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Query: UMLS:C0001175 (AIDS)
 120,706 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report describes a clinical case of a large cell, immunoblastic plasmacytoid malignant B-cell lymphoma of the rectum in an AIDS patient coinfected with HTLV-I. The malignant cells showed clonal genetic rearrangement of the HC (JH) and LCK genes. Infection by EBV was demonstrated serologically and with slot blots using genomic DNA of the cancer cells. Southern blot analysis with DNA extracted from the lymphoma cells were negative for HTLV-I. The patient received seven cycles of VACO-B which induced complete but transient clinical remission of the tumor. The final outcome of the patient is unknown.
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PMID:Primary B cell lymphoma of the rectum in a patient coinfected with HIV-1 and HTLV-I. 128 27

Hematopoietic growth factors may mitigate the cytopenias that frequently complicate HIV disease or its treatment. Clinical and in vitro studies have indicated the ability of granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte colony-stimulating factor (G-CSF) or erythropoietin (EPO) to overcome the myelosuppression of HIV or many of the drug therapies used in the care of HIV-infected individuals. In addition, neutrophil or monocyte functional abnormalities observed in AIDS patients may be improved by the use of GM-CSF. Issues which may distinguish the use of hematopoietic growth factors in AIDS as compared with in other clinical settings include: 1) interaction of the growth factor with other cytokines which are aberrantly expressed, 2) direct effects of the growth factor on the replicative activity of HIV, and 3) potential interactions of the growth factor with other concurrently administered medications. This review focuses on the potential roles and limitations of growth factor use in AIDS and reviews the clinical studies using GM-CSF in HIV-infected individuals.
Infection 1992
PMID:The use of GM-CSF in AIDS. 128 4

Infection with cytomegalovirus (CMV) is a major feature of acquired immunodeficiency syndrome (AIDS). Gastrointestinal involvement is being seen more frequently. Our collective experience involves nine patients with stomach involvement. Seven patients were intravenous drug abusers or homosexuals with AIDS. One developed CMV gastritis as a complication of leukemia and one patient was a West African with lymphoma and human immunodeficiency virus (HIV) infection. All our patients had biopsy-proven CMV inclusion bodies. The radiographic appearances varied widely. The findings included markedly thickened edematous folds, erosive gastritis with aphthous ulceration, and superficial and deep ulceration. One patient had deep ulceration with fistula formation. Computed tomographic (CT) scans confirmed the greatly thickened gastric wall and coarsened folds in two patients. Associated gastrointestinal infections included candida and herpes, and, in addition, pneumocystis carinii pneumonia (PCP) was present in two patients. CMV gastritis may mimic several other conditions including erosive gastritis, peptic ulceration, lymphoma, and carcinoma. It should be strongly considered in immunosuppressed patients.
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PMID:Cytomegalovirus gastritis: protean radiologic features. 131 63

Interleukin-6 (IL-6) is a cytokine produced by a number of cells, including macrophages, and is directly involved in the inflammatory response. The production of IL-6 can be stimulated by monokines such as IL-1 and tumor necrosis factor (TNF). Mycobacterium avium complex organisms frequently cause disseminated disease in patients with AIDS. M. avium is an intracellular bacterium that that mainly infects macrophages. Treatment of M. avium-infected macrophage monolayers with recombinant IL-6 decreased the ability of TNF to activate cultured macrophages to inhibit growth of or kill intracellular M. avium (68% +/- 14% decrease in intracellular killing compared with that in monolayers not treated with IL-6). To further evaluate whether this effect was dependent on the down regulation of membrane receptors to TNF, we examined 125I-TNF binding to macrophages previously exposed to IL-6: the expression of TNF receptors was decreased by 78% +/- 9%. The effect of IL-6 on TNF receptors was observed after 4 h and was reversible. Infection of macrophages with different M. avium serovars was associated with release of IL-6, and IL-6 production peaked at 48 h after infection in concentrations ranging from 328 +/- 87 ng/10(5) cells to 907 +/- 224 ng/10(5) cells. IL-6 did not have any influence on the rate of growth of the tested strains of M. avium within or outside macrophages. These results suggest that release of IL-6 by M. avium-infected macrophages may influence the host's immune response and the outcome of the disease.
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PMID:Interleukin-6 antagonizes tumor necrosis factor-mediated mycobacteriostatic and mycobactericidal activities in macrophages. 132 56

