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

We reported a case of 10-year-old girl with petechiae mainly on the truncus, although who had more than 10 x 10(4)/microliter of platelets. Smears of her bone marrow demonstrated extreme reduction of erythroblasts with giant proerythroblast like cells, which does not consist with idiopathic thrombocytopenic purpura. Human parvovirus B19 (B19) DNA was detected in her serum and throat swab using PCR and significant alterations of B19 specific IgM and IgG antibody titers were demonstrated. The petechiae subsided on the 8th day after her admission. She had not shown anemia less than Hb 10 g/dl, but her reticulocytes counts had increased up to 3.5% on the 11th day after her admission. Smears of her bone marrow on the 17th day became normal with moderate erythroblasts. It is demonstrated that the cellular receptor of this virus is an antigen of the blood group P recently. P antigen is presented not only on erythrocytes and on erythroblasts but also on megakaryocytes and endotherial cells. Therefore, it is suggested that direct injury by B19 to endothelial cells could cause petechiae in this case.
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PMID:[A case with petechiae due to human parvovirus B19]. 892 82

Parvovirus B19 (PVB19) is the causative agent of infectious erythema. In healthy children the virus causes transient erythroid aplasia, whereas in children with chronic hemolytic anemias it can cause severe aplastic crises, and in immunodeficient individuals it can produce chronic red cell aplasia. If contracted during pregnancy, the infection may induce serious damage to the fetus (abortion or hydrops fetalis). Shwachman-Diamond (S-D) syndrome, a rare autosomal recessive condition, consists of exocrine pancreatic insufficiency plus neutropenia; many patients develop either anemia or thrombocytopenia or both. We describe a newborn baby with severe congenital bone marrow failure who was diagnosed with S-D syndrome and persistence of PVB19 virus contracted by the mother in the third trimester of pregnancy.
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PMID:Severe Shwachman-Diamond syndrome and invasive parvovirus B19 infection. 894 Jul 40

Parvovirus B19 infection may cause chronic anemia in human immunodeficiency virus (HIV)-infected hosts. Small-scale studies and case reports have suggested that parvovirus B19 infection is a significant cause of anemia in HIV-infected patients. We studied single serum samples from 317 consecutive HIV-infected patients with use of parvovirus B19-specific serology and polymerase chain reaction for detection of viral DNA. Anemia was noted in 176 patients (55.5%); 126 (39.9%) had < 0.10 x 10(9) CD4+ cells/L. In this study group, 191 (60.3%) of the patients were positive for parvovirus B19 IgG. Seroprevalence rates did not differ between patients with low and higher CD4+ cell counts or between anemic and nonanemic patients. Parvovirus B19 DNA was detected in none of the sera. In a control group of 226 healthy male blood donors, the seroprevalence of parvovirus B19 IgG was 68.1%; two IgG-positive sera also contained parvovirus B19 DNA. This study demonstrates that chronic parvovirus B19 infection should not be considered a frequent cause of anemia in HIV-infected individuals.
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PMID:Prevalence of parvovirus B19 infection in patients infected with human immunodeficiency virus. 895 68

Anemia, mental status changes, and fatal respiratory failure complicated a febrile illness in a previously healthy 14-year-old black female. At autopsy, widespread fat emboli and bone marrow necrosis were found. Hemoglobin electrophoresis on an antemortem, pretransfusion specimen revealed hemoglobin S/beta+ thalassemia. Acute parvovirus B19 (PV B19) infection was suspected. Postmortem serum and a variety of paraffin-embedded tissues were assayed for PV B19 DNA using the polymerase chain reaction (PCR). The expected PCR product was identified in the serum specimen and in paraffin-embedded sections of bone marrow, kidney, spleen, parathyroid, thyroid, adrenal, and gastrointestinal tract: lung, liver, ovary, fallopian tube, uterus, brain, heart, and pancreas were negative. PV B19 infection is highly contagious and may be rapidly fatal in children with hemoglobinopathies by several mechanisms, including fat embolism. Therefore, there exists the risk of multiple deaths within a family. The acute infection may be easily and expeditiously diagnosed using serum or a variety of paraffin-embedded tissues.
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PMID:Fatal fat embolism syndrome in a child with undiagnosed hemoglobin S/beta+ thalassemia: a complication of acute parvovirus B19 infection. 896 32

Parvovirus B19, the only known human pathogenic parvovirus, is highly tropic to human bone marrow and replicates only in erythroid progenitor cells. The basis of this erythroid tropism is the tissue distribution of the B19 cellular receptor, globoside (blood group P antigen). In individuals with underlying hemolytic disorders, infection with parvovirus B19 is the primary cause of transient aplastic crisis. In immunocompromised patients, persistent B19 infection may develop that manifests as pure red cell aplasia and chronic anemia. B19 infection in utero can result in fetal death, hydrops fetalis or congenital anemia. Diagnosis is based on examination of the bone marrow and B19 virological studies. Treatment of persistent infection with immunoglobulin leads to a rapid, marked resolution of the anemia.
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PMID:Parvoviruses and bone marrow failure. 899 35

