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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

B19 parvovirus infection is a principal cause of transient bone marrow suppression in patients with chronic haemolytic anaemias. Acute infection is described in a family of five individuals with hereditary spherocytosis; three of them developed marked hypoplastic anaemia.
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PMID:B19 parvovirus infection causing aplastic crisis in 3 out of 5 family members with hereditary spherocytosis. 217 81

Hereditary spherocytosis was diagnosed in five of six children in one family after a human parvovirus B19 (B19-virus) infection. The diagnosis was made on the basis of severe anaemia, demonstrable haemolysis, decreased osmotic fragility and an increased number of spherocytes. Since in the serum of the patients an increased level of IgG and IgM antibodies against B19 virus was detectable two weeks after the crisis it was concluded that the B19-virus infection caused the severe anaemia.
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PMID:[A family with hereditary spherocytosis discovered after an infection with human parvovirus B19]. 217 45

Infection by parvovirus B19 is common and may become chronic if the patient is immunocompromised, leading to persistent erythroid hypoplasia. Parvovirus should be added to the list of pathogens that can complicate the course of HIV infection and should be considered in the evaluation of severe anemia or red cell aplasia in any immunocompromised patient.
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PMID:Pure red cell aplasia due to parvovirus B19 infection in a man with HIV infection. 217 78

Hydrops fetalis was diagnosed at 22 weeks. An ultrasound examination demonstrated cardiomegaly and a fetal blood specimen obtained by cordocentesis revealed thrombocytopenia, anaemia, and neutropenia. Fetal paracentesis yielded straw-coloured fluid with electrolytes indicative of a transudate. Non-enveloped icosahedral viral particles approximately 23 mm in diameter were visualized in the ascitic fluid by electron microscopy. Immune electron microscopy confirmed human parvovirus B19. Direct fetal digitalization led to a reduction in umbilical artery resistance, a decline in the abdominal circumference from 20.3 to 17.8 cm, and resolution of the ascites within 72 h. Despite this dramatic response to therapy, fetal death occurred on day 5 of treatment. The initial maternal serum was positive for anti-B19 IgM and IgG antibodies. Electron microscopy of fetal cardiac tissue obtained post-mortem revealed intranuclear viral particles typical of B19, confirming the antenatal diagnosis of myocarditis. This case demonstrates that direct viral identification is applicable to prenatal diagnosis. To our knowledge, this is the first reported case of the antenatal diagnosis and palliative treatment of fetal viral infection.
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PMID:Antenatal diagnosis and palliative treatment of non-immune hydrops fetalis secondary to fetal parvovirus B19 infection. 246 84

The occurrence of isolated erythroblastopenia is a common problem in paediatrics, and in most cases three diagnoses may be considered: Blackfan-Diamond anaemia (congenital erythroblastopenia), transient erythroblastopenia of childhood and erythroblastopenia consecutive to parvovirus B19 infection. These three diseases have distinctive features: age of onset, association with other laboratory and clinical abnormalities and above all, transient or chronic character are of assistance in making an exact diagnosis. The mechanisms responsible for Blackfan-Diamond anaemia and transient erythroblastopenia are imperfectly known. In vitro studies of the properties of erythroblast progenitors suggest intrinsic damage to these cells, whereas in transient erythroblastopenia their differentiation seems to be inhibited, perhaps by an immune mechanism. In both cases, the abnormality has not be identified. The selective tropism of parvovirus B19 towards actively dividing erythroblasts accounts for the acute erythroblastopenia observed in a context of chronic haemolysis. The responsibility of parvovirus B19 in chronic or relapsing erythroblastopenia in immunocompromised patients is a recent discovery. In view of the protean haematological pathology in this context and of the difficult therapeutic problems it creates, this diagnosis must systematically be envisaged, notably in children under chemotherapy.
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PMID:[Erythroblastopenia in children]. 255 85

Human parvovirus B19 is known to cause aplastic crisis in patients with hemolytic anemias due to cytotoxic effect of the infection to erythroid progenitor cells. We report here the first case of aplastic crisis by B19 in a patient with glucose-6-phosphate dehydrogenase deficiency. A five-year-old boy was admitted to the hospital because of severe anemia, fever and jaundice. Four weeks after admission, he developed erythema infectiosum. B19 infection was confirmed using countercurrent immunoelectrophoresis, Southern blotting and hybridization method, and radioimmunoassay for B19 specific IgM. B19 virus antigen was detected by an indirect immunofluorescent method in both the cytoplasm and nucleus of large mononuclear cells that had no granules in bone marrow. On admission, the hemoglobin was 3.1 g/dl and no reticulocytes were detected in the peripheral blood smear. Bone marrow examination revealed a normocellular marrow with erythroid hypoplasia and M/E ratio of 7.38. Large basophilic erythroblasts containing vacuoles were also noticed. Elevation of indirect bilirubin and hemoglobinuria suggested intravascular hemolysis. Transient mild thrombocytopenia associated with increased PAIgG was observed. It is likely that B19 virus infection caused hemolysis which contributed to severe anemia.
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PMID:[Aplastic crisis due to human parvovirus B19 infection in glucose-6-phosphate dehydrogenase deficiency]. 255 69

