Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The blood borne viruses must be separated into major and minor agents. Major viruses transmissible by blood transfusion are human immunodeficiency virus (HIV) and hepatitis B and C viruses (respectively HBV, HCV). The prevalence of virological markers in French blood donors has been continuously decreasing since the implementation of serological screening methods as soon as they were available. In 1998, the prevalences (per 10,000 donations) were 0.17 for antibody to HIV, 0.08 for antibody to human T-cell leukemia virus (HTLV), 2.23 for hepatitis B surface antigen (HBs Ag) and 2.52 for antibody to HCV. The values are, of course, higher in new donors when compared to regular donors: approximately five-fold for HIV, 50-fold for HCV and 300-fold for HBs Ag. The remaining major questions concern the residual risk due to infectious donations which could escape the preventive measures. It seems evident that the major risk is imputable mainly to donations collected during the window period. During the 1996-1998 period, the residual risk for HIV was 1 out of 1,350,000 donations, 0 for HTLV, 1 out of 375,000 for HCV, and 1 out of 220,000 for HBV. A few cases of "immunosilent" patients have been reported. They remain exceptional. The first data collected after the implementation of nucleic acid technology (NAT) confirm the very low residual risk. The recent introduction of leukodepletion probably brought an important contribution to diminishing the risk of transmission of leucotropic viruses such as cytomegalovirus (CMV), Epstein-Barr virus (EBV), human herpesviruses-6, -7 and -8, and HTLV. If the purification process of plasma-derived medicinal products including inactivation procedures makes it possible to be confident with the elimination of infectivity due to enveloped viruses, the detection of nucleic acid sequences derived from naked viruses in plasma pools such as parvovirus B19 or hepatitis A virus (HAV), and/or the introduction of a nanofiltration step during the purification process, when possible, may greatly contribute to their safety. The emergence of a new form of the Creutzfeldt-Jakob disease (nvCJD) introduces a new series of questions about the safety of blood products that, although the risks appear limited, are not yet resolved.
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PMID:[Viruses and unconventional transmissible agents: update on transmission via blood ]. 1091 17

Case records of 232 dogs and 29 cats with neutropenia were reviewed to examine the spectrum of underlying etiologies causing the neutropenia. Six etiological categories included nonbacterial infectious disease; increased demand due to marked inflammation, bacterial sepsis, or endotoxemia; drug-associated neutropenia; primary bone-marrow disease; immune-mediated neutropenia; and diseases of unclear etiology. The largest single category associated with the development of neutropenia was nonbacterial infectious disease (e.g., feline leukemia virus [FeLV], feline immunodeficiency virus [FIV], histoplasmosis, cryptococcosis, and parvovirus), with parvovirus infection accounting for 47.1% of all cases. The least common (0.38%) cause was naturally occurring immune-mediated neutropenia.
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PMID:Neutropenia in dogs and cats: a retrospective study of 261 cases. 1130 May 19

Inhibitors against factor XI (FXI) have been frequently described in patients who acquired inhibitors (due to auto-immune disorders, malignancies or infections), but less often in those with a congenital deficiency of this factor, who had received plasma infusions. The present report concerns one such inhibitor found in the plasma of a patient with chronic myelomonocytic leukaemia and infected by B19 parvovirus, who was neither a heterozygote nor a homozygote for FXI deficiency, and who had no bleeding tendency despite a very low FXI level. Taking this case into account, we discuss and present the clinical and biological features of acquired FXI deficiency caused by an inhibitor.
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PMID:A case of chronic myelomonocytic leukaemia and factor XI deficiency with a circulating anticoagulant. 1144 50

