Abstract:Several reports have noted pancytopenia associated with Human parvovirus B19 (PVB19)or Ebstein-Barr virus (EBV) infections in patients who have no history of immunodeficiency. To our knowledge, we report the first case of severe aplastic anemia associated with both EBV and PVB19 infections in a previously healthy 22-year-old man. He was admitted to our hematology service due to anemia and thrombocytopenia. He had no symptoms or signs of infections of these viruses. His bone marrow biopsy revealed a hypocellula… Show more
“…In patients with chronic haemolysis or erythropoietic stress it can cause a transient but often severe red cell aplasia [Wong et al, 1993;Heegaard and Brown, 2002]. However, in immunocompromised patients such as solid organ transplant recipients [Moudgil et al, 1997;Wicki et al, 1997;Wong et al, 1999;Lui et al, 2001;Choi et al, 2002], human immunodeficiency virus (HIV)-infected [Yap, 1994;Ramratnam et al, 1995;Hung et al, 2001] and hematological malignancies [Azzi et al, 1993;Sharma et al, 2000;Kaptan et al, 2001;Castelli et al, 2002;Song et al, 2002;Isobe et al, 2004;Mouthon et al, 2005;Eid et al, 2006], PVB 19 infection can persist, resulting in pure red cell aplasia, chronic anemia and pancytopaenia [Heegaard and Brown, 2002].…”
A 42-year-old male with stage IV mantle cell lymphoma received chemotherapy and autologous peripheral blood stem cell transplantation. He developed pancytopaenia, and bone marrow examination indicated a parvovirus B19 (PVB 19)-induced red cell aplasia, confirmed by virological tests. Multiple doses of intravenous immunoglobulin (IVIG) were given over the following months, with blood samples being taken after each dose for quantitative PVB 19 DNA and hematological testing to assess the response. Each dose of IVIG produced a 1-3 log(10) drop in PVB 19 DNA levels. Eventually, after the fifth dose of IVIG, the PVB 19 DNA was reduced to <10 copies/ml serum, with a gradual improvement in his hematological parameters. This report demonstrates how close monitoring of the virological and hematological response to IVIG therapy for persistent PVB 19 infection in an immunocompromised patient can optimize the usage of this relatively expensive, and sometimes scarce intervention.
“…In patients with chronic haemolysis or erythropoietic stress it can cause a transient but often severe red cell aplasia [Wong et al, 1993;Heegaard and Brown, 2002]. However, in immunocompromised patients such as solid organ transplant recipients [Moudgil et al, 1997;Wicki et al, 1997;Wong et al, 1999;Lui et al, 2001;Choi et al, 2002], human immunodeficiency virus (HIV)-infected [Yap, 1994;Ramratnam et al, 1995;Hung et al, 2001] and hematological malignancies [Azzi et al, 1993;Sharma et al, 2000;Kaptan et al, 2001;Castelli et al, 2002;Song et al, 2002;Isobe et al, 2004;Mouthon et al, 2005;Eid et al, 2006], PVB 19 infection can persist, resulting in pure red cell aplasia, chronic anemia and pancytopaenia [Heegaard and Brown, 2002].…”
A 42-year-old male with stage IV mantle cell lymphoma received chemotherapy and autologous peripheral blood stem cell transplantation. He developed pancytopaenia, and bone marrow examination indicated a parvovirus B19 (PVB 19)-induced red cell aplasia, confirmed by virological tests. Multiple doses of intravenous immunoglobulin (IVIG) were given over the following months, with blood samples being taken after each dose for quantitative PVB 19 DNA and hematological testing to assess the response. Each dose of IVIG produced a 1-3 log(10) drop in PVB 19 DNA levels. Eventually, after the fifth dose of IVIG, the PVB 19 DNA was reduced to <10 copies/ml serum, with a gradual improvement in his hematological parameters. This report demonstrates how close monitoring of the virological and hematological response to IVIG therapy for persistent PVB 19 infection in an immunocompromised patient can optimize the usage of this relatively expensive, and sometimes scarce intervention.
“…There are very few published data reporting parvovirus B 19 as a pathogen, associated with SAA in immunocompetent and otherwise healthy individuals [11–14], while it is known to induce prolonged bone marrow aplasia in immunosuppressed patients [15, 16]. Although the connection between SAA and viral infections (hepatitis viruses, EBV, CMV, parvovirus B 19, HHV-6, and HIV) has not yet been reliably documented, direct effect or immune-mediated mechanisms of bone marrow failure are discussed [11, 17]. An attempt to clarify the role of parvovirus B 19 in SAA was made by Qian et al in 2002 [18].…”
Although bone marrow transplantation (BMT) from an HLA identical sibling is considered as treatment of choice in pediatric patients with severe aplastic anemia (SAA), a significant number of them experience graft failure (GF) after BMT. We report a case of an 8-year-old male patient with SAA who presented with a complicated posttransplant course due to parvovirus B19 infection and GF. A subsequent attempt to support the graft by antithymocyte globulin (ATG) and a peripheral stem cell boost resulted in transitory autologous recovery of hematopoiesis followed by mixed chimerism, supported by donor lymphocyte infusions (DLIs) and finally graft rejection with relapse of SAA. Permanent complete chimerism was achieved by a second BMT. Dynamics of graft function, measured by a single nucleotide polymorphism (SNPs) analysis, are discussed.
“…Since no population-based data about the presence of HPV-B19 DNA in healthy subjects is available, studies with larger sample size are warranted before refuting association between HPV-B19 and FHF. Additionally, several reports in the literature have described AA secondary to HPV-B19 infection, including successful treatment with myeloablation and BMT (19)(20)(21). It would seem that in the appropriate clinical scenario of FHF with positive PCR for HPV-B19, especially without any other identifiable cause, causative association between HPV-B19 and FHF cannot be denied.…”
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