Anti-B19-IgG antibodies were tested for by the ELISA method in 768 sera, 76 from children and juveniles, aged 1-15 years, attending the Outpatients Department of the Children's Clinic, University of Munich, and 692 from persons, aged 18-68 years, attending the blood donor service of the Bavarian Red Cross in Munich. 38.4% of sera were positive, with a significant difference between men and women (32.5% vs. 47.5%, P less than or equal to 0.01). A fresh B19 infection was present in 42 subjects by demonstrating anti-B19-IgM in the ELISA test. The sera came from seven patients with infectious erythema, 26 with skin rash of uncertain cause, two with erythroblastosis fetalis, two with enteritis, one with transitory anaemia, one with juvenile polyarthritis, one with lymphadenitis and arthralgia, and two with an asymptomatic course. Viral B19-DNA was demonstrated by nucleic acid hybridization in a blood unit from an asymptomatic blood donor and in amniotic fluid in a case of erythroblastosis fetalis.
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PMID:[Incidence of parvovirus B19 infection. Seroepidemiologic studies]. 282 Jun 87

Two patients, a 43-year-old mother and her 12-year-old son developed severe anemia after a disease with fever, myalgia, rash and gastrointestinal symptoms. The infectious proved to be caused by human parvovirus B19 (IgM antibody titer rises). Investigations revealed that both patients suffered from spherocytosis, apparently hereditary and not known before. This emphasizes the importance of thorough hematological investigations in patients showing symptoms resembling a viral disease when seen in connection with severe anemia in order to reveal underlying chronic hemolytic disease. In patients with these diseases transient aplastic crisis will give a much more pronounced anemia than in otherwise healthy individuals.
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PMID:Human parvovirus B19 infection with severe anemia affecting mother and son. 284 54

In two children with acute lymphocytic leukaemia in whom severe anaemia developed, serum samples collected over 9-12 months showed high concentrations of B19 parvovirus, the aertiological agent of fifth disease. In one patient, anaemia recurred with the reappearance of virus in serum; in the other, the anaemia persisted. Smears of bone marrow aspirates obtained during periods of viraemia showed giant pronormoblasts and either absent mature erythroid cells or erythroid hypoplasia. Parvovirus replication in the marrow was detected by Southern blot of cellular DNA. An underlying immune deficit was suggested by low titres of specific antibodies against B19 parvovirus. Treatment of one patient with plasma containing specific antibodies against parvovirus resulted in a transient fall in serum virus levels, the appearance of reticulocytes, and symptoms of fifth disease.
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PMID:Persistent B19 parvovirus infection as a cause of severe chronic anaemia in children with acute lymphocytic leukaemia. 290 76

From March to August 1984, 26 patients with hereditary hemolytic anemia in northeastern Ohio developed acute, profound red cell aplasia. The patients included 14 males and 12 females 2 to 23 years old, with sickle cell anemia (20 cases), hemoglobin SC-disease (4 cases), sickle-beta-thalassemia (1 case), or hereditary spherocytosis (1 case). All had an acute onset of severe reticulocytopenia and anemia and prodromal symptoms of illness including fever, abdominal symptoms, headache, and arthralgias. Twenty-two received transfusions. Reticulocytosis occurred spontaneously within 2 to 14 days of presentation. In five acute-phase sera, 10(8) to 10(12) viral particles/mL were detected by electron microscopy. Human parvovirus B19 DNA was demonstrated in high concentration by hybridization in the same five acute-phase sera and in low concentration in sera of eight additional patients. The five highly viremic sera inhibited erythroid colony formation in vitro. B19-specific IgM was detected in sera of 24/26 patients, and B19-specific IgG in 21 of 22 patients tested. Our results indicate that human parvovirus B19 was the etiologic agent in this large epidemic of life-threatening acute red cell aplasia in patients with hereditary hemolytic anemia.
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PMID:Human parvovirus B19-induced epidemic acute red cell aplasia in patients with hereditary hemolytic anemia. 300 91


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