Cats with feline leukemia virus (FeLV)-associated enteritis (FAE), enteritis of other known viral etiology (parvovirus [PV], enteric coronavirus [CoV]), and enteritis of unknown etiology with histologic features similar to those of FAE and PV enteritis (EUE) and FeLV-negative and FeLV-positive cats without enterocyte alterations were examined. Amount and types of infiltrating leukocytes in the jejunum and activity and cellular constituents of mesenteric lymph nodes, spleen, and bone marrow were determined. PV and CoV infections were confirmed by immunohistologic demonstration of PV and CoV antigen, ultrastructural demonstration of viral particles in the intestinal content, and in situ hybridization for PV genome. FeLV infection was detected by immunohistology for gp70, p27, and p15E. Latent FeLV infection was excluded by polymerase chain reaction methods for exogenous FeLV DNA. Enterocyte lesions involved the crypts in cats with PV enteritis, FAE, and EUE and the villous tips in cats with CoV enteritis. Inflammatory infiltration was generally dominated by mononuclear cells and was moderate in the unaltered intestine and in cats with PV enteritis and marked in cats with FAE, CoV enteritis, and EUE. In cats with EUE, myeloid/histiocyte antigen-positive macrophages were relatively numerous, suggesting recruitment of peripheral blood monocytes. Lymphoid tissues were depleted in cats with PV enteritis and with EUE but were normal or hyperplastic in cats with FAE. Bone marrow activity was decreased in cats with PV enteritis; in cats with FAE or EUE and in FeLV-positive cats without enterocyte alterations, activity was slightly increased. In cats with FAE and PV enteritis, a T-cell-dominated response prevailed. EUE showed some parallels to human inflammatory bowel disease, indicating a potential harmful effect of infiltrating macrophages on the intestinal epithelium.
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PMID:Comparative examination of cats with feline leukemia virus-associated enteritis and other relevant forms of feline enteritis. 1146 70

A preleukaemic phase, typified by pancytopenia and bone marrow (BM) hypoplasia, is an uncommon but well-documented prelude to acute lymphoblastic leukaemia (pre-ALL) in children. Parvovirus B19 (B19) exhibits a marked tropism to human BM and replicates only in erythroid progenitor cells acting as a confounding, but treatable agent in immunocompromised patients. We present the first case of B19-associated pre-ALL characterized by severe and recurring transient pancytopenia in a child who developed ALL 5 months later. The advent of B19-specific IgG at the time of infection and the subsequent disappearance 1.5 years later has not previously been described. In this patient the observed cytopenias were probably the result of B19 acting in concert with the failing BM and B19 is possibly one of several factors capable of triggering the onset of pre-ALL.
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PMID:Transient pancytopenia preceding acute lymphoblastic leukaemia (pre-ALL) precipitated by parvovirus B19. 1249 95

This review addresses three related bone marrow failure diseases, the study of which has generated important insights in hematopoiesis, red cell biology, and immune-mediated blood cell injury. In Section I, Dr. Young summarizes the current knowledge of acquired aplastic anemia. In most patients, an autoimmune mechanism has been inferred from positive responses to nontransplant therapies and laboratory data. Cytotoxic T cell attack, with production of type I cytokines, leads to hematopoietic stem cell destruction and ultimately pancytopenia; this underlying mechanism is similar to other human disorders of lymphocyte-mediated, tissue-specific organ destruction (diabetes, multiple sclerosis, uveitis, colitis, etc.). The antigen that incites disease is unknown in aplastic anemia as in other autoimmune diseases; post-hepatitis aplasia is an obvious target for virus discovery. Aplastic anemia can be effectively treated by either stem cell transplantation or immunosuppression. Results of recent trials with antilymphocyte globulins and high dose cyclophosphamide are reviewed. Dr. Abkowitz discusses the diagnosis and clinical approach to patients with acquired pure red cell aplasia, both secondary and idiopathic, in Section II. The pathophysiology of various PRCA syndromes including immunologic inhibition of red cell differentiation, viral infection (especially human parvovirus B19), and myelodysplasia are discussed. An animal model of PRCA (secondary to infection with feline leukemia virus [FeLV], subgroup C) is presented. Understanding the mechanisms by which erythropoiesis is impaired provides for insights into the process of normal red cell differentiation, as well as a rational strategy for patient management. Among the acquired cytopenias paroxysmal nocturnal hemoglobinuria (PNH) is relatively rare; however, it can pose formidable management problems. Since its first recognition as a disease, PNH has been correctly classified as a hemolytic anemia; however, the frequent co-existence of other cytopenias has hinted strongly at a more complex pathogenesis. In Section III, Dr. Luzzatto examines recent progress in this area, with special emphasis on the somatic mutations in the PIG-A gene and resulting phenotypes. Animal models of PNH and the association of PNH with bone marrow failure are also reviewed. Expansion of PNH clones must reflect somatic cell selection, probably as part of an autoimmune process. Outstanding issues in treatment are illustrated through clinical cases of PNH. Biologic inferences from PNH may be relevant to our understanding of more common marrow failure syndromes like myelodysplasia.
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PMID:New Insights into the Pathophysiology of Acquired Cytopenias. 1170 33

