Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0002874 (aplastic anemia)
 5,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Congenital human parvovirus B19 infection presented in this case as nonimmune hydrops fetalis that resulted from aplastic anemia at 20 weeks' gestation. Intravascular transfusion therapy led to resolution of the hydrops and a term delivery of an appropriately grown neonate.
 ...
PMID:Intrauterine transfusion treatment of nonimmune hydrops fetalis secondary to human parvovirus B19 infection. 184 4

Some generalizations can be drawn from a review of virus-associated bone marrow failure. The story of B19 parvovirus illustrates that viral infection may be an occult cause of marrow failure. Although the epidemiology of transient aplastic crisis suggested a viral aetiology, the implication of a single virus was surprising; the sporadic appearance of chronic bone marrow failure in immunosuppressed persons has had none of the features of a viral illness. The incrimination of parvovirus in these cases required development of specific immunological and molecular assays. Human and animal retrovirus studies have shown that small changes in the virus genome can have dramatic effects on the biology of the infectious agent and its pathogenicity in infected hosts. In Epstein-Barr virus infection, the host's immune response may play a more important role in mediating disease than virus cytotoxicity. Finally, the association of aplastic anaemia with hepatitis may be underestimated because of the inability to diagnose virus infection without obvious liver disease. The true spectrum of bone marrow disease due to virus infection is not known.
 ...
PMID:Viruses and bone marrow failure. 253 67

Recovery of bone marrow function in aplastic anemia patients treated with immunosuppressive therapy first suggested a role for the immune system in bone marrow failure. High recovery rates in patients treated with immunosuppressive therapy suggested that an immune mechanism may be a final common pathway of marrow failure in this disease. In vitro studies have shown that aplastic peripheral blood and marrow cells and their supernatants are capable of suppressing hematopoiesis by autologous and normal marrow. Soluble factors identified in this system include gamma interferon and lymphotoxin. The interaction of these molecules with positive growth factors, the role of synergy with other negative regulators, and their role in the pathogenesis of bone marrow failure are discussed. Lymphokine and lymphocyte abnormalities in aplastic anemia may be manifestations of an underlying viral etiology. Three examples are discussed: Epstein-Barr virus-associated aplastic anemia; B19 parvovirus bone marrow failure; and HIV-induced neutropenia.
 ...
PMID:Autoimmune aspects of aplastic anemia. 297 24

We recently observed that more than one third of pediatric patients who presented with non-A, non-B fulminant liver failure (FLF) also developed aplastic anemia (AA) either before or shortly after liver transplantation. Factors involved in the suppression of bone marrow could be the same as those causing hepatic failure. We considered parvovirus B19 a candidate etiologic agent because of the known tropism of B19 for erythroid precursors. Archived liver and serum from six patients undergoing liver transplantation for non-A, non-B, non-C FLF with associated AA were analyzed for the presence of B19 DNA and anti-B19 serology. An age- and gender-matched control group (N = 44) was analyzed in parallel. B19 DNA studies and anti-B19 serology were performed in a blinded fashion. B19 serologies were performed by antibody capture enzyme-linked immunosorbent assay (ELISA). B19 DNA was detected after polymerase chain reaction (PCR) amplification of target B19 DNA sequences in liver and serum. Liver tissue showed evidence of B19 DNA in four of six (66%) patients with FLF and associated AA. Two of 4 patients with cryptogenic FLF but without AA had B19 DNA detected in the liver tissue. Of the 34 remaining controls, only 5 (15%) showed evidence of B19 DNA in liver tissue (66% vs. 15%, P = .016). B19 DNA was not detected in any of the test or control sera. This study provides evidence to support the role of parvovirus B19 in the development of FLF and associated AA.
 ...
PMID:Parvovirus B19 as a possible causative agent of fulminant liver failure and associated aplastic anemia. 748 71

Parvovirus B19 DNA was detected in serum samples from 10 out of 42 patients with chronic anaemia, the majority of whom suffered from aplastic anaemia, haemolytic anaemia, pure red cell anaemia or myelodysplastic syndrome. Nested PCR methods with sensitivities of 0.005-0.05 fg DNA were developed. In nine patients, B19 DNA could only be detected by nested PCR. Conventional PCR with a sensitivity of 50 fg B19 DNA could only detect B19 DNA in one patient. In the majority of B19-DNA-positive patients, the DNA concentration was estimated at 0.005-0.05 fg per 5 microliters serum.
 ...
PMID:Estimation of serum concentration of parvovirus B19 DNA by PCR in patients with chronic anaemia. 770 74

The diverse manifestations of human parvovirus B19 infection have been well established. Erythema infectiosum, fetal hydrops, adult arthropathy, and aplastic anemia in patients with hemoglobinopathies or underlying immunocompromise have been described. Recently we successfully treated a patient who, after heart transplantation, had fever, rash, and pneumonia with respiratory failure caused by human parovirus B19. Human parovirus B19 has not been reported previously as a pathogen causing pulmonary disease after pediatric heart transplantation, and we wish to report it at this time.
 ...
PMID:Severe pneumonia after heart transplantation as a result of human parvovirus B19. 803 18

