View clinical trials related to Alcoholism.
Filter by:The purpose of this grant is to develop and test a proven computer based quality improvement/behavior change e-Health system (CHESS--Comprehensive Health Enhancement Support System) to help prevent relapse in alcohol dependent patients being discharged from residential treatment. The investigators' primary hypothesis is that ACHESS (Addiction CHESS) will improve competence, relatedness and autonomy, which will reduce the days of risky drinking over a 12-month period.
This study will evaluate the safety and efficacy of ALKS33 (RDC-0313) compared with placebo in adults with alcohol dependence. There will be 11 study visits conducted over a period of about 4 months. The study period includes a screening visit, a 12-week treatment period, and a follow-up visit.
The primary objectives of this study are to assess the efficacy of levetiracetam XR in increasing the percentage of subjects with no heavy drinking days and in reducing the weekly percentage of heavy drinking days in subjects with alcohol dependence confirmed by DSM-IV criteria and who frequently consume 10 or more drinks per drinking day for men and 8 or more drinks per drinking day for women (designated as "very heavy" drinkers).
Alcohol is one of the most commonly abused drugs in the world. Up to 40% of medical and surgical patients have alcohol related problems, and alcohol use accounts for more than 10% of U.S. health care costs. In the intensive care unit (ICU), patients with a history of alcohol abuse are common where their rates of mortality and ICU-related morbidity are significantly higher when compared to patients without a history of alcohol abuse. Though ICU patients are a heterogeneous group, Acute Respiratory Distress Syndrome (ARDS), a devastating form of acute lung injury, is one of the more frequent diagnoses among these critically ill patients. In 1996, we made the novel observation that a prior history of chronic alcohol abuse is associated with an increased incidence and severity of ARDS in critically ill patients. In our epidemiological studies of over 570 critically ill patients, 50% of all patients with ARDS have a significant history of chronic alcohol abuse. Since ARDS affects approximately 150,000 patients per year in the United States, and mortality is 40-50% even in previously healthy individuals, alcohol-related ARDS is an enormous national health care problem. We estimate that between 15,000 and 25,000 deaths per year in the United States are associated with alcohol-related ARDS, a number consistent with or even exceeding the number of deaths due to many other alcohol-related diseases such as cirrhosis of the liver and alcohol-related traffic accidents. Further investigations of the association between chronic alcohol abuse and ARDS are needed to develop therapies that improve morbidity and mortality in this important patient population. The clinical syndrome of ARDS is defined as refractory hypoxemia with bilateral infiltrates on chest radiograph in the absence of left atrial hypertension. Pathophysiologically, ARDS is characterized by diffuse alveolar damage, increased pulmonary alveolar-capillary permeability, and the subsequent accumulation of extravascular lung water. In animal models of chronic alcohol abuse, we showed that chronic ethanol ingestion causes chronic oxidative stress, depletes lung glutathione, impairs alveolar-capillary barrier function, and exaggerates endotoxin-mediated acute lung injury. Ethanol-mediated disruption of the alveolar-capillary barrier, and the associated susceptibility to acute edematous injury, is modified by glutathione (GSH) replacement therapy in animal models. Responding to NIH emphasis on studies of the mechanisms of disease and evaluation of therapies in human subjects, our group has initiated translational studies that expand our basic observations of the effects of chronic alcohol abuse on ARDS to the clinical setting. We recently reported that lung epithelial lining fluid from individuals with a prior history of chronic alcohol abuse is deficient in GSH, an essential antioxidant. The translational experiments outlined in this proposal will identify alterations in the structure and function of the lung in individuals with a history of chronic alcohol abuse and test a novel medical therapy that may ultimately decrease the morbidity and mortality for 50,000-75,000 ARDS patients with a prior history of chronic alcohol abuse per year in the United States. We propose the following hypothesis that antioxidant deficiency is a cause of abnormal alveolar-capillary barrier function in individuals with a history of chronic alcohol abuse, and oral anti-oxidant replacement therapy will correct the abnormality. If this hypothesis can be confirmed, this work would pave the way for testing antioxidant replacement as prophylaxis against acute lung injury in alcoholic patients at risk for the development of ARDS. Specific Aim: To determine the safety and efficacy of in vivo antioxidant replacement therapy on alveolar-capillary barrier function in individuals with a history of chronic alcohol abuse.
A 12-week, double-blind, placebo-controlled parallel group study will be conducted with 150 outpatients with alcohol dependence, with random assignment to pregabalin 300 mg/d, duloxetine 40 mg/d, or placebo in conjunction with manual-guided behavioral counseling and follow-up visits 1 week and 3 months post-treatment. A cue reactivity session will be conducted at Week 2 to assess the predictive validity of the human laboratory model for determining the clinical efficacy of pregabalin and duloxetine.
