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)

This study evaluates the association of cocaine use with short-term change in CD4 counts among human immunodeficiency virus type 1 (HIV-1) seropositive, minority injecting drug users prior to the introduction of zidovudine (AZT). Ninety-eight HIV-1 seropositive subjects were recruited from six inner-city, methadone maintenance clinics. A baseline assessment included a short questionnaire regarding drug behavior and quantitation of CD4 cell counts. These measures were repeated on all subjects 3 to 4 months later. Thirty-eight subjects reported using cocaine between baseline and 4-month follow-up evaluations. Males and African Americans were more likely to be cocaine users (P < .01). Cocaine users were more likely to engage in heroin and needle use (P < .001). Cocaine users experienced a significant decline in CD4 cells compared with nonusers (P = .013); no marked difference in CD4 decline was noted between heroin users and nonusers (P = .19). Multivariate analysis showed that a decline in CD4 counts was 2.82 times more likely to occur in cocaine users than in cocaine nonusers (90% two-sided confidence interval of 1.08, 7.37). These findings support the hypothesis of a possible link between cocaine use and short-term CD4 decline in HIV-1 seropositive injecting drug users.
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PMID:Short-term declines in CD4 levels associated with cocaine use in HIV-1 seropositive, minority injecting drug users. 847 71

Our appreciation of the impact on health of illicit drug use is growing. Once considered a maternal risk, prenatal drug exposure may target fetal neurobehavior, affecting attention and learning as the child grows into adulthood. Cocaine, opiates, marijuana, and amphetamines have each been scrutinized for adverse actions on placental transport, fetal behavior states, newborn withdrawal, and childhood learning and attentive skills. Neurotransmitter analysis in the animal model after prenatal drug exposure now provides biological support for these clinical findings. The increasing prevalence of drug use by pregnant women, the effect of illicit drug use on transmission of the human immunodeficiency virus, and the maternal and fetal consequences of illicit drug exposure make illicit drug use in pregnancy a central challenge in maternal-fetal medicine and a need-to-know field in general obstetrics.
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PMID:Adverse consequences of prenatal illicit drug exposure. 897 11

We evaluated maternal sexual behavior and injection drug use practices as possible risk factors for vertical transmission of human immunodeficiency virus type 1 (HIV-1). Data were analyzed from the Mothers and Infants Cohort Study, a prospective study in Brooklyn and the Bronx, New York. A total of 207 mother-infant sets were enrolled between 1986 and 1991 and followed for up to 4 years after the enrollment visit during pregnancy. HIV-1 transmission occurred in 49 of 201 mother-infant sets, yielding an overall transmission rate of 24.4% (95% confidence interval (CI) = 18.7% to 31.0%). Increased frequency of vaginal intercourse after the first trimester of pregnancy was positively associated with vertical transmission of HIV-1 (trend p = 0.03). A lifetime history of injection drug use was not associated with vertical transmission. However, a history of combined cocaine and heroin injection after the first trimester of pregnancy was associated with vertical HIV-1 transmission, particularly among women with CD4+ lymphocyte levels of 20% or higher (risk ratio = 4.0; 95% CI = 2.0 to 8.1). Cocaine and heroin injection drug use after the first trimester accounted for most of the relation between preterm birth and vertical HIV-1 transmission in this cohort. Maternal coinfection with hepatitis C virus or human T-cell lymphotropic virus types I and II could not explain these observations, because coinfection with these viruses had no detectable effect on HIV-1 transmission. These results suggest that maternal sexual behavior and injection drug use practices during the second and third trimester of pregnancy may modify the risk of vertical HIV-1 transmission.
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PMID:Sexual behavior and injection drug use during pregnancy and vertical transmission of HIV-1. 921 58

Self-reports of drug use are extensively employed in research on drug use and in evaluations of drug abuse treatment and human immunodeficiency virus (HIV) prevention interventions. The chapter first summarizes recent research addressing the validity of drug use self-reports in high-risk populations. The results of two self-report validity studies are then compared, one for a sample of patients in methadone maintenance and the other for a sample of criminally involved young adults. Cocaine use was more accurately reported by the methadone patients; the possible reasons for this are explored.
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PMID:The validity of self-reported cocaine use in two high-risk populations. 924 64

