Aplastic anemia associated with interferon alpha 2a in a patient with chronic hepatitis C virus infection: a case report

Abstract

IntroductionHepatitis-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 presentationWe 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.ConclusionsThe 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.

Pro-inflammatory cytokines: Emerging players regulating HSC function in normal and diseased hematopoiesis

“…Thus, apoptosis of IFN-exposed HSCs forced back into cycle likely accounts for the decreased engraftment observed upon transplantation of IFN-exposed HSCs (Baldridge et al, 2010, de Bruin et al, 2013, Pietras et al, 2014). Importantly, the protection quiescence provides against IFN-mediated killing likely explains the limited effectiveness of IFN-Is in eliminating quiescent CML LSCs, as well as the relative absence of bone marrow failure in patients chronically exposed to IFNs absent other complications (Ionnou et al, 2010). Altogether these findings indicate that HSC quiescence acts as a protective mechanism that limits IFN-induced apoptosis during chronic exposure ( Fig.…”

Type I interferon potentiates metabolic dysfunction, inflammation, and accelerated aging in mtDNA mutator mice

“…Future research on the mutator strains described here should yield new insight into roles for IFN-I dysregulation in both aging-and MD-related cardiomyopathy. Elevated IFN-I signaling has also been linked to anemia in aging and in various human diseases and animal models (61,73,86). A recent report characterized a unique subset of splenic hemophagocytes that differentiate from IFN-I expanded Ly6C hi monocytes, which are responsible for anemia in a model of macrophage activation syndrome and lupus (37,73).…”

Pure red cell aplasia caused by ribavirin and interferon treatment

“…RIB is often associated with dose-dependent hemolytic anemia [7], and up to 25% of patients require dose reduction for treatment continuation [8]. INF-a can also suppress bone marrow and lead to significant hemoglobin reduction or even aplastic anemia [9][10][11]. INF-a has also very rarely been associated with hemolytic anemia in patients being treated for viral hepatitis [12].…”