Bone Marrow of Contention: A Rare Case of Recurrent Acute Hepatitis
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Bone Marrow of Contention: A Rare Case of Recurrent Acute Hepatitis Alba Rocco1 · Debora Compare1 · Antonio Maria Risitano2 · Costantino Sgamato1 · Bruno Amato3 · Gerardo Nardone1 Accepted: 7 October 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Hepatitis-associated aplastic anemia is a well-recognized clinical syndrome in which marrow failure follows the development of hepatitis. Although aplastic anemia is intimately related to paroxysmal nocturnal hemoglobinuria, until now, no cases of PNH-associated hepatitis have been described. We report a case of recurrent acute hepatitis preceding the clinical onset of PNH. Treatment of PNH with the complement inhibitor eculizumab ( Soliris®) prevented both recurrences of episodes of intravascular hemolysis and liver enzyme alteration. This is the first known published case of PNH-associated hepatitis. Keywords Hypertransaminasemia · Jaundice · Acute hepatitis · Paroxysmal nocturnal hemoglobinuria Abbreviations AA Aplastic anemia PNH Paroxysmal nocturnal hemoglobinuria AST Aspartate aminotransferase ALT Alanine aminotransferase LDH Lactate dehydrogenase Ig Immunoglobulin WBC White blood cells GGT Gamma GT RBC Red blood cells Plt Platelets GPI-APs Glycosyl phosphatidylinositol-anchored proteins HA-AA Hepatitis-associated aplastic anemia
* Gerardo Nardone [email protected] 1
Department of Clinical Medicine and Surgery, Gastroenterology, University of Naples “Federico II”, Via S. Pansini n° 5, 80131 Naples, Italy
2
Department of Hematology, University of Naples “Federico II”, Via S. Pansini n° 5, 80131 Naples, Italy
3
Department of Surgery, University of Naples “Federico II”, Via S. Pansini n° 5, 80131 Naples, Italy
Case Report A 23-year-old man was admitted to our institution due to pancytopenia and splenomegaly. He denied alcohol, tobacco, or drug abuse. In the family history, he reported a case of hepatocellular carcinoma in his grandfather. Personal medical history included two acute episodes of jaundice, dark urine, and hypertransaminasemia that occurred about six and eighteen months before hospitalization, respectively. The first clinical manifestation of the disease consisted of sudden onset of jaundice and dark urine. Mild splenomegaly was found at physical examination and confirmed by abdominal ultrasound. Though the blood cell count was normal, the biochemical tests documented a significant increase of aspartate aminotransferase (AST) (1440 IU/L; nl 0–40) and alanine aminotransferase (ALT) (2560 IU/L; nl 0–40) and a mild increase of bilirubin (total 3.4 mg/dL; direct 0.4 mg/ dL) and lactate dehydrogenase (LDH) 620 U/L (nl 125–450) levels. Hepatitis A, B, and C virus markers and cytomegalovirus, Herpes, and IgM and IgG Coxsackie virus antibodies were undetectable. The titer of Epstein-Barr virus (EBV) IgG was 280 arbitrary units (AU)/ml [nl
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