Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The acquired immune deficiency syndrome (AIDS) is a novel epidemic form of immunodeficiency that has been widely recognized within the last six years. AIDS is characterized by Kaposi's sarcoma, B cell lymphoma, and/or life-threatening opportunistic infections superimposed on an immune deficiency state which consists of lymphopenia with a selective depletion of the CD4 T cells. In addition, lymphocytes from AIDS patients show decreased responses to antigen or mitogen stimulation in vitro. Although the secondary infections and malignancies seen in these patients may be successfully treated, the underlying immune defect persists, leaving the patient susceptible to further complications.
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PMID:Acquired immune deficiency syndrome (AIDS) and neoplasia. 349 18

Blood specimens from 165 intravenous drug users who were seropositive for the human immunodeficiency virus (HIV), from 158 seropositive homosexual men with lymphadenopathy, and from 77 patients with acquired immunodeficiency syndrome (AIDS) were assessed immunologically. Immunologic parameters were analyzed by the Guttman scalogram technique to determine if immunologic abnormalities occurred in a nonrandom pattern. The following four patterns emerged: (i) seropositivity for HIV with no immunologic abnormalities; (ii) seropositivity for HIV with a depressed T4/T8 cell ratio; (iii) seropositivity with a depressed T4/T8 cell ratio and T4-cell depletion; and (iv) seropositivity with a depressed T4/T8 cell ratio, T4-cell depletion, and lymphopenia. Ninety-two to 100% of subjects in each of the three groups of patients were found "to scale" because the abnormalities occurred in the cumulative, ordered fashion described. This nonrandom occurrence of abnormalities indicates an ordered progression of immunologic abnormalities in individuals infected with HIV, a finding useful in the staging of both symptomatic and asymptomatic HIV-seropositive subjects.
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PMID:Nonrandom development of immunologic abnormalities after infection with human immunodeficiency virus: implications for immunologic classification of the disease. 349 3

Unresponsiveness to skin testing with PPD and tetanus toxoid was commonly seen in patients with haemophilia A but not infected with human immunodeficiency virus but was uncommon in controls. Vaccination history indicated that the unresponsive patients had not been immunised in childhood. Other tests of immune competence (skin tests with other antigens, lymphocyte stimulation with mitogens and antigens, and viral serology) showed that the haemophilia A patients had an adequate response to pathogens to which they had been exposed. Five of 12 such patients had a mild T4 lymphopenia, and this may have been related to parenteral administration of large quantities of protein.
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PMID:Unresponsiveness to skin testing with bacterial antigens in patients with haemophilia A not apparently infected with human immunodeficiency virus (HIV). 349 42

Between February 1983 and April 1986 we studied peripheral blood and bone marrow samples from 20 patients with human immunodeficiency virus (HIV) related disease. 14 patients had AIDS, three had ARC, two had PGL and one had ITP as a sole manifestation of HIV related disease. Peripheral blood abnormalities included marked anisocytosis and poikilocytosis, rouleaux formation, neutropenia, lymphopenia, monocytopenia, a left shift in the granulocyte series and, in the patients with AIDS, vacuolated monocytes. The most frequent bone marrow abnormalities were reticuloendothelial iron block, dyserythropoiesis, megaloblastic change and erythroid hypoplasia. Excess histiocytes were noted in four marrows, one exhibiting haemophagocytosis. None of the bone marrows showed lymphopenia. Eight of the 20 marrows were difficult or impossible to aspirate. None of the trephine biopsies showed increased reticulin. The causes of these abnormalities are probably multiple and include opportunistic infections, drug therapy, immune mechanisms and possibly direct insult by the HIV virus.
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PMID:Peripheral blood and bone marrow abnormalities in patients with HIV related disease. 356 82

A 7-year-old horse with no previous history of illness was determined to have a systemic infection of Rhodococcus equi. Rhodococcus equi was isolated from blood, tracheal fluid, and feces. Lymphopenia, failure to respond to concanavalin A and phytohemagglutinin lymphocyte stimulation testing, decreased concentrations of immunoglobulin (Ig)M, IgA, and IgG, low R equi antibody titer, histologic depletion of lymphoid tissue, and a failure to respond to antigenic stimulation led to the conclusion that both humoral and cell-mediated immunity were compromised. No cause for the acquired immunodeficiency could be determined.
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PMID:Acquired immunodeficiency in a seven-year-old horse. 357 Sep 21

Development of cell-mediated immunity in young ruminants appears to be under the influence of the thymus. In sheep, prenatal removal of the thymus has little effect on postnatal growth of lambs. However, lambs are immunodeficient compared with normal controls, and they exhibit depressed delayed hypersensitive skin responses to antigens such as tuberculin purified protein derivative. Lymphopenia accompanying the immunodeficiency appears to be due to depletion of a particular population of T-cells (thymus derived) that have reduced response to mitogens and decreased numbers as the lamb matures. Young lambs are less responsive than adult sheep to vaccination with irradiated Trichostrongylus colubriformis larvae. The basis of this lowered responsiveness appears to be not only the immaturity of the cell-mediated immune response but also the segregation of the lambs into high and low responders. This immune responsiveness is possibly under the genetic control of the ovine major histocompatibility complex. It may be possible to select and breed sheep and cattle for responsiveness to vaccination against parasitic, viral, and bacterial diseases.
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PMID:Development of cell-mediated immunity in young ruminants. 388 81

