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)

Ninety-five randomly selected human immunodeficiency virus (HIV)-seropositive Air Force personnel were psychiatrically examined during a routine medical evaluation. Of the 95, 95% did not have acquired immunodeficiency syndrome and were largely asymptomatic; 61.1% had clinical axis I diagnoses, which included simple phobia, adjustment disorders, hypoactive sexual desire disorder, alcohol use disorder, major depression, and organic mental disorders; 30.5% had personality disorders. Significantly higher frequencies (p less than 0.05) of simple phobia and hypoactive sexual desire disorder were noted with knowledge of HIV seropositivity. Disorders that occurred more commonly than in age-matched Epidemiologic Catchment Area (ECA) participants included: simple phobia, antisocial personality disorder, alcohol abuse, and organic mental disorders. The high prevalence of major psychiatric illness in this sample supports the notion that screening for psychiatric illness, and counseling where indicated, should be integral to HIV screening programs.
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PMID:Prevalence of psychiatric disorders in a mandatory screening program for infection with human immunodeficiency virus: a pilot study. 210 56

We screened inpatient and outpatient parenteral drug users with no clinical evidence of AIDS for immunodeficiency and antibodies to HTLV-III by ELISA. Among 20 outpatient drug users, 5 (25%) were seropositive. Three of these (and 2 who were seronegative) had low T-cell ratios. Over 6 months, 1 seropositive patient with a low ratio developed oral thrush and weight loss. We also studied 13 parenteral drug users hospitalized for conditions other than AIDS. Eight had low T-cell ratios, and at least 6 of these developed AIDS or ARC within 4 months. Serum from 8 of 13 inpatients was available for HTLV-III testing: 6/8 were seropositive and 3 of these 6 were among those developing AIDS or ARC. Abnormal T-cell ratios among all patients were associated with abnormal HTLV-III serology (p = .02). Of the 7 patients who developed AIDS or ARC, 4 were tested for both antibodies and T-cell ratios: all 4 were seropositive and had low ratios. A low ratio (p = .0004), a positive ELISA (p = .014), and abnormalities of both tests (p = .001) were associated with the development of AIDS or ARC. Of the 26 patients without AIDS or ARC, 3 were lost to follow-up and 23 did not develop AIDS or ARC. Six of these 26 had abnormal ratios. Of the 21 patients who did not develop AIDS or ARC and who were tested for HTLV antibodies, 2 were lost to follow-up. Seven of 21 were seropositive and 2/21 were both seropositive and had a low ratio. One of these 2 seropositive patients with low ratios also had lymphadenopathy, but he was lost to follow-up. The other had no adenopathy and remained well until her death from trauma a year later. This study found two populations with very different risks. Six of 13 hospitalized parenteral drug users and only 1 of 20 healthy outpatients developed AIDS or ARC.
Am J Drug Alcohol Abuse 1987
PMID:Serologic, immunologic, and clinical features of parenteral drug users from contrasting populations. 296 Dec 53

Acquired Immunodeficiency Syndrome (AIDS) is characterized by a range of risk factors that determine susceptibility to HIV and the clinical expression of the disease. These include sexual practices, intravenous drug use, and blood exchange. Appropriate preventive measures have been formulated for these risk factors. This paper reviews alcohol abuse as a prominent feature of the homosexual experience, and suggests that it may merit consideration as a risk factor in relation to AIDS. The presumably high prevalence of alcohol abuse among homosexuals and the damaging effects of alcohol on the immune system are discussed as a basis for linking alcoholism, homosexuality, and AIDS. The implications of the potentiating effects of alcohol misuse as the human immunodeficiency virus infiltrates the heterosexual population are presented in terms of high risk populations and the need for additional preventive measures.
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PMID:Assessing alcoholism as a risk factor for acquired immunodeficiency syndrome (AIDS). 306 Oct 19

Parenteral drug abusers are at risk for acquired immunodeficiency syndrome (AIDS), which is caused by human immunodeficiency virus (HIV). We tested stored sera for antibody to HIV (anti-HIV) using two enzyme-linked immunosorbent assay (ELISA) methods and Western blot. The patients were parenteral drug abusers who had undergone percutaneous liver biopsy for chronic liver disease. Current or former alcohol abuse was noted in 88 (80%) of the 110 patients. The sensitivities of the two ELISA tests in comparison with Western blot, the more specific test for HIV, were 100 and 94%, respectively; the specificities were 94 and 99%. Western blot was positive in 36 (33%) of 110 patients. False-positive ELISA reactions for anti-HIV were seen in five (7%) of 70 patients with negative Western blot analyses. Compared to true-negatives, false-positives had significantly more years of alcohol abuse, younger ages of onset of alcohol abuse, greater frequencies of jaundice and edema, higher levels of alkaline phosphatase, total billirubin, total protein, and globulins, and lower levels of serum albumin. In a stepwise logistic regression, only hyperglobulinemia was significantly associated with a false-positive anti-HIV. We conclude that: (a) ELISA tests for anti-HIV are useful for screening abusers of alcohol and parenteral drugs with chronic liver disease for HIV infection, but positive results must be confirmed with more specific tests such as Western blot; (b) false-positive ELISA reactions in this population are associated with hyperglobulinemia; and (c) studies of HIV testing are needed in other populations of patients with alcoholism or liver disease.
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PMID:Specificity of antibody tests for human immunodeficiency virus in alcohol and parenteral drug abusers with chronic liver disease. 306 17