Cocaine can cause a variety of neuropsychiatric and neurobehavioral complications; however, it is uncertain whether cocaine causes persistent cerebral structural and neurochemical abnormalities in asymptomatic users. We studied 52 African-American men (26 human immunodeficiency virus-negative asymptomatic heavy cocaine users and 26 normal subjects). Ventricle-to-brain ratio (VBR) and white matter lesions (WML) were quantified on magnetic resonance imaging. N-acetyl-containing compounds (NA), total creatine, choline-containing compounds, myo-inositol, and glutamate + glutamine were measured with in vivo proton magnetic resonance spectroscopy, VBR and WML were not significantly different in the cocaine users compared to the normal controls. Elevated creatine (+7%; p = .05) and myo-inositol (+18%; p = .01) in the white matter were associated with cocaine use. NA, primarily a measure of N-acetyl aspartate and neuronal content, was normal. Normal NA suggest no neuronal loss or damage in the brain regions examined in these cocaine users. Therefore, we conclude that neurochemical abnormalities observed might result from alterations in nonneuronal brain tissue.
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PMID:Neurochemical alterations in asymptomatic abstinent cocaine users: a proton magnetic resonance spectroscopy study. 942 80

Earlier studies have supported a significant role for cocaine in the susceptibility to and the progression of human immunodeficiency virus type 1 (HIV-1) infection. Recently, several unique HIV-1 entry coreceptors (e.g., CCR5 and CCR3) and a trio of HIV-1-specific suppressor chemokines, namely, RANTES (regulated-upon-activation T expressed and secreted), macrophage inflammatory protein 1alpha (MIP-1alpha) and MIP-1beta, were identified. Although cocaine has been linked to the immunopathogenesis of HIV-1 infection, the corresponding cellular and molecular mechanism(s) have not been well defined. We hypothesize that cocaine mediates these pathologic effects through the downregulation of HIV-1-suppressing chemokines and/or upregulating HIV-1 entry coreceptors in HIV-1-infected subjects, resulting in disease progression to AIDS. Our results show that cocaine selectively downregulates endogenous MIP-1beta secretion by normal peripheral blood mononuclear cells (PBMC), while cocaine did not affect the MIP-1beta production by PBMC from AIDS patients. Cocaine also selectively suppresses lipopolysaccharide-induced MIP-1beta production by PBMC from HIV-infected patients. Further, cocaine significantly downregulates endogenous MIP-1beta gene expression, while it upregulates HIV-1 entry coreceptor CCR5 by normal PBMC. These studies suggests a role for cocaine as a cofactor in the pathogenesis of HIV infection and support the premise that cocaine increases susceptibility to and progression of HIV-1 infection by inhibiting the synthesis of HIV-1 protective chemokines and/or upregulating the HIV-1 entry coreceptor, CCR5.
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PMID:Cocaine differentially modulates chemokine production by mononuclear cells from normal donors and human immunodeficiency virus type 1-infected patients. 1061 85

For various ethnic and socioeconomic reasons the pattern of renal disease in the inner city displays distinctive features. Hypertension is frequent, often intractable, and generally conditioned by salt sensitivity and a high sodium intake. Chronic hypertensive nephrosclerosis, found predominantly in African Americans, comprises marked cardiomegaly, renal shrinkage, and hypertensive retinopathy. It has been overdiagnosed in the past, but actually accounts for less than 20% of end-stage renal disease (ESRD) in African Americans. Malignant hypertension, less frequent nowadays, may cause renal shutdown, which is reversible in a few cases; the heart and kidneys are often of normal size. Idiopathic focal segmental glomerulosclerosis is the most common cause of the primary nephrotic syndrome in blacks, but its incidence has also been rising in whites and Hispanics; it does not respond well to treatment, and almost one half of the patients develop ESRD within 10 years. Systemic lupus erythematosus is also more common in African Americans, in whom the severe proliferative forms of lupus nephritis pursue a more virulent course: one half of such patients develop ESRD in 5 years. Cocaine, the use of which has assumed epidemic proportions, may cause accelerated hypertension, acute renal failure from rhabdomyolysis, and progression of preexisting renal disease. Heroin nephropathy has all but disappeared and has been replaced by human immunodeficiency virus (HIV) nephropathy. The prognosis of HIV-infected patients maintained by dialysis has greatly improved. Sickle glomerulopathy, consisting of mesangial expansion, basement membrane duplication, and the absence of immune deposits, may cause the nephrotic syndrome in 4% of patients with severe sickle cell anemia, heralding death within 2 years in one half of patients and ESRD in two thirds; survival has not improved with dialysis. Diabetes is now the most common cause of ESRD. Familial aggregation of ESRD is frequently encountered. Interventions useful in the general population, such as vascular bypass procedures, should be undertaken with great caution and restraint in dialysis patients.
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PMID:Renal disease in the inner city. 1145 21