Infection with the human immunodeficiency virus-1 is associated with a marked increase in the incidence of Kaposi's sarcoma. Recent studies suggest that the risk of Kaposi's sarcoma in human immunodeficiency virus infection is increased with oral-fecal contact and that a sexually transmitted agent possibly related to human papillomavirus-16 could be involved. Exposure to this or another sexually transmitted agent apparently alters both the morphology and growth regulation of the Kaposi's sarcoma progenitor cells. These changes include the expression of the alpha chain of the interleukin-6 receptor with the acquisition of an interleukin-6-dependent autocrine growth loop. Subsequent perturbation of multiple cytokines during human immunodeficiency virus infection, including Oncostatin-M, interleukin-1 beta and tumor necrosis factor-alpha alters the subsequent growth of Kaposi's sarcoma. These studies suggest that control of cytokine perturbations or the underlying human immunodeficiency virus-1 infection should result in a significant reduction in the rate of growth of acquired immunodeficiency syndrome-related Kaposi's sarcoma.
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PMID:Pathogenesis of human immunodeficiency virus-related Kaposi's sarcoma. 133 10

P carinii is an opportunistic pathogenic agent able to produce severe infection that must be diagnosed promptly. We analyzed 138 samples from 100 patients suspected of having infection by P carinii. The ortho-toluidine blue and the methenamine stains were used to analyze the samples. Infection was demonstrated in 18 patients, 13 adults and 5 children. Underlying disease was AIDS in 7 and other immunosuppressive disorders in the rest. No immunocompetent patient was infected with P carinii. Proper sample collection is important for diagnosis. When bronchoalveolar lavage is not possible, pharyngo-tracheal aspirate in children and sputum sampling after assisted coughing in adults are recommended. At least 2 staining methods and proper controls are advisable.
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PMID:[Pneumocystis carinii infection. Various aspects on its clinical and laboratory diagnosis]. 134 92

The purpose of this paper was to evaluate the prevalence of HIV infection and AIDS in Argentina, to study the dynamics of the spread of HIV and to predict the future course by means of an epidemic model. The model was constructed using differential equations to describe the interactions between members of the various groups at risk. The functional form of the solutions was used in a back calculation procedure using data from cohort studies which were done in other countries (U.S.A. and France) together with data of AIDS cases reported to the National AIDS Program, to determine the time evolution of HIV-infection in each of the groups at risk defined. Results show that HIV was introduced in Argentina during the early 80's and affected persons of the homosexual/bisexual group in a first stage. In April 1990 it was estimated that there were a total of 34,131 HIV-infected persons. Intravenous drug users (IVDU) represented 39.5%, homosexual/bisexual men 47.6% and heterosexual adults 11%. It is estimated that in December 1992 there will be 107,946 HIV-infected persons where heterosexuals contribute with more than 20% of that value. AIDS cases predicted for the same period are 4130, with 1958 among homosexual/bisexual, 1483 among IVDU, 449 in heterosexual adults, 153 in children under 4 years old and 87 among hemophiliacs or patients with blood coagulation disorders. By the end of 1994 the model predicts more than 200,000 HIV infected persons with an important proportion of heterosexual adults and more than 12,000 AIDS cases. The values of this period must be considered as a future possible scenario if the present spread conditions are preserved. Infection among heterosexual adults is at the present time in a first and exponential phase of spread and dominated by transmission from IVDU group and bisexual men. It is concluded that the future course of AIDS epidemic in Argentina may be particularly influenced by changes in the heterosexual behavior particularly in those with a higher degree of exposure to HIV-infection.
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PMID:Epidemic model of HIV infection and AIDS in Argentina. Status in 1990 and predictive estimates. 134 88

