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)

The authors reviewed the means by which human immunodeficiency virus (HIV) seropositivity was acquired for the 134 seropositive children seen at Duke University Medical Center prior to September 1990. Perinatal transmission occurred in 111 (83%) and blood product transmission in 15 (11%). Of the 108 mothers (there were three sets of siblings) responsible for perinatal transmission, 44 (41%) had acquired their infection while residing in North Carolina. Intravenous (IV) drug use by the mother or her sexual partner was the significant risk factor for maternal infection in 91 (84%) of the total cases and in 38 (86%) of the 44 women infected in North Carolina. The proportion of women who acquired their HIV infection from a sexual partner who was an IV drug user was significantly greater for mothers who were resident in North Carolina when infected compared with mothers infected elsewhere (P less than .001). On the basis of admission to drug treatment programs during the 1990 fiscal year, cocaine is the predominant IV drug used in North Carolina. Admissions to cocaine abuse programs occurred throughout the state, and mothers who acquired HIV infection from IV drug use were more likely to live in counties with a higher frequency of cocaine abuse treatment.
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PMID:The introduction of human immunodeficiency virus into the North Carolina pediatric population. 160 43

The incidence of syphilis and chancroid began to increase in the United States among heterosexuals in the mid-1980s, with most cases reported among minorities living in Eastern cities and in the South. A number of studies have established a link between increasing syphilis incidence rates and cocaine use, specifically the smoked form of the drug, which is known as "crack." A similar link was hypothesized for chancroid, but supporting data became available only recently. In New Orleans, we showed that Haemophilus ducreyi infection in male patients was strongly associated with crack cocaine use. However, our studies also demonstrated that drug use by the patient actually was a marker for a more important risk factor: sexual exposure to a cocaine-using woman. Thus, although the details of the relationships among crack, sexual behavior, and the size and nature of core transmitter groups are not known, it is clear that crack cocaine abuse is the driving force behind the recent syphilis and chancroid epidemics in the United States. Although it is not possible to predict the effects of these events on human immunodeficiency virus (HIV) transmission, the potential for significant synergism between them exists. New approaches to HIV surveillance should be developed taking this possibility into account. During the last 3 to 4 years, incidence rates of syphilis and chancroid have fallen in the United States, despite continued problems throughout the country with crack cocaine abuse. However, our studies and those of others have shown how difficult it is to recognize chancroid clinically, suggesting that the disease may be grossly underreported.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Recent changes in the epidemiology of genital ulcer disease in the United States. The crack cocaine connection. 804 23

Cocaine abuse is a common clinical problem among opioid-dependent patients who are in methadone maintenance treatment. In an open prospective study, 16 DSM-III-R, cocaine-dependent, methadone maintenance treatment patients were treated with fluoxetine, at a mean dose of 45 mg/day for 9 weeks. Eleven subjects (69%) were infected with the human immunodeficiency virus. Cocaine use was significantly reduced by the end of treatment, although most subjects did not achieve abstinence. Comparison of intake to week 9 showed a significant decrease in self-reported cocaine use, craving, and quality of high. Actual cocaine use was measured by a quantitative analysis of cocaine and benzoylecgonine (BE) concentrations in plasma and urine. Median BE and cocaine concentrations in urine decreased significantly from intake to week 9 of fluoxetine treatment. This decrease would not have been detected if BE had been measured only qualitatively, as present or absent in the urine. Fluoxetine was well tolerated in combination with methadone and did not appear to alter methadone concentrations in plasma. Few adverse effects were noted. No subjects had to discontinue fluoxetine. Fluoxetine may be a promising treatment approach for cocaine abuse in methadone maintenance patients. Quantitative determination of exact cocaine and BE concentrations in biofluids may be a more accurate method of measuring cocaine use outcome than qualitative urinalysis.
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PMID:Fluoxetine for cocaine dependence in methadone maintenance: quantitative plasma and urine cocaine/benzoylecgonine concentrations. 780 96

Buprenorphine, an opioid mixed agonist-antagonist, is a potent analgesic that appears to be effective for the treatment of opiate abuse. Recent preclinical studies have shown that buprenorphine also significantly reduces cocaine self-administration by rhesus monkeys for periods up to 120 days. This unexpected finding has led to clinical trials to evaluate buprenorphine's effectiveness for the treatment of dependence on both cocaine and opiates, as defined by DSM-III-R criteria. Buprenorphine's safety in combination with cocaine and opiates and its effects on electroencephalographic sleep patterns and regional cerebral blood flow were evaluated during inpatient studies. Buprenorphine (4 or 8 mg/day given sublingually) did not accentuate the cardiovascular and respiratory changes induced by an acute challenge dose of cocaine (30 mg given intravenously) or morphine (10 mg given intravenously) alone. In an outpatient open trial, buprenorphine significantly reduced both opiate and cocaine abuse by patients who had abused these drugs for more than 10 years. Most of these patients had failed in other drug abuse treatment programs. Reports of needle sharing also decreased significantly, and no patient tested positive for human immunodeficiency virus (HIV). The apparent safety and effectiveness of buprenorphine, combined with a high level of patient acceptance, led the Food and Drug Administration to grant a compassionate extension of the approved period for outpatient buprenorphine treatment from 26 to 52 weeks. Clinical trials of buprenorphine are ongoing. Possible mechanisms underlying buprenorphine-cocaine interactions are now under investigation.
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PMID:Buprenorphine treatment of opiate and cocaine abuse: clinical and preclinical studies. 938 44

