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Systematic PubMed searches were conducted including December 2014, using the keywords: "cocaine", dopaminergic drug ("disulfuram-methylphenidate-bupropion-bromocriptine-sibutramineapomorphine- caffeine") and ("psychosis-psychotic symptoms-delusional-paranoia"). Articles in English, Spanish, Portuguese, French, and Italian were included. Articles in which there was no history of cocaine abuse/dependence, absence of psychotic symptoms, systematic reviews, and animal studies, were excluded.
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There is low evidence, at the present, supporting the clinical use of disulfiram for the treatment of cocaine dependence. Larger randomised investigations are needed investigating relevant outcomes and reporting data to allow comparisons of results between studies. Results from ongoing studies will be added as soon as their results will be available.
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These practice guidelines for the biological treatment of alcohol use disorders are an update of the first edition, published in 2008, which was developed by an international Task Force of the World Federation of Societies of Biological Psychiatry (WFSBP). For this 2016 revision, we performed a systematic review (MEDLINE/PUBMED database, Cochrane Library) of all available publications pertaining to the biological treatment of alcoholism and extracted data from national guidelines. The Task Force evaluated the identified literature with respect to the strength of evidence for the efficacy of each medication and subsequently categorised it into six levels of evidence (A-F) and five levels of recommendation (1-5). Thus, the current guidelines provide a clinically and scientifically relevant, evidence-based update of our earlier recommendations. These guidelines are intended for use by clinicians and practitioners who evaluate and treat people with alcohol use disorders and are primarily concerned with the biological treatment of adults with such disorders.
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Exposure of dark- or light-adapted mice to 1--3 ATA oxygen for times ranging from 15 min to 4 h caused a progressive increase in P-450, which peaked and then decayed. The rate of decay appears to be independent of PO2. A linear, inverse relationship was noted between the PO2 in the range of 1--4 ATA and the duration of exposure needed to obtain maximum P-450 levels. Cytochrome P-450 was induced by hyperoxia in vitro in a suspension of hepatocytes, and this induction was prevented by inhibitors of transcription and translation and by disulfiram. Cytochrome P-450 induction is not a general phenomenon of stress, albeit physical restraint may decrease the level of P-450 induced. Induction was a specific effect of increased oxygen tensions and was not due to pressure per se. Neither equivalent pressures of compressed air in the in vivo experiments nor equivalent pressures of nitrogen in the in vitro experiments induced P-450. Induction in vivo was inhibited by disulfiram and metyrapone. Hyperoxia is the most rapid inducer of P-450 yet found, and this response may represent a protective mechanism against hyperoxia.
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As a quality improvement metric, the US Veterans Health Administration (VHA) monitors the proportion of patients with alcohol use disorders (AUD) who receive FDA approved medications for alcohol dependence (naltrexone, acamprosate, and disulfiram). Evidence supporting the off-label use of the antiepileptic medication topiramate to treat alcohol dependence may be as strong as these approved medications. However, little is known about the extent to which topiramate is used in clinical practice. The goal of this study was to describe and examine the overall use, facility-level variation in use, and patient -level predictors of topiramate prescription for patients with AUD in the VHA.
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A cohort study of n = 209 alcoholic patients (DSM-IV) during 6 months of outpatient treatment. Eight medical doctors from two hospitals were involved. Co-responsible participation in treatment was a necessary condition. At admission, we documented socio demographic factors, use of other drugs and severity of alcohol consumption. During the 6 months, we observed medication for prevention of alcohol relapse [disulfiram (DIS), acamprosate], number of sessions with the doctor, number of phases of the consultation and medication for depression. Primary outcome variables were time to first heavy relapse and abstinence of heavy alcohol consumption. These were measured with Timeline Followback. Five or more alcohol units of 10 g in one relapse day were considered heavy relapse.
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Disulfiram-modified cytoplasmic aldehyde dehydrogenase binds covalently to the thiol groups of reduced thiopropyl-Sepharose 6B under conditions in which mitochondrial aldehyde dehydrogenase does not bind. After washing the resin, the uncontaminated form of the enzyme is eluted by dithiothreitol solution.
