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

Intermediate- and high-grade B-cell non-Hodgkin lymphoma (NHL) occurring in a human immunodeficiency virus (HIV)-infected patient is considered diagnostic of the acquired immunodeficiency syndrome (AIDS). Other neoplasms (both hematopoietic and nonhematopoietic) have also been reported in patients with HIV infection, although none except Kaposi sarcoma carries the same diagnosis of AIDS as B-cell NHL in an HIV-infected host. There have been previous reports in the literature of Hodgkin disease (HD) in HIV-infected patients. We describe our clinical and pathological experience with HD from 1984-1989, in 18 patients with documented HIV infection and also review the literature on HD in HIV-infected patients. Almost all patients described herein presented with advanced disease and mixed cellularity histology and did very poorly despite some good initial responses to therapy. By statistical analysis, we found that the patients with HIV-associated HD had a strong tendency to be outside the age range seen in non-HIV-associated HD (P less than 0.005). We also discuss the possible relationship between HIV and HD and consider whether HIV-associated HD, like B-cell NHL, is a manifestation of AIDS.
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PMID:HIV-associated Hodgkin disease: a clinical study of 18 cases and review of the literature. 201 71

We wished to determine the incidence of human immunodeficiency virus-related high-grade non-Hodgkin's lymphoma (NHL) and identify factors associated with the development of NHL in patients receiving zidovudine. Data are from a 2-year prospective, observational, multisite study of 1030 patients with the acquired immunodeficiency syndrome (AIDS) and advanced AIDS-related complex who received zidovudine. Non-Hodgkin's lymphoma developed in 24 (2.3%) of 1030 patients who received zidovudine during 1463 person-years of follow-up (rate, 1.6 per 100 person-years of therapy). The relative hazard for development of NHL was stable throughout 2 years of therapy, with the risk of developing NHL 0.8% for each additional 6 months of therapy. Factors associated with development of NHL were a prior diagnosis of Kaposi's sarcoma, herpes simplex virus infection, or lower mean neutrophil count. Less strongly associated was a prior diagnosis of oral hairy leukoplakia or homosexual transmission of HIV. By Cox proportional hazards analysis, a prior diagnosis of Kaposi's sarcoma, cytomegalovirus disease, or oral hairy leukoplakia was most strongly associated with development of NHL. Our study demonstrates a relatively high incidence of NHL in patients with advanced human immunodeficiency virus disease who are undergoing antiretroviral therapy and suggests possible risk factors for development of NHL.
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PMID:Non-Hodgkin's lymphoma in patients with advanced HIV infection treated with zidovudine. 201 53

Epithelial and submucosal mesenchymal (SM) cells from normal human small intestine and colon could be directly infected by several strains of the human immunodeficiency virus (HIV). Macrophage-derived virus strains were more potent than the HTLVIIIB prototype strain. Persistent release of virus over several months implies that the human gastrointestinal tract may serve as a site for primary infection and as a reservoir for the virus. Furthermore, HIV infection of SM cells may be an in vitro model of Kaposi's sarcoma.
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PMID:HIV replication and persistence in human gastrointestinal cells cultured in vitro. 201 70

The combined use of zidovudine (ZDV) and interferon (IFN) alfa-2a has been shown to have antiretroviral and antitumor potential benefit in the treatment of acquired immune deficiency syndrome (AIDS)-associated Kaposi's sarcoma (KS). However, the clinical use of this combination is frequently complicated by the overlapping myelotoxicity of these agents. We report here the results of a phase I/II study in which granulocyte-macrophage colony-stimulating factor (GM-CSF) was used for those KS patients who became neutropenic while receiving ZDV (1,200 mg/d) and IFN (9 x 10(6) U/d). Nineteen of 29 patients (66%) developed an absolute neutrophil count (ANC) of less than 1,000 cells per cubic millimeter and were begun on GM-CSF. All experienced a prompt increase in the ANC. Those patients receiving GM-CSF/ZDV/IFN alfa-2a had an improved end of study ANC when compared with the ZDV/IFN alfa-2a group, but did not have an increased rate of tumor response, end of study CD4 cell count, or improvement in any other hematologic variable. The use of GM-CSF was not associated with increased toxicity and, in particular, was not associated with a change in serum human immunodeficiency virus (HIV) p24 antigen. Tumor response was noted in 50% of the assessable patients (33% overall) despite "high-risk" characteristics in 80%. Of the responding patients, seven were on GM-CSF and might have otherwise required an alteration in ZDV/IFN alfa-2a dose level. Further study of GM-CSF as an alternate to dose modification of this (ZDV/IFN alfa-2a) and other combination therapies for AIDS patients is warranted.
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PMID:Granulocyte-macrophage colony-stimulating factor mitigates the neutropenia of combined interferon alfa and zidovudine treatment of acquired immune deficiency syndrome-associated Kaposi's sarcoma. 196 May 65