The authors present a case of a 13-year-old girl with a history of congenital hemolytic anemia (spherocytosis) who developed acute lymphoblastic leukaemia. She received treatment according to the ALL-BFM 91 protocol standard risk group. During maintenance therapy an aplastic crisis caused by Parvovirus B 19 infection had developed. Chemotherapy was stopped in September 1999, and the patient remained in complete remission. In January, 2000 the patient presented with jaundice, caused by a stone in the ductus choledochus. Cholecystectomy and splenectomy were performed, and the the girl became symptomfree. The authors review the most frequent complications of congenital hemolytic anemias (aplastic crisis, haemolytic crisis and cholelithiasis). The occurrence of acute lymphoblastic leukaemia in a patient with congenital hemolytic anemia has not been previously reported.
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PMID:[Acute lymphoblastic leukemia in a patient with congenital hemolytic anemia: case report]. 1176 Apr 56

There have been few reports of large granular lymphocyte (LGL) leukemia with neutropenia complicated with pure red cell aplasia (PRCA) that developed after human parvovirus (HPV) B19 infection. We report here the case of a 35-year-old female who developed HPV B19-associated PRCA with T-LGL leukemia. LGL count of peripheral blood was lower than 2 x 10(9) l(-1), although phenotypic analysis of LGL showed CD3+, CD16-, CD56-, CD57+ with double positive for CD3 and CD57, and genetic study showed the clonal rearrangement of T-cell receptor gene. Microscopically, the patient's bone marrow showed characteristic giant proerythroblasts. A serologic study of HPV B19 was positive for IgM, but negative for IgG, with a positive result on Dot-blot hybridization assay for HPV B19 DNA. Severe anemia and reticulocytopenia ameliorated without treatment 10 days after the initial examination, but slight anemia, neutropenia, a moderate increase of LGL counts with rearrangement of TCR gene, and positive result of HPV B19 DNA has persisted 7 months after the initial examination. We suggest that this viral infection may play an etiologic role in some patients with LGL leukemia who develop PRCA.
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PMID:Pure red cell aplasia associated with parvovirus B19 infection in T-large granular lymphocyte leukemia. 1191 33

The goal of this study was to evaluate the efficacy of a virus-inactivating process for use during the preparation of porcine-derived extracellular matrix biomaterials for human clinical implantation. Porcine small intestine, the source material for the tissue-engineered, small intestinal submucosa (SIS) biomaterial, was evaluated. Relevant enveloped, non-enveloped, and model viruses representative of different virus families were included in the investigation: porcine parvovirus (PPV), porcine reovirus, murine leukemia retrovirus (LRV), and porcine pseudorabies (herpes) virus (PRV). Samples of small intestine were deliberately inoculated with approximately 1 x 10(7) plaque-forming units (PFU) of virus which were thereafter exposed to a 0.18% peracetic acid/4.8% aqueous ethanol mixture for time periods ranging from 5 minutes to 2 hours. Enveloped viruses were more easily inactivated than non-enveloped viruses, but material processed for 30 minutes or longer inactivated all of the viruses. D(10) values were calculated and used to extrapolate the extent of inactivation after 2 hours. Viral titers were reduced by more than 14.0 log(10) PPV, 21.0 log(10) reovirus, 40.0 log(10) PRV, and 27.0 log(10) LRV, meeting international standards for viral sterility. These results demonstrate that treatment of porcine small intestine with a peracetic acid/ethanol solution leads to a virus-free, non-crosslinked biomaterial safe for xenotransplantation into humans.
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PMID:Virus safety of a porcine-derived medical device: evaluation of a viral inactivation method. 1211 37

The reconstitution of blood and its components is hampered by factors of compatibility, availability, and the risk of transmission of infectious diseases. Protozoal agents such as plasmodium malariae and trypanosoma cruzi are only regionally relevant. Bacterial transmissions are easy to prevent and treat. Antibody, antigen, and nucleic acid screening have been implemented to prevent transmission of blood-borne viruses. Transfusion-relevant viruses include hepatitis B and C virus (HBV and HCV), human immunodeficiency virus (HIV), human T leukemia virus (HTLV-I), and in certain circumstances, parvovirus B19, hepatitis A virus (HAV), and cytomegalovirus (CMV). Of great concern is the possible transmission of prion protein causing transmissible spongiform encephalopathy. Of future interest will be whether other viruses such as Nipah and Hendra virus are blood-borne and whether viruses such as TT, SEN, and GBV-C are involved in diseases or their progression, while not causing hepatitis.
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PMID:Virus safety of human blood, plasma, and derived products. 1237 92


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