An 18-year follow-up of a young woman who presented at the age of 10 years with a malabsorption syndrome and recurrent chest infections is reported. The serum immunoglobulins, and in particular the IgA, were increased, cell-mediated immunity was impaired but free alpha heavy chains were not detected. A jejunal biopsy showed plasma cell infiltration of the bowel with villous atrophy. Bronchiectasis, recurrent skin infections, and sinusitis were treated with frequent courses of antibiotics and corticosteroids. An initial presumptive diagnosis of cystic fibrosis was excluded by a normal sweat test. Although difficult to classify her exact type of immune deficiency state, the data would appear to conform to the syndrome of cellular immunodeficiency with normal or near normal immunoglobulins and lymphopenia (Nezelof's syndrome).
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PMID:Plasma cell infiltration of the small intestine, recurrent pulmonary infections, and cellular immunodeficiency (Nezelof's syndrome). 405 Jul 63

A severe combined immunodeficiency disorder was demonstrated in two Arabian foals which were full siblings. The defect in the B-lymphocyte system was shown by hypogammaglobulinemia, lymphopenia, and absence of germinal centers. The almost total absence of thymic tissue in one foal and the lack of thymic dependent lymphocytes in the spleens of both foals demonstrate a T-lymphocyte defect. In a retrospective study of total available Arabian foal cases, 4 of 15 had evidence of immunodeficiency.
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PMID:Hypogammaglobulinemia and thymic hypoplasia in horses: a primary combined immunodeficiency disorder. 419 58

Fourteen previously healthy young patients with unusual community-acquired opportunistic infections were seen over a period of three years. They differ from patients previously described in that 11 were heterosexual drug abusers (including two women) and only three were homosexual men. There were eight Puerto Ricans, five blacks, and one white. Infections included Pneumocystis carinii pneumonia (seven), disseminated Mycobacterium intracellulare infection, histoplasmosis, cryptococcosis, and cytomegalovirus infection (one each), oral thrush (13), and Candida esophagitis (two). All patients had impaired cellular immunity manifested by cutaneous anergy and lymphopenia, and all 11 tested had a markedly decreased ratio of T helper/inducer cells to T suppressor/cytotoxic cells. Twelve had evidence of associated viral infection (Epstein-Barr virus in nine, cytomegalovirus in five, Herpes simplex type 2 in two). Clinical presentation was with a severe opportunistic infection or with a prodrome consisting of oral thrush and nonspecific findings including malaise, fever, lymphadenopathy, or cough. The syndrome of immunodeficiency and opportunistic infection occurs in nonwhite heterosexual drug abusers, not exclusively in white homosexual men, and patients may present for medical care before the onset of a severe opportunistic infection.
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PMID:Community-acquired opportunistic infections and defective cellular immunity in heterosexual drug abusers and homosexual men. 621 79

Deoxyadenosine (AdR) appears to be central to the molecular events mediating immunodeficiency in children born with adenosine deaminase (ADA) deficiency but it is still uncertain whether lymphotoxicity is due to AdR directly inhibiting transmethylation reactions in which S-adenosylmethionine is the methyl group donor, or is due to phosphorylation of AdR to deoxyadenosine triphosphate (dATP) which then inhibits ribonucleotide reductase or is due to other mechanisms. Using AdR and the ADA inhibitor deoxycoformycin (dCF) and assessing cell viability, nucleoside incorporation into RNA and DNA, as well as measuring deoxyribonucleoside triphosphate (dNTP) concentrations and S-adenosylhomocysteine (SAH) hydrolase activity, we have studied various types of human lymphoid cells and demonstrated in them the relative importance of the above two mechanisms of AdR toxicity. Treatment of normal resting peripheral blood lymphocytes in culture with AdR and dCF resulted in impaired viability. Although elevated dATP levels as well as decreased SAH hydrolase activities were both observed, the failure of a known inhibitor of ribonucleotide reductase (hydroxyurea) to produce toxicity, and the inability of deoxycytidine (CdR) to achieve a rescue effect, point to another mechanism, possibly inhibition of trans-methylation or ATP depletion being the more likely causes of toxicity in resting lymphocytes. The same mechanism may well account for the rapid and severe lymphopenia in patients treated with dCF. On the other hand, in cultured lymphoblasts in the exponential phase of growth. AdR and dCF produced marked inhibition of growth and cell death both in a Thy-ALL line and in a c-ALL line, in the absence of significant inhibition of SAH hydrolase, but with a substantial elevation in dATP concentrations and depressed levels of the other dNTP. Minor toxicity occurred in a proliferating B lymphoblast line despite almost complete inactivation of SAH hydrolase. These observations indicate inhibition of ribonucleotide reductase as the more likely mechanism of toxicity in rapidly proliferating lymphocytes. Other T-cells actively synthesizing DNA, such as PHA-stimulated or MLC activated lymphocytes and T-lymphoid colony forming cells, are also likely to be affected by the same mechanism. Indeed in PHA-stimulated lymphocytes, deoxycytidine caused significant although incomplete rescue from toxicity due to dCF and AdR. In patients with ADA deficiency or treated with ADA inhibitors, both mechanisms could be operative. These observations are also relevant to the possible use of dCF and AdR as immunosuppressive agents and for the removal of T-cells or residual Thy-ALL blasts from bone marr
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PMID:Mechanisms of deoxyadenosine toxicity in human lymphoid cells in vitro: relevance to the therapeutic use of inhibitors of adenosine deaminase. 623 Oct 47


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