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Query: UMLS:C0002874 (aplastic anemia)
 5,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Maternal infection with parvovirus B19 during pregnancy can cause aplastic anemia in the fetus. Severe anemia may lead to nonimmune hydrops or fetal demise. In the case reported, the demise of one twin was diagnosed by ultrasonography in an asymptomatic 21-year-old para 1-0-2-1 African American at the gestational age of 25 weeks. The deceased twin (A) was grossly hydropic with anasarca, ascites, pleural and pericardial effusions, and a thickened placenta. Parvovirus B19 DNA was found in the amniotic fluid of Twin A using the polymerase chain-reaction technique. Serial scans of Twin B showed normal growth and no evidence of hydrops. The pregnancy was managed expectantly until 29 weeks when delivery was indicated by maternal disseminated intravascular coagulation. Maternal IgM antiparvovirus B19 antibodies were detected at the time of delivery. Antiparvovirus B19 IgM antibodies were not present in Twin B. These serologic studies suggest a recent acute maternal infection and refute such an infection in Twin B. We present a case of differential transmission of parvovirus B19 in a twin pregnancy with in utero death of the infected twin and subsequent maternal disseminated intravascular coagulation.
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PMID:Differential transmission of parvovirus B19 in a twin gestation: a case report. 1552 55

Erythema infectiosum (fifth Disease) is the major clinical manifestation of human parvovirus B19 (HPV B19) infection. HPV B19 is known to be associated with adverse effects on fetuses such as hydrops fetalis, aplastic anemia, intrauterine fetal death, and chronic anemia in immunocompromised individuals. The objective of this study was to assess seroprevalence to HPV B19 in three different groups in Shiraz, Iran. The first group included 91 to-be-married girls. The second group included 184 pregnant women and the third group consisted of 184 neonates, who were born to the women in the second group. Specific IgG and IgM antibodies to HPV B19 were measured using ELISA technique. Results showed that the prevalence for IgG to HPV B19 was 56 (61.5%), 127 (69%), and 127 (69%) for the first, second, and third groups, respectively. Overall, 183 out of the 275 (66.5%) women of childbearing age had IgG to HPV B19. The seroprevalence for IgM to HPV B19 was 2.2% for the second group. There was no detectable IgM in umbilical cord sera or in the first group blood samples. In conclusion, approximately one-third of individuals in the study who were of childbearing age were at risk for primary HPV B19 infection.
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PMID:The seroprevalence of parvovirus B19 infection among to-be-married girls, pregnant women, and their neonates in Shiraz, Iran. 1585 87

Aplastic anemia is characterized by pancytopenia with hypoplastic bone marrow. Various factors including viral infections have been implicated as the precipitating factors. Human parvovirus B19 has been associated with red-cell aplasia, leukopenia, and thrombocytopenia. The present study was carried out to determine the role of parvovirus B19 in aplastic anemia patients. Twenty-seven aplastic anemia patients and 20 healthy controls were tested for the presence of parvovirus B19 infection by detecting parvovirus B19-specific IgM by ELISA and viral DNA by PCR. Parvovirus B19 IgM and viral DNA were detected in significantly higher numbers of patients in comparison to the controls (40.7% vs. 5%, P < 0.01; 37% vs. 0%, P < 0.001, respectively). The presence of parvovirus DNA in aplastic anemia patients indicates active or recent infection. However, more studies are needed to explore the mechanism of bone-marrow aplasia due to human parvovirus B19 infection.
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PMID:Human parvovirus B19 in patients with aplastic anemia. 1592 6

An otherwise healthy 73-year-old female was admitted to our department in 1997 because of easy bruising and a platelet count of 12 x 10(9)/L. The patient was taking no medications. Bone marrow examination revealed erythroid hyperplasia, megakaryocytic hypoplasia, and no sign of malignancy. Chromosome analysis showed a normal karyotype. There was serological evidence of previous infection with parvovirus B19. No antibodies to HBV, HCV, CMV, or EBV were found. ANA and cardiolipin antibodies were not detected. Treatment with prednisolone was without effect, but 3 weeks after i.v. gamma-globulin therapy, the platelet count was normal, 233 x 10(9)/L. Two years later, the patient was readmitted with a platelet count of 11 x 10(9)/L. At this time, treatment with corticosteroids, azathioprine, and gamma-globulin had only a temporary effect, and further therapy was stopped because of side effects. During the next 3 years, the patient developed transfusion-dependent anemia, and her white blood cell count decreased to 1.8 x 10(9)/L. A new bone marrow examination showed aplastic anemia with bone marrow cellularity about 10%. After an intracerebral hemorrhage, the patient accepted treatment with rituximab and received 4 weekly doses of 375 mg/m2. This therapy was followed by an increase in the platelet count to 232 x 10(9)/L, white blood cell count to 6.8 x 10(9)/L, and no more need for blood transfusions. A bone marrow examination 5 months after treatment with rituximab showed hyperplastic myelopoiesis, normoblastic erythropoiesis, and slightly reduced megakaryopoiesis. The use of anti-CD20 monoclonal antibody in aplastic anemia warrants further investigation.
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PMID:Aplastic anemia successfully treated with rituximab. 1631 56