The term "emerging diseases" is a loosely defined category of entities comprising resurgent or recurrent old diseases (usually caused by "new" or mutated previously known agents), diseases truly new to man, but caused by preexisting ("old") zoonotic agents, and syndromes newly defined by the discovery of new agents through advances in biotechnology. Identification and solution of these problems depends, first, on recognition of their differences, and then upon tailoring appropriate strategies for their control. Thus, new influenza viruses appear each year to challenge immunity to their antecedents, but evoke the unchanged and centuries old symptom complex of influenza. Tuberculosis, is resurgent because of mycobacterial mutation to antibiotic resistance, immunosuppression by AIDS, and laxity in public health surveillance. Parvovirus B19 and herpesvirus 6 were revealed as cryptic infectors of white blood cells in studies of hepatitis B and AIDS, but since have been shown to be important causes of childhood rashes, aplastic anemia, and neurologic disease. The encroachment of human habitation on wilderness perimeters (ecosystem change) has increased contact with vectors of zoonotic viruses and bacteria, as evidenced by Lyme disease, Ebola virus infection, and the hemorrhagic fevers. The term "holistic epidemiology" embraces all these problems, from the molecular to the macroenvironmental level. Humans, parasites, and their environment will continue their ancient, fluctuating, dynamic relationship in the future, and new diseases will continue to emerge.
 ...
PMID:The emergence of "emerging diseases": a lesson in holistic epidemiology. 869 62

Parvovirus B19 has been identified as the etiological agent of "fifth disease" in childhood. It is also a rarely reported cause of anemia in transplanted patients. During a period of 18 months we observed four cases (2 male and 2 female; 53 +/- 4.24 years) of severe aplastic anemia due to parvovirus B19 in kidney transplant patients. The overall incidence of the disease was 6.3% of all our transplanted patients. Symptoms of the disease occurred 22.5 +/- 9.75 days post-operatively. Serum creatinine was 1.5 +/- 0.35 mg/dl. Hb was 6.58 +/- 0.6 g/dl. All patients recovered with 15 days of high doses of commercial immunoglobulins. We conclude that B19 parvovirus infection is probably an underestimated disease in transplant patients. It is a first-period infection, probably donor-transmitted. High dose immunoglobulins are an effective but costly therapy.
 ...
PMID:Aplastic anemia due to B19 parvovirus infection in cadaveric renal transplant recipients: an underestimated infectious disease in the immunocompromised host. 923 23

The role of known hematopoietic growth factors in the pathogenesis of aplastic anemia and congenital hypoplastic anemia has been extensively studied and no evidence has been obtained that deficiency of these factors contributes to the hypoproliferative state in these disorders. Clonal hematopoiesis seems to be present at least in a small percentage of cases of aplastic anemia, a finding that needs further investigation. Androgens were shown to be beneficial only for women with aplastic anemia treated with antilymphocyte globulin. Unrelated-donor bone marrow transplantation is becoming a realistic approach for children and very young adults with aplastic anemia, but in older groups the survival is very poor. New observations on abnormalities of lymphokines and cytokines in Fanconi's anemia have been described, but their pathogenetic significance remains unknown. A large number of studies have excluded the possibility that abnormalities of c-kit/SCF genes and their expression are responsible for the erythroid aplasia in Diamond-Blackfan syndrome. Cyclosporine was found to be an effective treatment for pure red cell aplasia associated with chronic lymphocytic leukemia. The cell membrane receptor for B19 parvovirus has been identified as the P antigen. Long-term studies showed that in 20% of patients with homozygous sickle cell disease, infection by B19 does not cause erythroid aplasia.
 ...
PMID:Aplastic anemia and pure red cell aplasia. 937 Dec 75

Hepatitis-associated aplastic anemia is rare in general, but occurs in up to 28% of patients receiving liver transplantation for fulminant non-A, non-B hepatitis. Cases are commonly young men with mild hepatitis but severe aplastic anemia. Although cases have been reported in association with hepatitis A, B, and C, most appear to be due to a non-A-B-C virus. We report two cases of acute hepatitis subsequently complicated by marrow hypoplasia in patients with acute parvovirus B19 infection. Hepatic manifestations of parvovirus B19 infection range from liver chemistry abnormalities to fulminant hepatic failure and aplastic anemia. Our cases demonstrate a less severe form of hepatitis-associated aplastic anemia, and together with other data, suggest that parvovirus B19 is at least one cause of hepatitis-associated aplastic anemia, and may be a heretofore underrecognized hepatotrophic virus.
 ...
PMID:Hepatitis-associated aplastic anemia and acute parvovirus B19 infection: a report of two cases and a review of the literature. 951 62


1 2 3 4 5 6 7 8 Next >>