We used structured diagnostic interviews and rating scales to assess lifetime prevalence of psychiatric disorders, by DSM-III criteria, among an unselected sample of 56 ambulatory homosexual men in four groups: men with acquired immunodeficiency syndrome (AIDS), men with AIDS-related complex (ARC), men asymptomatic or mildly symptomatic but seropositive for antibody to human immunodeficiency virus (HIV), and HIV-seronegative men. An age- and demographically matched comparison group of 22 healthy, heterosexual controls was also studied. The homosexual men had lifetime rates of alcohol or nonopiate drug abuse (22/56 [39.3%]), generalized anxiety disorder (22/56 [39.3%]), and major depression (17/56 [30.3%]) that often preceded diagnosed medical illness or knowledge of HIV status. The six-month point prevalence of these disorders in homosexual men was also high, especially alcohol abuse in patients with AIDS-related complex, and the occurrence of a DSM-III disorder within the previous six months significantly exceeded that in heterosexual controls. The data suggest that there may be a higher prevalence of anxiety disorder and major depressive illness in homosexual men when compared with sociodemographically matched heterosexual men and that the psychiatric morbidity may have preceded the onset of the AIDS epidemic. These findings indicate that awareness of psychiatric history is necessary to comprehensive medical care of men at high risk for AIDS, even among relatively healthy outpatients.
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PMID:Prevalence of psychiatric disorders among men infected with human immunodeficiency virus. A controlled study. 341 27

Chronic ethanol (EtOH) abuse in humans leads to a variety of immunomodulatory events that can alter resistance to a number of infectious agents. Whether alcohol abuse affects the susceptibility to human immunodeficiency virus infection or the subsequent development of acquired immune deficiency syndrome (AIDS) is a matter of extreme importance; however, available information in humans or animal models is limited. The goal of this study was to evaluate the effect of chronic EtOH feeding in mice on the development of immunodeficiency in the murine model of AIDS (MAIDS). C57BI/6 mice were placed on the Lieber-DeCarli liquid EtOH diet (25% or 31% total caloric intake) or a nutrient-matched isocaloric liquid control diet. Seven days later, mice were infected with the LP-BM5 murine leukemia virus mixture, and groups of infected and noninfected mice were assayed at defined time points postinfection for antigen-specific and nonspecific immune responses. In the absence of retroviral infection, chronic EtOH feeding (5-8 weeks) led to reductions in spleen weights, compared with isocaloric controls. In spite of reduced spleen size, mitogenic responses of spleen cells to concanavalin A (ConA) and lipopolysaccharide (LPS) were elevated in EtOH-fed mice, as compared with mice fed the control diet. Chronic EtOH feeding also enhanced the allogeneic mixed lymphocyte response and increased antigen-specific priming of both B-cells and CD4+ T-cells to the antigen, sheep red blood cells. In MAIDS-infected mice, chronic EtOH feeding delayed but did not prevent the onset of virus-induced immunodeficiency and MAIDS-induced autoantibody synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ethanol as a possible cofactor in the development of murine AIDS. 748 39