The paucity of virus-laden CD4+ cells in individuals infected with human immunodeficiency virus type-1 (HIV-1) contrasts with the greatly reduced numbers and function of these lymphocytes. A pathway is described whereby dendritic cells carry HIV-1 to uninfected T cells, amplifying the cytopathic effects of small amounts of virus. After exposure to HIV-1, dendritic cells continue to present superantigens and antigens, forming clusters with T cells that are driven to replicate. Infection of the dendritic cells cannot be detected, but the clustered T cells form syncytia, release virions, and die. Carriage of HIV-1 by dendritic cells may facilitate the lysis and loss of antigen specific CD4+ T cells in acquired immunodeficiency syndrome.
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PMID:Dendritic cells exposed to human immunodeficiency virus type-1 transmit a vigorous cytopathic infection to CD4+ T cells. 135 13

A prospective study was designed to evaluate the efficacy and effects on pulmonary function tests of weekly 600 mg aerosolised pentamidine as prophylaxis against Pneumocystis carinii pneumonia (PCP) amongst two groups of patients infected with the human immunodeficiency virus. Group 1 (primary prophylaxis) consisted of patients with either diseases indicative of AIDS other than PCP or whose absolute CD4 positive lymphocyte count was below 200/mm3, and Group 2 (secondary prophylaxis) comprised patients with previous proven episodes of PCP. Fifty-five patients (30-Group 1, 25-Group 2) were studied over a period of 36 months, and no patients reached a study end point of either relapse or death due to PCP after a mean duration of treatment of 14.9 months (range 9-36 months). There were no significant differences between the pulmonary function tests (forced expiratory volume in the first second, forced vital capacity and carbon monoxide diffusion capacity) performed at the start and end of the study on both groups of surviving patients. Ten patients (18%) reported coughing and eight patients (15%) were documented to have bronchoconstriction, which was found to be preventable by prior administration of disodiumcromoglycate. The results showed that weekly 600 mg aerosolised pentamidine is effective and well tolerated for primary and secondary prophylaxis against PCP without additional adverse effects. Further prospective randomized trials are needed to determine whether doses higher than the current recommended 300 mg monthly dosage of aerosolised pentamidine provide more efficacy before such an alternative prophylactic treatment is generally adopted for patients who cannot tolerate other systemic agents.
Infection
PMID:Efficacy and effects on pulmonary function tests of weekly 600 mg aerosol pentamidine as prophylaxis against Pneumocystis carinii pneumonia. 135 50

Infection with the human immunodeficiency virus (HIV) ultimately results in profound immunodeficiency characterized by severe depletion of CD4+ T helper cells. In symptomatic infection a general perturbance of immune function is observed. Here recent insights in the sequence of events in progression to AIDS is reviewed. Following seroconversion a rapid persistent loss of inducible B cell function is observed. In addition, in long term infection, antigen-presenting cell functions of monocytes and dendritic cells are increasingly affected. T-cell non-responsiveness, preceding CD4 cell loss, appears to be induced through several different, sequential mechanisms. In early infection, the in-vivo deletion of memory cells can account for the in-vitro decreased responsiveness. Later on in infection, when the balance between memory and naive T cells is normalized, both CD4 and CD8 cells are non-responsive to nominal antigen and low dose anti-CD3 monoclonal antibodies. This anergy is at the level of IL-2 gene expression since early signal transduction events following CD2 and CD2 receptor occupancy are normal. This state of anergy, probably due to inappropriate activation in vivo, may be related to programmed cell death (PCD) observed in vitro for both CD8 and CD4 cells reflecting a systemic interference with maturation and differentiation of T cells. In progression to symptomatic infection, the proportion of non-responsive CD8 cells with immature or activated phenotypes increases and in about fifty percent of the cases, CD4 cell decline may accelerate in association with emergence of syncytium-inducing HIV variants. During this progressive stage, anti-CD3 reactivity is severely decreased, and alloantigen reactivity and finally the capacity to respond to phytohemagglutinin (PHA) are affected. These functional parameters appear useful for staging of HIV-infected individuals and for evaluation of anti-viral therapy.
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PMID:Immunological abnormalities in the natural history of HIV infection: mechanisms and clinical relevance. 135 68


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