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Delayed fulminant hepatic failure: case report A 35-year-old woman developed delayed fulminant hepatic failure following treatment with dydrogesterone, estradiol and progesterone for in-vitro fertilization (IVF). The woman (G5P2) was admitted for management of elevated transaminases and painless jaundice at 14 weeks of gestation. She had reported the onset of scleral jaundice three days prior to hospital admission with pruritus affecting the palms of the hands and soles of the feet. Her past medical history included gestational diabetes, an ectopic pregnancy, an elective termination of pregnancy and two spontaneous vaginal deliveries and a left salpingectomy. She had traveled to Thailand four months prior for an IVF therapy. She had received a regular IVF regimen including oral estradiol 1mg, oral dydrogesterone 10mg and per vaginal progesterone for three months. She returned to Australia for ongoing antenatal care after the successful implantation. She had been receiving routine pregnancy supplements including vitamin B complex, ascorbic acid/ferrous sulfate [Ferrograd-C] and colecalciferol [cholecalciferol]. Examination revealed she was hypotensive. She was jaundiced with significant scleral icterus. Abdominal examination showed a non-tender smooth liver edge. Peripheral blood investigations on admission showed elevated transaminases, total and conjugated bilirubin levels, albumin, total white cell count, neutrophils, ferritin and lactate dehydrogenase. Her INR was also mildly elevated. The investigational parameters were indicative of a viable fetus at that point of time. The woman received supportive care during her admission including unspecified albumin, unspecified N-acetyl infusion and vitamin K supplementation. Her AST and ALT levels reduced over the following week and biochemical deterioration was noted with profound exacerbations of hyperbilirubinaemia, hypoalbuminemia, thrombocytopenia and coagulopathy. A 24-hour urine copper collection showed a mildly elevated copper level. An atypical form of concurrent Wilson’s disease was considered. However, an ophthalmic review ruled out Kayser-Fleischer rings. Transjugular biopsy of the liver were consistent with submassive hepatic necrosis including 40% of the parenchyma. Focal steatosis with cholestasis and variable ballooning along with Kupffer cells and lymphocyte infiltrates were noted. The liver biopsy excluded Wilson’s disease. Possible differential diagnoses included a druginduced liver injury attributed to dydrogesterone, an undiagnosed fulminant viral hepatitis or toxic hepatic injury. Despite the supportive care, she continued to deteriorate biochemically. On day 10 of hospital admission, she was activated for liver transplantation as it was considered to be a viable option which may sustain fetal survival. At day 21–22 following the admission, she clinically decompensated and had developed acute encephalopathy. Her Glasgow coma scale reduced, and she developed sinus tachycardia with oliguria. Biochemistry revealed AST of 110 U/L, ALT of 119 U/L,