Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Feline haematology profiles of patients presented to the University of Bristol Small Animal Hospital from January 2000 to October 2005 were evaluated for thrombocytosis (defined as a platelets count of >700x10(9)/l and confirmed on smear evaluation). Thrombocytosis was found in 79 cats (4.64% of the hospital feline population), with values ranging from 703 to 1895x10(9)/l. Signalment, clinical presentation, concurrence of other haematological abnormalities, diagnoses and outcome were evaluated in 51 cases in which complete medical records were available. Other variables (feline immunodeficiency virus/feline leukaemia virus status, thyroxine level, haemoplasma PCR, toxoplasma antibody titres) were also evaluated. No association was found between the presence of thrombocytosis and breed or gender. Gastrointestinal signs were the most common clinical presentation. Lymphopenia was the most common concurrent haematological abnormality. Based on final diagnosis reached, cats were grouped both according to the DAMNITV classification and according to the body system affected. Amongst the DAMNITV classification, inflammatory/infectious conditions were most commonly associated with thrombocytosis. According to body systems, gastrointestinal involvement was most represented, followed by endocrine cases. No association was found between the severity of thrombocytosis and outcome.
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PMID:Thrombocytosis in cats: a retrospective study of 51 cases (2000-2005). 1738 28

An important indication for bone marrow investigation is the presence of bone marrow failure, which manifests itself as (pan)cytopenia. The causes of cytopenia are varied and differ considerably between childhood and adulthood. In the paediatric age group inherited bone marrow failure syndromes are important causes of bone marrow failure, but they play only a minor role in later life. This review gives a comprehensive overview of bone marrow failure disorders in children and adults. We classified the causes of bone marrow failure according to the main presenting haematological abnormality, i.e. anaemia, neutropenia, thrombocytopenia or pancytopenia. The following red cell disorders are discussed: red cell aplasia, sideroblastic anaemia, congenital dyserythropoietic anaemia, haemolytic anaemia, paroxysmal nocturnal haemoglobinuria, iron deficiency anaemia, anaemia of chronic disease and megaloblastic anaemia. The neutropenias occur in the context of Shwachman-Diamond syndrome (SDS), severe congenital neutropenia, cyclic neutropenia, immune-related neutropenia and non-immune neutropenia. In addition, the following causes of thrombocytopenia are discussed: congenital amegakaryocytic thrombocytopenia, thrombocytopenia with absent radii, immune-related thrombocytopenia and non-immune thrombocytopenia. Finally, we pay attention to the following pancytopenic disorders: Fanconi anaemia, dyskeratosis congenita, aplastic anaemia, myelodysplastic syndromes and human immunodeficiency virus (HIV) infection.
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PMID:The pathology of bone marrow failure. 2072 24

Anemia is the most common hematological abnormality in human immunodeficiency virus (HIV)-infected patients. Besides chronic disease, opportunistic infections, nutritional deficiencies and antiretroviral drug toxicity, the direct role of HIV in the development of anemia has not yet been fully investigated. To explore the HIV-related mechanisms involved in the genesis of anemia, we used two experimental designs. In the first, HPCs purified from cord blood were challenged with HIV-1IIIb or recombinant gp120 (rgp120) and then committed to erythrocyte differentiation (EPO-post-treated HPCs). In the second, HPCs were first committed to differentiate towards the erythroid lineage and only afterwards challenged with HIV-1IIIb or rgp120 (EPO-pre-treated HPCs). Our results showed that HPCs and EPO-induced HPCs were not susceptible to HIV-1 infection. In addition, the two experimental designs (EPO post or pre-treated HPCs) independently showed that HIV-1IIIb or rgp120 were able to induce the impairment of survival, proliferation, and differentiation albeit differing in kinetics and extent. Interestingly, the gp120 interaction with CD4 and CXCR4 played a pivotal role in the impairment of erythrocyte differentiation by inducing TGF-b1 expression. These observations reveal an important additional mechanism involved in the genesis of anemia suggesting a complex competition between EPO-positive regulation and HIV-negative priming regarding erythrocyte survival, proliferation and maturation.
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PMID:HIV-1 gp120 impairs the differentiation and survival of cord blood CD34+ HPCs induced to the erythroid lineage. 2692 82