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Aplastic anemia associated with interferon alpha 2a in a patient with chronic hepatitis C virus infection: a case report
INTRODUCTION: Hepatitis-associated aplastic anemia is a common syndrome in patients with bone marrow failure. However, hepatitis-associated aplastic anemia is an immune-mediated disease that does not appear to be caused by any of the known hepatitis viruses including hepatitis C virus. In addition,...
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2010
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2925355/ https://www.ncbi.nlm.nih.gov/pubmed/20704699 http://dx.doi.org/10.1186/1752-1947-4-268 |
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author | Ioannou, Savvas Hatzis, Gregorios Vlahadami, Ioanna Voulgarelis, Michael |
author_facet | Ioannou, Savvas Hatzis, Gregorios Vlahadami, Ioanna Voulgarelis, Michael |
author_sort | Ioannou, Savvas |
collection | PubMed |
description | INTRODUCTION: Hepatitis-associated aplastic anemia is a common syndrome in patients with bone marrow failure. However, hepatitis-associated aplastic anemia is an immune-mediated disease that does not appear to be caused by any of the known hepatitis viruses including hepatitis C virus. In addition, to the best of our knowledge there are no reported cases of patients with chronic hepatitis C virus infection developing aplastic anemia associated with pegylated interferon alpha 2a treatment. CASE PRESENTATION: We report the case of a 46-year-old Greek man who developed severe aplastic anemia during treatment with pegylated interferon alpha 2a for chronic hepatitis C virus infection. He presented with generalized purpura and bruising, as well as pallor of the skin and mucous membranes. His blood tests showed pancytopenia. He underwent allogeneic bone marrow transplantation after completing two courses of immunosuppressive therapy with antithymocyte globulin and cyclosporin A. CONCLUSIONS: The combination of a specific environmental precipitant represented by the hepatitis C virus infection, an altered metabolic detoxification pathway due to treatment with pegylated interferon alpha 2a and a facilitating genetic background such as polymorphism in metabolic detoxification pathways and specific human leukocyte antigen genes possibly conspired synergistically in the development of aplastic anemia in this patient. Our case clearly shows that the causative role of pegylated interferon alpha 2a in the development of aplastic anemia must not be ignored. |
format | Text |
id | pubmed-2925355 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-29253552010-08-24 Aplastic anemia associated with interferon alpha 2a in a patient with chronic hepatitis C virus infection: a case report Ioannou, Savvas Hatzis, Gregorios Vlahadami, Ioanna Voulgarelis, Michael J Med Case Reports Case Report INTRODUCTION: Hepatitis-associated aplastic anemia is a common syndrome in patients with bone marrow failure. However, hepatitis-associated aplastic anemia is an immune-mediated disease that does not appear to be caused by any of the known hepatitis viruses including hepatitis C virus. In addition, to the best of our knowledge there are no reported cases of patients with chronic hepatitis C virus infection developing aplastic anemia associated with pegylated interferon alpha 2a treatment. CASE PRESENTATION: We report the case of a 46-year-old Greek man who developed severe aplastic anemia during treatment with pegylated interferon alpha 2a for chronic hepatitis C virus infection. He presented with generalized purpura and bruising, as well as pallor of the skin and mucous membranes. His blood tests showed pancytopenia. He underwent allogeneic bone marrow transplantation after completing two courses of immunosuppressive therapy with antithymocyte globulin and cyclosporin A. CONCLUSIONS: The combination of a specific environmental precipitant represented by the hepatitis C virus infection, an altered metabolic detoxification pathway due to treatment with pegylated interferon alpha 2a and a facilitating genetic background such as polymorphism in metabolic detoxification pathways and specific human leukocyte antigen genes possibly conspired synergistically in the development of aplastic anemia in this patient. Our case clearly shows that the causative role of pegylated interferon alpha 2a in the development of aplastic anemia must not be ignored. BioMed Central 2010-08-12 /pmc/articles/PMC2925355/ /pubmed/20704699 http://dx.doi.org/10.1186/1752-1947-4-268 Text en Copyright ©2010 Ioannou et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Case Report Ioannou, Savvas Hatzis, Gregorios Vlahadami, Ioanna Voulgarelis, Michael Aplastic anemia associated with interferon alpha 2a in a patient with chronic hepatitis C virus infection: a case report |
title | Aplastic anemia associated with interferon alpha 2a in a patient with chronic hepatitis C virus infection: a case report |
title_full | Aplastic anemia associated with interferon alpha 2a in a patient with chronic hepatitis C virus infection: a case report |
title_fullStr | Aplastic anemia associated with interferon alpha 2a in a patient with chronic hepatitis C virus infection: a case report |
title_full_unstemmed | Aplastic anemia associated with interferon alpha 2a in a patient with chronic hepatitis C virus infection: a case report |
title_short | Aplastic anemia associated with interferon alpha 2a in a patient with chronic hepatitis C virus infection: a case report |
title_sort | aplastic anemia associated with interferon alpha 2a in a patient with chronic hepatitis c virus infection: a case report |
topic | Case Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2925355/ https://www.ncbi.nlm.nih.gov/pubmed/20704699 http://dx.doi.org/10.1186/1752-1947-4-268 |
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