Disulfiram (DSF) causes the ALDH-mediated deterrence of alcohol consumption. We review recent meta-analyses showing the superior effectiveness of supervised disulfiram (SD) in alcoholism treatment compared with oral naltrexone or acamprosate (ACP). The success of SD is also consistent with the almost complete absence of alcoholism in Japanese homozygotes for 'inefficient' ALDH. However, SD is an underused treatment and some clinicians have ethical objections to DSF. We examine these objections and argue that they are based on a misunderstanding of how DSF works. In particular, we argue that SD is not as is often claimed a variety of aversion therapy but aids cognitive, behavioural, educational and psychosocial interventions. It has some unique features that need to be better understood if it is to be properly compared with other treatments and effectively employed to help alcoholic patients, especially those who have not responded to other evidence-based interventions.
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Raji cells were subjected to different treatments and thereafter MTT assay, flow cytometry were used to determine IC50 and apoptotic status. We also tested the cytotoxicity of DS/Cu in acute lymphoblastic leukemia cell line Molt4 in vitro. In vivo experiments were also performed to demonstrate the anticancer efficacy of DS/Cu in Raji cells xenografted nude mice.
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Clinical case report.
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Seven studies, 492 participants, met the inclusion criteriaDisulfiram versus placebo: no statistically significant results for dropouts but a trend favouring disulfiram, two studies, 87 participants, RR 0.82 (95% CI 0.66 to 1.03). One more study, 107 participants, favouring disulfiram, was excluded from meta-analysis due high heterogeneity, RR 0.34 (95% CI 0.20 to 0.58). For cocaine use, it was not possible to pool together primary studies, results from single studies showed that, one, out of four comparisons, was in favour of disulfiram (number of weeks abstinence, 20 participants, WMD 4.50 (95% CI 2.93 to 6.07).Disulfiram versus naltrexone: no statistically significant results for dropouts but a trend favouring disulfiram, three studies, 131 participants, RR 0.67 (95% CI 0.45 to 1.01). No significant difference for cocaine use was seen in the only study that considered this outcome.Disulfiram versus no pharmacological treatment: for cocaine use: a statistically significant difference in favour of disulfiram, one study, two comparisons, 90 participants: maximum weeks of consecutive abstinence, WMD 2.10 (95% CI 0.69 to 3.51); number of subjects achieving 3 or more weeks of consecutive abstinence, RR 1.88 (95% CI 1.09 to 3.23).
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Four experiments were conducted to determine the effect of dietary cholecalciferol (vitamin D3), 25-hydroxycholecalciferol (25-OHD3) and 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) on the changes in growth, feed efficiency and bone ash, and the incidence, severity and number of #3 scores of tibial dyschondroplasia caused by the addition of disulfiram to the diet. The basal diet used was low in calcium and high in phosphorus and chlorine and known to promote a high incidence of tibial dyschondroplasia in broiler chickens. The chickens in all experiments received enough ultraviolet radiation from fluorescent lights in the pens to nearly satisfy their need for vitamin D. The addition of disulfiram to the diet caused an increase in most of the measurements indicating development of tibial dyschondroplasia in all of the experiments, and caused a decrease in bone ash in two of the experiments and a decrease in growth and gain:feed in one experiment. The addition of D3 to a diet containing no D3 caused higher bone ash and lower incidence of tibial dyschondroplasia in the absence or presence of disulfiram. The effects of the addition of 25-OHD3 to diets containing approximately five times the requirement of D3 in the absence and presence of disulfiram caused variable results. The addition of 1,25-(OH)2D3 to the D3-supplemented diet in the absence or presence of disulfiram caused dramatic increases in bone ash and a decrease in most of the criteria used to measure development of tibial dyschondroplasia. There was no indication of interaction of the effects of D3, 25-OHD3 and 1,25-(OH)2D3 with the action of disulfiram.
The effects of acidic tumor-like microenvironment on cytotoxicity of antabuse (disulfiram, DSF)/Cu(2+) complexes to MCF-7 breast carcinoma and HT-29 colon carcinoma cells were studied.
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During screening examinations and, when appropriate, other health-related visits, family physicians should be alert for signs and symptoms of common psychosocial disorders in men. Health issues of concern include alcohol and substance abuse, domestic violence, midlife crisis and depression. Alcohol remains the most abused drug in America. The highest rates of alcohol abuse are in men 25 to 39 years of age, although alcoholism is also a considerable problem after 65 years of age. Disulfiram and the opioid antagonist naltrexone are the two medications currently labeled by the U.S. Food and Drug Administration for the treatment of chronic alcohol dependence. Like alcohol abuse, domestic violence is a sign of psychosocial distress in men. Domestic violence may be a problem in up to 16 percent of marriages. Most men move through the midlife period without difficulty. Major depressive illness occurs in about 1 percent of elderly men, whereas minor depression or subsyndromal depression affects 13 to 27 percent of older men. Selective serotonin reuptake inhibitors have become first-line therapy for depression.