Anemia, a potentially correctable cardiovascular risk factor, continues to be a major problem in kidney-transplant patients. Erythropoietin levels increase rapidly after successful kidney transplantation, and by 3 months, most patients achieve hemoglobin levels greater than 12 g/dL. Anemia may be caused by problems commonly seen in the general population such as iron deficiency or gastrointestinal blood loss, by immunosuppressive medications, or by more rare abnormalities such as hemolytic uremic syndrome or parvovirus B19-induced aplastic anemia. Iron deficiency is common at the time of transplantation and beyond and frequently contributes to anemia. Markers of iron deficiency (ferritin or transferrin saturation) are frequently inconclusive because of the presence of inflammation and infection. Immunosuppressive medications, such as azathioprine and mycophenolate mofetil (MMF), are a common cause of mild bone-marrow suppression and, thus, anemia. Sirolimus can cause more severe bone-marrow suppression, although this effect can lessen over time. The transplant patient with chronic kidney disease (CKD) frequently develops anemia, yet agents such as epoetin-alpha and darbepoetin are greatly underutilized. Evaluation of anemia should be undertaken when hemoglobin fails to normalize by 3 months after transplantation. Later after transplantation, especially in the setting of chronic allograft dysfunction, evaluation should take place when the hemoglobin falls to less than 11 g/dL in premenopausal females or to less than 12 g/dL in males and postmenopausal females.
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PMID:Anemia in the kidney-transplant patient. 1641 65

Following its identification by Yvonne Cossart in 1975, human Parvovirus B19 has been recognized as the causative agent of a wide range of diseases. In childhood, the most common disease is a typical exanthema called "fifth disease". In adults, viral infection may be responsible for fetal loss and for aplastic anaemia in immuno-compromised patients. Because persistent viral infection may induce an autoimmune response, Parvovirus B19 is emerging as an environmental factor linked to the pathogenesis of autoimmunity. As a result of its expanding disease spectrum, Parvovirus B19 is the subject of intense efforts to clarify the pathogenesis of virus-related disorders as well as improve diagnostic laboratory testing including standardization of serological and nucleic acid-based detection assays. Enzymatic immunoassays based on conformational antigens have proven to be the most important tools for accurate diagnosis in the majority of cases. In other selected clinical cases, the detection of Parvovirus B19 infection can be complemented by PCR and, more recently, by the real-time PCR.
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PMID:Serologic and molecular detection of human Parvovirus B19 infection. 1676 38

Acute viral hepatitis with hepatitis A, B, C, D, and E viruses in the etiology of fulminant hepatic failure either single or in combinations has been described. Parvovirus B19 is also an etiologic agent of acute liver failure and hepatitis-associated aplastic anemia. We present a patient diagnosed with fulminant hepatitis A referred for liver transplantation. Parvovirus B19 superinfection was detected when the patient developed anemia during the course of the disease. We discuss possible roles of both viruses in fulminant hepatitis and pure red cell aplasia.
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PMID:Hepatitis A and parvovirus B19 infections in an infant with fulminant hepatic failure. 1683 Mar 3

An 11-year-old boy presented with hepatic failure secondary to parvovirus B19 infection, requiring urgent liver transplantation. His recovery was complicated by primary Epstein-Barr virus and cytomegalovirus infections. He subsequently developed aplastic anaemia that has been refractory to antithymocyte globulin and cyclosporine therapy and may now require bone marrow transplantation. We present this case to emphasize parvovirus as a rare cause of hepatic failure and of aplastic anaemia as a complication of the virus.
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PMID:Urgent liver transplantation for acute liver failure due to parvovirus B19 infection complicated by primary Epstein-Barr virus and cytomegalovirus infections and aplastic anaemia. 1731 40

The human parvovirus B19 is a small single-strand DNA virus with specific tropism for the membranous receptor P expressed on erythrocytes and endothelial cells. About 60 - 70 % of the adult population is parvovirus B19 seropositive. The contamination usually occurs through droplets from the nasopharyngeal airways. The major systemic infections present as episodes of aplastic anemia and development of hydrops fetalis. Arthropathies, encephalitis, or glomerulonephritis are less frequently encountered. This review focuses on its cutaneous manifestations including erythema infectiosum, and the purpuric syndromes whose principal manifestation is the papulo-purpuric gloves and socks syndrome. Several other cutaneous manifestations have been reported to be associated with the parvovirus B19 without however strong evidence. These include vasculitis, erythema nodosum, the lupus eythematosus-like syndrome, some vesiculo-pustular eruptions, pityriasis lichenoides and scleroderma.
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PMID:[Cutaneous manifestations of parvovirus B19 infection]. 1785 70

We present an elderly female patient with fever, aplastic anemia, arthralgic symptoms and atypical pneumonia. Serological and clinical findings suggested Parvovirus B19 and Chlamydophila pneumoniae infection. These supposed infections delayed the recognition of underlying sarcoidosis which definitive diagnosis was reached through a lung biopsy and histological demonstration of nonnecrotizing granulomas containing giant cells and noncaseating epithelioid cells. The present case highlights the potential difficulty to diagnose sarcoidosis in the presence of unusual infections which may complicate the course of this disease.
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PMID:Detection of parvovirus B19 and Chlamydophila pneumoniae in a patient with atypical sarcoidosis. 1790 38


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