamicin. On day 1 after birth, abdominal ultrasonography demonstrated mild ascites. Head ultrasonography did not show any evidence of intracranial calcifications. On day 2 after birth, she was treated with unspecified surfactant. Echocardiography showed mild right ventricular dysfunction and coronary vasculopathy with mild ectasia of both coronary arteries and a small pericardial effusion. On day 3 after birth, she was extubated and respiratory support was weaned without further complications. She developed coagulopathy. Therefore, on day 5 after birth, fresh frozen plasma was transfused. Investigations also revealed hyperbilirubinaemia and hypoalbuminaemia. She was diagnosed with hepatitis and lactic acidosis secondary to antiretroviral therapy. She subsequently developed NIHF secondary to hepatitis. Lamivudine and nevirapine were held, due to acute liver injury. Zidovudine was continued. She was treated with ursodiol. Her ammonia levels were noted to be spuriously high. In the second week of birth, her generalised oedema, bilirubin levels and liver enzyme levels improved. Four weeks after birth, ursodiol was discontinued. Total parenteral nutrition was also discontinued with advancement of her diet. She developed hypoglycaemia requiring slow weaning of glucose fluids. At three weeks of age, echocardiography revealed improved coronary artery sizes with no evidence of
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