Experiments on rats were made to study the effect of alcohol and teturam on the function of spermatozoa and spermatogenesis of males and their progeny. The male-mediated damaging action of alcohol on the gonads of the progeny was ascertained. That might be one of the causes of the maldevelopment in subsequent generations of the progeny. Teturam was demonstrated to have an insignificant gonadotropic action and not to potentiate an adverse alcohol action on the male gonads.
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These data suggest that disulfiram-mediated inhibition is predominantly selective for CYP2E1. The magnitude of CYP2E1 inhibition was similar after both acute and chronic disulfiram administration. The effects on caffeine N3-demethylation (CYP1A2) and dapsone metabolism suggest that chronic disulfiram administration may affect multiple drug metabolizing enzymes, which could potentially complicate the use of chronically administered disulfiram as a diagnostic inhibitor of CYP2E1.
We have examined the role of serotonergic and/or dopaminergic mechanism in the mediation of the nicotine-induced depression of brainstem auditory evoked responses (BAER) to auditory stimuli. Nicotine produced dose- and time-dependent decreases in BAER amplitude. Administration of serotonin-depleting drugs (reserpine or p-chlorophenylalanine (PCPA), prevented this decrease. Administration of catecholamine-depleting drugs (alpha-methyl-p-tyrosine, disulfiram or Dopa), on the other hand, had no effect. These data thus suggest a role for serotonergic mechanisms in the mediation of nicotine-induced depression of the brainstem auditory pathway.
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Disulfiram, an alcohol antagonistic drug has been on the market since 1949 with 80% bioavailability and an established safety profile. Recently it has been reported as a P-glycoprotein efflux pump modulator. Herein we report its antifungal potential. The MIC50 and MIC90 of disulfiram for yeast isolates is 4 and 8 microg/ml, respectively, and the MIC range is 1-16 micro g/ml for both fluconazole sensitive and resistant strains. Interestingly, disulfiram also showed fungicidal activity on Aspergillus spp. with MIC50 and MIC90 of 2 and 8 microg/ml, respectively.
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Following active disulfiram treatments and cocaine 0.25 mg/kg administration, plasma cocaine AUC (0-480 min) was increased (p=0.003 and 0.001) and cocaine clearance decreased (p<0.001). Disulfiram treatments also decreased cocaine clearance for the 0.5 mg/kg cocaine dose (p=0.002 and<0.001). Neither disulfiram dose with cocaine altered cardiovascular responses relative to cocaine alone. Following cocaine 0.25 mg/kg, 'any high' (p=0.021 and 0.019), 'cocaine high' (p=0.017 and 0.018) and 'rush' (p=0.013 and 0.047) significantly decreased with either disulfiram dose.
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The behavioral and biochemical effects of amantadine hydrochloride (ATD) on some ethanol (ETOH) mediated responses in rats and mice were studied. Administration of ATD, 0.5 mM/kg IP, prior to a narcotic dose of ETOH significantly decreased the central depressant action of ETOH, as measured by the duration of ETOH-produced narcosis in mice. The time required for the onset of ETOH-narcosis was significantly delayed in ATD-treated mice compared to controls. Analyses of whole blood and brain ETOH concentrations showed that ATD-treatment prior to ETOH significantly reduced brain content of ETOH from saline-pretreated mice at the time of onset of ETOH narcosis as well as 30 min after ETOH injection without concomitant change in blood ETOH concentrations at the respective time intervals. Administration of ATD 0.5mM/kg IP, reduced voluntary intake of ETOH by rats voluntarily selecting 5% ETOH solution over water as the drinking fluid. There were no changes in cytoplasmic rat liver alcohol dehydrogenase (L-ADH) and mitochondrial aldehyde dehydrogenase (L-ALDH) activities in rats maintained on water or 5% ETOH as the drinking fluid and administered ATD, 0.5 mM/kg IP, once or identical dose once daily for six consecutive days. However, ATD produced in vitro non-competitive inhibiton of both L-ADH and L-ALDH at a concentration range between 10(-3) M and 3 x 10(-3) M assay mixture. The results indicate the potency of ATD in negating ETOH-mediated responses measured and suggest for a possible clinical trial for ATD in the management of alcoholic patients provided it is devoid of disulfiram-like reaction in man.