We examined the effects of human immunodeficiency virus (HIV) infection and chronic alcohol consumption on cerebral phosphorus metabolites to determine if chronic alcohol abuse is a risk factor for the progression of neurological effects of HIV infection. We studied 15 HIV- alcoholics, 8 HIV- light/nondrinkers, 32 HIV+ alcoholics, and 41 HIV+ light/nondrinking men, with both HIV+ groups having similar CD4 lymphocyte counts. We used localized 31-phosphorus magnetic resonance spectroscopy after magnetic resonance imaging to examine two brain volumes in superior white matter and subcortical gray matter. Chronic alcohol consumption was associated with reduced white matter concentrations of phosphodiester (PDE) and phosphocreatine (PCr). Also in the white matter, acquired immune deficiency syndrome (AIDS) and AIDS-related complex (ARC) were associated with reduced concentrations of PDE and PCr, compared with both HIV- and clinically asymptomatic HIV+ subjects. Because no alcohol-by-HIV interactions were detected, the effects of HIV infection and alcohol abuse were cumulative. This is reflected in a successive decrease of white matter PDE and PCr concentrations in the order HIV- light/nondrinkers/HIV- alcoholics/HIV+ light/nondrinkers/HIV+ alcoholics. Subcortical gray matter PDE concentrations were lower in ARC/AIDS alcoholics than in HIV- light/nondrinking individuals. These findings suggest altered brain phospholipid metabolites and energy metabolites with alcohol abuse and HIV infection. They demonstrate that the adverse metabolic effects of HIV on the brain are augmented by chronic alcohol abuse.
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PMID:Effects of chronic alcohol abuse and HIV infection on brain phosphorus metabolites. 757 94

Both alcohol and human immunodeficiency virus (HIV) infection have been shown to produce central nervous system (CNS) morbidity in frontal brain regions. The degree to which the CNS morbidity in HIV infection, as it affects frontal cortex function, may be preferentially increased by alcohol abuse was examined using the auditory P3A evoked potential. The P3A indexes an orienting response, maximal over frontal cortex that occurs when novel nontarget stimuli are presented in the midst of a target detection paradigm. Four groups of subjects were compared: HIV+ alcohol abusers, HIV+ light/nondrinkers, HIV- alcohol abusers, and HIV- light/nondrinkers. The alcohol abuser and light/nondrinker HIV+ groups were matched on percent CD4 lymphocytes, insuring that the results reflected specific CNS effects and were not a result of differences between the groups in the degree of systemic immune suppression. Alcohol abuse and HIV infection had at least additive effects on P3A latency, consistent with alcohol abuse worsening the effect of HIV disease on frontal cortex function. Post-hoc analyses suggested that concomitant alcohol abuse results in the effects of HIV infection on P3A latency becoming manifest earlier in the HIV disease process.
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PMID:Alcohol abuse and HIV infection have additive effects on frontal cortex function as measured by auditory evoked potential P3A latency. 749 32

Rapid progression of infection with human immunodeficiency virus type 1 (HIV-1) to AIDS after seroconversion is rare; it has been associated with coinfection by cytomegalovirus or human T lymphotrophic virus type I. We describe an alcoholic patient whose condition progressed to AIDS 3 months after HIV-1 seroconversion occurred. Culture of peripheral blood mononuclear cells yielded a syncytium-inducing variant of HIV-1. T lymphocytes showed no spontaneous cytotoxic activity against HIV-infected cells, nor could such activity be demonstrated following stimulation with HIV-1 antigen in the presence of recombinant interleukin-2. We hypothesize that our patient's accelerated course was due to alcohol abuse, which may have suppressed T cell function and stimulated HIV replication.
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PMID:Alcoholism and rapid progression to AIDS after seroconversion. 798 12

Whether ethanol (ETOH) abuse could contribute to the development of acquired immunodeficiency syndrome (AIDS) among human immunodeficiency virus (HIV)-positive drug abusers is a critical question for which little experimental information is available. This study was designed to determine if chronic ETOH feeding and murine AIDS virus infection cooperatively affected liver antioxidant defense systems in C57B1/6 female mice. Mice were divided into two groups and fed the Lieber-DeCarli liquid ETOH diet containing ETOH at a concentration to provide 31% of total caloric intake or an isocaloric liquid control (control) diet in which dextrin-maltose replaced ETOH. One week after the initiation of ETOH feeding, half of the mice in each diet group (8 mice) were injected intraperitoneally with murine retrovirus (MAIDS) stock. After 3 and 5 weeks of ETOH feeding, half of the mice in each of the four treatment groups (4 mice) were killed, and livers were excised for biochemical analysis. Liver reduced glutathione (GSH) levels and activities of glutathione peroxidase (GP), glutathione reductase (GR), glutathione transferase (GT), catalase and superoxide dismutase (SOD), and serum ETOH concentrations were determined. The results demonstrated that serum ETOH concentrations were significantly elevated in ETOH-MAIDS group when compared with the ETOH group. Moreover, chronic ETOH feeding and MAIDS infection independently depressed liver antioxidant defense capability, and together led to an additive inhibition of GSH and SOD activities. In addition, MAIDS infection inhibited an ETOH-induced increase in catalase and GT activities. These results suggest that alcohol abuse could contribute to the development of AIDS by inhibiting the protective capability of an infected individual against oxidative stress.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of chronic alcohol feeding and murine AIDS virus infection on liver antioxidant defense systems in mice. 827 61


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