We reviewed the literature on relationships between human parvovirus B19 infection and rheumatic diseases. Parvovirus B19 causes erythema infectiosum in childhood, transient anemia in immunocompetent individuals, and potentially severe infections in fetuses; laboratory evidence that the virus is directly responsible for these disorders has been obtained. Acute arthropathy meeting American College of Rheumatology criteria for rheumatoid arthritis and disorders meeting some of the classification criteria for systemic lupus erythematosus are the most striking rheumatic manifestations of parvovirus B19 infection. Purpuric lesions have also been reported. Parvovirus B19 infection may be capable of inducing a number of manifestations that have not yet been described in the literature. Although the relationship between human parvovirus B19 infection and rheumatic diseases has been the focus of many studies, compelling evidence that the virus is directly involved in the pathogenesis of rheumatic diseases has not yet been obtained.
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PMID:Parvovirus B19 infection and rheumatic diseases. 901 Sep 73

Congenital hypoplastic anemias are a rare and heterogeneous group of disorders. This paper reviews new molecular diagnostic tests in two distinct forms of congenital anemias, anemia due to transplacental infection with B19 parvovirus and Fanconi anemia. In both instances, molecular assays making use of amplification of DNA by the polymerase chain reaction have been used to diagnose either a specific viral infection or gene mutation responsible for a disorder. Recognition of these entities has important prognostic and therapeutic implications.
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PMID:New molecular diagnostic tests for two congenital forms of anemia. 902 20

The relationship between transient erythroblastopenia of childhood (TEC) and parvovirus B19 infection remains uncertain. Large series using primarily serologic evaluation have not shown an association, whereas smaller series have reported parvovirus B19 infection in such patients. Further, parvovirus DNA or antigen has been detected in some patients seronegative for the virus at presentation. Polymerase chain reaction (PCR) amplification has never been used to evaluate patients with TEC for parvovirus B19. We used the PCR in an attempt to detect parvovirus B19 in DNA extracted from archived bone marrow coverslips of 16 patients diagnosed with TEC. The patients ranged in age from 3 to 23 months and presented with a mean hemoglobin value of 5.4 g/dL. Sixty-nine percent were neutropenic and none was thrombocytopenic. None of the patients had histologic evidence of parvovirus B19 infection in the bone marrow. DNA amplification for parvovirus B19 was negative in each case. In contrast, parvovirus B19DNA was amplified from DNA isolated from archived bone marrow coverslips of a patient with known parvovirus B19 infection, indicating that the PCR assay was sufficiently sensitive to detect virus from archieved bone marrow coverslips. Review of the literature indicates that the patients with parvovirus-associated TEC are generally older and often present with concomitant thrombocytopenia, whereas patients with parvovirus B19-negative TEC are younger and present without thrombocytopenia, similar to the patients in our study. Our results suggest that parvovirus B19 is not the cause of anemia in the young patient with typical features of TEC. Rather, parvovirus B19 infection of older, previously healthy children may occasionally cause a protracted anemia, often with thrombocytopenia, which may be diagnosed by some as TEC.
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PMID:Polymerase chain reaction amplification of archival material for parvovirus B19 in children with transient erythroblastopenia of childhood. 902 46

To learn whether fetal congestive heart failure causes a characteristic tissue iron storage pattern, we selected 15 neonatal autopsy cases of hydrops fetalis in which both the clinical and gross autopsy findings suggested intrauterine congestive heart failure. The latter appeared to be due to functional causes in 10 (3 nonhemolytic anemia, 4 cardiac dysrhythmia, 3 dilated cardiomyopathy) and was associated with cardiac malformation in 5. We graded the amount of hepatocellular siderosis, reticuloendothelial siderosis, and renal tubular siderosis in Perls-stained microscopic sections of liver, spleen, and kidney and compared the iron storage pattern with that in 15 normally developed neonatal autopsy controls (4 preterm, 11 term) and a further 7 with hemolytic anemia (5 alpha-thalassemia, 2 parvovirus B19 infection). Liver cell siderosis was absent in the three cases with nonhemolytic anemia. It was increased in 11 of the remaining 12 cases, as in hemolytic anemia controls. Among the five cardiac malformation cases, three had proximal renal tubular siderosis (as in hemolytic anemia controls) attributed to turbulent blood flow through the heart. Among the five, hydrops appeared to be due to prenatal closure of the foramen ovale in one and to prenatal constriction of the ductus arteriosus in another. In one of the five, and despite complex malformation of the heart, hydrops appeared to be due to complete heart block. We concluded that, although clinical information and morphologic assessment of the heart were basic to identifying a cardiac cause of fetal hydrops, histologic assessment of the pattern of iron storage helped confirm the pathologic diagnosis. Analysis of the pathologic findings led to a scheme for categorizing cardiogenic fetal hydrops.
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PMID:Tissue iron storage patterns in fetal hydrops associated with congestive heart failure. 902 54

Parvovirus B19, the only known human pathogenic parvovirus, is associated with a wide range of disease manifestations. In healthy individuals, the major presentation of B19 infection is erythema infectiosum. In patients with underlying hemolytic disorders, infection is the primary cause of transient aplastic crisis. In immunosuppressed patients, persistent infection may develop that presents as pure red cell aplasia and chronic anemia. In utero infection may result in hydrops fetalis or congenital anemia. Diagnosis is based on examination of bone marrow and virologic studies. Much is known of the pathophysiology of the virus, and studies are in progress to develop a vaccine to prevent this widespread infection.
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PMID:Parvovirus B19 in human disease. 904 45


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