Cocaine use, marijuana use, alcohol use, and polysubstance use (e.g., alcohol and cocaine, alcohol and marijuana) are associated with high-risk sexual behavior and higher rates of sexually transmitted diseases (STDs) and human immunodeficiency virus (HIV). The purpose of this study was to examine readiness for using condoms among three groups (cocaine users, noncocaine drug users, and non-drug users) of African Americans living in low-income urban settings. African Americans in this sample differed in sex risk behaviors according to their drug use status. Noncocaine drug users reported higher levels of sex risk behaviors than non-drug users, and cocaine users reported the highest levels of risk. Cocaine users also reported lower levels of condom use with their main and nonmain sexual partners than both other groups. Results of multivariate analyses indicate that, compared to the other two groups, cocaine users are at earlier stages of readiness for condom use with main partners. Cocaine users have accurate perceptions of their HIV risk, but are more likely to factor into their decisions for using condoms cost and the trouble that it takes to get condoms. Different approaches to sexually transmitted disease and human immunodeficiency virus prevention will be necessary to meet the needs of these three different subgroups.
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PMID:Intention to use condoms among three low-income, urban African American subgroups: cocaine users, noncocaine drug users, and non-drug users. 1261 4

Cocaine abuse is associated with increased rates of infections, including human immunodeficiency virus, and cocaine has immunomodulatory effects in experimental animal and cellular models. When challenged by antigens, tissues release cytokine polypeptides that signal a complex balance of cellular and humoral immune responses. Placement of indwelling venous catheters also leads to surrounding tissue inflammation, mediated partially by local production and release of the proinflammatory cytokine, IL-6. Thus, catheter placement provides a model for examination of cocaine's immunological effects. Thirty healthy men and women with a history of cocaine use participated in this study of neuroendocrine and immunological responses to iv injection of 0.4 mg/kg cocaine or saline placebo. After injection, blood samples were collected from the antecubital vein of the opposite arm via an indwelling venous catheter at 2, 4, 8, 12, 16, 20, 30, 40, 60, 80, 120, 180, and 240 min. Cocaine, ACTH, cortisol, and dehydroepiandrosterone concentrations peaked at 8, 12, 40, and 20 min, respectively. Stimulation of IL-6 at 240 min was markedly reduced in subjects receiving cocaine compared with subjects receiving placebo (3.85 +/- 0.49 vs. 11.64 +/- 2.21 pg/ml; P = 0.0019, by two-tailed t test). Gender and menstrual cycle phase did not significantly influence most endocrine or IL-6 measures, although the small number of subjects limits the power of these comparisons. Because cocaine stimulates the hypothalamic-pituitary-adrenal axis, IL-6 suppression may be a consequence of corticosteroid release. Cocaine-induced suppression of proinflammatory IL-6 may mediate impaired host defenses to infections.
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PMID:Diminished interleukin-6 response to proinflammatory challenge in men and women after intravenous cocaine administration. 1262 5

Cocaine, often abused by human immunodeficiency virus (HIV) infected patients, has been suggested to worsen the HIV associated dementia via unknown mechanisms. Here we report that subchronic treatment with a dose of cocaine (30 mg/kg i.p.), unable per se to cause neuronal death, increases the number of apoptotic cells typically observed in the neocortex of rats treated with HIV-1 gp120 (100 ng given i.c.v.). A pre-treatment with MK801 (0.3 mg/kg i.p.), a NMDA receptor antagonist, L-NAME (10 mg/kg i.p.) and 7-nitroindazole (50 mg/kg i.p.), two specific inhibitors of NOS, or with 1400 W (1 mg/kg s.c.), a selective inhibitor of inducible NOS (iNOS), minimized neurotoxicity by combined administration of cocaine and gp120 thus implicating iNOS. This conclusion is supported by the evidence that cocaine increases brain neocortical citrulline, the co-product of NO synthesis.
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PMID:Inducible nitric oxide synthase is involved in the mechanisms of cocaine enhanced neuronal apoptosis induced by HIV-1 gp120 in the neocortex of rat. 1503 25


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