A number of studies have illustrated the effectiveness of hematopoietic growth factors in managing treatment-related cytopenias in patients with human immunodeficiency virus (HIV) infection. One of these factors, granulocyte-macrophage colony-stimulating factor, has been shown to restore absolute neutrophil counts in patients with acquired immunodeficiency syndrome (AIDS) and Kaposi's sarcoma receiving a combination of zidovudine (AZT) and interferon alfa. A combination of granulocyte colony-stimulating factor and erythropoietin has also been demonstrated to alleviate both neutropenia and anemia in patients with advanced AIDS or AIDS-related complex receiving zidovudine. Hematopoietic growth factors, in combination with each other and with antiretroviral agents, thus have an important supportive role to play in the treatment of patients with HIV disease.
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PMID:Antiretroviral therapy and immunomodulators in patients with AIDS. 201 46

In vitro studies have shown that 3'-azido-3'-deoxythymidine (zidovudine, AZT) and interferon synergistically inhibit the replication of the human immunodeficiency virus type 1 (HIV) in peripheral blood mononuclear cells at concentrations achievable in patients. Interferon alfa can cause lesions to regress in patients with acquired immunodeficiency syndrome (AIDS)-related Kaposi's sarcoma (KS). Although zidovudine has no significant effect on the regression of these lesions, it does have antiviral activity in these patients as manifested by a decline in serum HIV antigen. However, when used separately, the two drugs can have serious side effects in some patients. In addition, the development of zidovudine-resistant strains has been noted in patients with advanced HIV disease receiving zidovudine for nine months or longer. Three in vivo trials have been initiated to assess possible advantages of combination therapy with zidovudine and interferon alfa in patients with AIDS-related KS. The incidence of serious adverse reactions, therapeutic efficacy, and the rate of emergence of zidovudine-resistant strains of HIV were evaluated. Preliminary results indicate that combination therapy with interferon alfa and zidovudine can safely be administered to patients with AIDS-related KS in doses that elicit antitumor and antiviral responses and discourage the potential emergence of zidovudine-resistant HIV strains.
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PMID:Antiretroviral therapy in combination with interferon for AIDS-related Kaposi's sarcoma. 201 47

Although Kaposi's sarcoma has been well described in homosexual men at risk for infection with the human immunodeficiency virus, there have been fewer reports of KS in women, and most of these have been in women who became infected with HIV through intravenous drug use. This report describes a woman who had no history of intravenous drug use in whom intraoral KS and hairy leukoplakia were the first indication of her infection with HIV.
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PMID:Oral Kaposi's sarcoma in a woman as a first indication of HIV infection. 202 89

Magnetic resonance (MR) imaging was used to assess for the presence of bacterial myositis, rare outside the tropics, in 13 patients with either the acquired immunodeficiency syndrome (AIDS) (n = 11) or positive results of serologic tests for the human immunodeficiency virus but without other evidence of AIDS (n = 2). Bacterial myositis was diagnosed in six patients: in five it was caused by pyogenic bacteria, and in the other, by Mycobacterium tuberculosis; in each patient, little or no subcutaneous tissue alteration occurred. On T1-weighted images in three patients, muscle abscesses showed a rim of increased signal intensity corresponding to margins between drainable pus and edematous muscle. Subcutaneous tissues appeared normal in patients with bacterial myositis but was not in the others, in whom muscle abnormalities tended to be less prominent. The latter group included patients with lymphoma (n = 1), Kaposi sarcoma (n = 2), and carbunculosis (n = 1), and three patients in whom no diagnosis was made; lymphedema was presumed to account for imaging abnormalities in four of the latter group.
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PMID:Differential diagnosis of bacterial myositis in AIDS: evaluation with MR imaging. 202 69

Kaposi's sarcoma (KS) is an important finding in patients infected with human immunodeficiency virus (HIV), with a distinctive spectrum of clinical presentations. Three cases of dermatophytosis in HIV-infected patients are presented which clinically mimic the appearance of KS. This new observation underscores the importance of histopathologic examination in the evaluation of skin lesions suspicious for the diagnosis of KS. The other clinical mimickers of KS are reviewed.
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PMID:Dermatophytosis mimicking Kaposi's sarcoma in human immunodeficiency virus disease. 205 Feb 35

Through epidemiological considerations we conclude that full-blown AIDS may occur only if the index patient is infected by the human immunodeficiency virus (HIV) and, in addition, by some other infectious coagent. Since the dynamical behavior of the spread of AIDS cases with manifestation of Kaposi's sarcoma differs fundamentally from that of the non-Kaposi cases, we conjecture that two independent coagents (together with HIV) are responsible for the outbreak of full-blown AIDS with or without manifestation of Kaposi's sarcoma, respectively. Our formal epidemiological considerations appear to be supported by recent microbiological findings.
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PMID:Linkage and independence of AIDS and Kaposi disease: the interaction of human immunodeficiency virus and some coagents. 205 Apr 19


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