The epidemiology of cocaine abuse and potential relationships of cocaine withdrawal to human immunodeficiency virus type 1 (HIV-1)-associated dementia (HAD) are discussed. Neuroendocrinological changes in HIV-1 infection of the central nervous system (CNS) are discussed with the relevant impact of cocaine abuse. HIV-1 load in the brain tissue of infected substance users is described along with possible associations with neuropathology and HAD. Finally, the molecular epidemiology and sequence heterogeneity of HIV-1 and their implications for neuropathogenesis are summarized. The complex context of addressing cocaine abuse in the setting of HIV-1 infection appears more tractable when decomposed into its components.
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PMID:Cocaine abuse and HIV-1 infection: epidemiology and neuropathogenesis. 961 Jun 77

A comprehensive study of an urban methadone clinic with supervised urine analyses for illicit drugs was conducted over an 18 month period for a 133 patient cohort as they entered or remained in methadone maintenance for narcotic addiction. Overall retention during the study was 85%, with significantly (p < .05) higher daily methadone doses (mean 67.1 mg +/- 2.1) in those patients still in treatment at the end of the study. Predictably, illicit opioid use was dramatically reduced, to 10% as measured by urine toxicology in the last month of treatment. Moreover, significantly more patients stopped regular cocaine abuse (69%) than started using cocaine (10%, Fisher's exact test, p = .02). Thus, with effective methadone maintenance using adequate dosages, the majority of patients remain in treatment and reduce cocaine abuse as well as illicit opioid use, with implications for public health by reducing the spread of infectious diseases including hepatitis B, C, D and human immunodeficiency virus (HIV-1).
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PMID:Cocaine abuse sharply reduced in an effective methadone maintenance program. 1063 64

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

Atherosclerosis increases cardiovascular risk and the possibility of developing acute myocardial infarction (AMI) or stroke. Patients infected with human immunodeficiency virus (HIV) often present morphological and metabolic alterations (hypercholesterolemia, hypertriglyceridemia, insulin resistance, diabetes) that can increase vascular risk. The frequent coexistence of classic risk factors (atherogenic diet, smoking, physical inactivity, cocaine abuse), the progressive increase in mean age of HIV-1 infected patients, and the polymedication they receive make it difficult to estimate the direct effect that new therapies may have on cardiovascular risk. Retrospective clinical studies with diverse designs in large cohorts offer contradictory results for cardiovascular risk in the HIV-infected population. Longer observational periods are needed and the effect of other classic risk factors needs to be controlled, in order to establish the possible detrimental effect the new therapies may have on cardiovascular risk in this population.
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PMID:[Cardiovascular risk in patients with chronic HIV-1 infection: a controversy with therapeutic, clinical and prognostic implications]. 1475 7

Cocaine abuse has been implicated as a cofactor in human immunodeficiency virus (HIV)-1-associated dementia (HAD). In this study, we tested the hypothesis that exposure of microglial cells, the resident macrophages of the brain, to cocaine would potentiate HIV-1 expression. Because kappa-opioid receptor (KOR) agonists have been shown to suppress neurochemical and neurobehavioral responses to cocaine and to inhibit HIV-1 expression in microglial cell cultures, we also postulated that KOR ligands would inhibit cocaine-induced potentiation of HIV-1 expression. Human microglial cells were infected with HIV-1(SF162), an R5 isolate, and viral expression was quantified by measurement of p24 antigen in culture supernatants. Treatment of microglia with the KOR agonists trans-(+/-)-3,4-dichlor-N-methyl-N-(2[1-pyrrolidnyl])benzeneacetamide methanesulfonate and 8-carboxamidocyclazocine inhibited viral expression (maximal suppression of 42 and 48%, respectively). Consistent with the hypotheses, treatment of microglia with cocaine promoted HIV-1 expression (maximal enhancement of 54%), and pretreatment of microglia with these KOR agonists as well as with the KOR-selective antagonist nor-binaltorphimine abrogated cocaine-induced potentiation of viral expression. Results of flow cytometry studies suggested that the mechanism whereby KOR ligands inhibit cocaine's stimulatory effect on viral expression involves the suppression of cocaine-induced activation of extracellular signal-regulated kinase1/2, thereby blunting cocaine-enhanced up-regulation of the HIV-1 entry chemokine coreceptor CCR5. The findings of this study suggest that in addition to its neurotoxic effects, cocaine could foster development of HAD by potentiating viral expression in the brain and that this phenomenon is inhibited by KOR ligands.
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PMID:Kappa-opioid receptor ligands inhibit cocaine-induced HIV-1 expression in microglial cells. 1475 49

Cocaine is a suspected cofactor in human immunodeficiency virus (HIV)-associated dementia but cocaine's effects are not clear. Herein the authors describe investigations of the mechanisms by which cocaine increases HIV-1 invasion through brain microvascular endothelial cells (BMVECs). Cocaine binds to a site on BMVECs, which is not a biogenic amine transporter, a binding site for estrogen, or a muscarinic receptor and for which benztropine and tamoxifen have the highest affinity. Cocaine treatment of BMVECs disrupts intercellular junctions and induces cell ruffling, which could account for their increased permeability and decreased electrical resistance. HIV-1 enters BMVECs by macropinocytosis and is transported to lysosomes and inactivated. In cocaine-treated BMVECs, the virus enters and persists in large cytoplasmic "lakes." Cocaine exposure of BMVECs up-regulates transcription of genes important in cytoskeleton organization, signal transduction, cell swelling, vesicular trafficking, and cell adhesion. The toxicity of cocaine for the blood-brain barrier may lead to increased virus neuroinvasion and neurovascular complications of cocaine abuse.
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PMID:Cocaine increases human immunodeficiency virus type 1 neuroinvasion through remodeling brain microvascular endothelial cells. 1603 8


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