Method: This study is designed as an accompaniment to an already funded study - a 12-week treatment trial with prazosin for patients with PTSD and AD. The study design will consist of III phases. In phase I, all subjects will participate in three laboratory sessions to determine their reactivity to stress. Stress reactivity will be measured using: traumatic experiences, stressful non-trauma experiences and neutral experiences, presented randomly. Laboratory sessions will be conducted in an outpatient setting. Phase II is a randomized clinical trial evaluating prazosin versus placebo for 12 weeks in a double-blind, controlled fashion in an outpatient setting. The treatment will last for 12 weeks and outcomes will include symptoms of PTSD and alcohol use. In phase III, subjects will again participate in a laboratory session. This phase of the study will be conducted after at least 6 weeks of treatment while patients are on medication (prazosin or placebo). Hypotheses: Primary: The investigators hypothesize that prazosin will be more effective than placebo in reducing trauma-related stress reactivity in a laboratory paradigm, particularly anxiety, craving for alcohol, and hormonal response, in individuals with PTSD and AD. Secondary: The investigators hypothesize that stress reactivity will have a moderating effect on treatment with prazosin, such that individuals with high levels of stress reactivity will have fewer heavy drinking days, a significant reduction in PTSD symptoms, and shorter time to relapse than individuals with low levels of stress reactivity.
The overarching aim of this trial is to evaluate naltrexone's efficacy in light of genetic variation and brain response to alcohol cues utilizing a neuroimaging paradigm. This trial has four specific aims. First, this trial will evaluate whether the presence of the OPRM1 Asp40 allele substitution is associated with improved treatment response to naltrexone in treatment-seeking alcoholics. Second, it will evaluate whether there is a difference in the naltrexone dampening of the alcohol cue-induced brain activation dependent on OPRM1 genotype. Third, it will explore whether alcohol cue-induced brain activation dampening by naltrexone might be a mediating factor in the treatment effects of naltrexone, the OPRM1 gene, or their interaction that might be observed in the first aim. Finally, this trial will evaluate the effect of medication compliance, or adverse effects, on the observed medication by genotype treatment response. A secondary aim will measure medication compliance and side effects based on OPRM1 genotype.
The purpose of the project is to improve adolescent behavioral counseling services in healthcare settings with a new Internet/Intranet-based Motivational Enhancement Therapy (iMET) intervention that targets the use of tobacco, alcohol, and other drugs.
Objective: Alcoholism is highly co-morbid with post traumatic stress disorder (PTSD). Since stress and negative affective states are major relapse triggering factors for alcohol use, the negative symptoms associated with PTSD are thought to promote alcohol dependence. Substance P, which is released in the amygdala in response to stress, acts at NK1 receptors (NK1Rs) to mediate behavioral stress responses. Blockade of the NK1R represents a novel approach for anti-stress actions. In a recent double blind, placebo controlled study involving detoxified anxious alcoholics, we found that NK1R antagonism decreased alcohol cravings, attenuated cortisol response to stress, and significantly decreased insula activation in response to negative sensory input. The present study is intended to expand the findings and determine whether the NK1R is a candidate target for treating alcohol dependent patients with PTSD. Study Population: On hundred twenty participants with PTSD and co-morbid alcohol dependence will be recruited and stratified by PTSD etiology (60 participants each with civilian and combat PTSD, resp). Within each stratum, the treatment groups will be balanced for sex using urn randomization. Stratification is indicated since civilian and combat-related PTSD can theoretically have a different pathophysiology. Civilians typically experience a single trauma exposure of invariably high magnitude, resulting in symptoms immediately. Combat-related PTSD typically results from multiple traumatic exposures over a prolonged period of time, of variable magnitude, and frequently with delayed emergence of symptoms. Design: Participants will be admitted to the National Institute on Alcohol Abuse and Alcoholism (NIAAA) research inpatient unit at the NIH Clinical Research Center (CRC) under protocol number 05-AA-0121 for assessment and treatment of people with alcohol drinking problems, which provides diagnostic assessments and standard withdrawal treatment if needed. Participants will enter into the present protocol once such treatment, if needed is completed. Following inclusion, all participants will receive 1 week of single blind placebo, and will then be randomized to double blind treatment with aprepitant or placebo. Randomized treatment will be for 3 weeks. Spontaneous cravings for alcohol, and ratings of psychopathology will be obtained twice weekly on the inpatient unit throughout the study. Cravings as well as endocrine and immune responses will also be assessed in a challenge session that combines a social stressor and exposure to physical alcohol cues. During the final week, three sessions utilizing scripts will be carried out, on separate days in counter-balanced order, exposing the participant to personalized trauma, alcohol-associated or neutral stimuli. Cravings as well as endocrine and immune responses will also be assessed during the script presentations. A functional magnetic resonance imaging (fMRI) session will be carried out last to assess responses to affective stimuli. Participants will remain hospitalized throughout the study, and will remain on the unit for a three day post-medication monitoring period. Outcome Measures: The primary outcome will be craving alcohol and changes in PTSD symptoms resulting from the script sessions. Secondary outcomes will include cravings and changes in PTSD symptoms resulting from the combined social stress-alcohol cure challenge session, spontaneous craving and PTSD symptoms during hospitalization, and brain responses on the fMRI session. Changes in PTSD symptoms and cravings for alcohol are intended to be surrogate markers for the overall effect of the drug treatment and are not intended to represent global improvement for either PTSD or alcoholism.
The current study investigates the effects of two potential alcohol treatment medications on drinking in a laboratory setting. Aripiprazole (APZ), effects dopamine and serotonin receptors with fewer limiting side effects seen with other atypical antipsychotics. Topiramate (TPMT), an antiepileptic, affects glutamate and GABA-A receptors and shows promise in reducing heavy drinking. Few studies have used two medications with such a diverse combination of actions to examine a potential synergistic effect on reducing alcohol consumption. The primary aims are to: 1. determine if APZ and TPMT are each more effective than placebo, and the combination of APZ and TPMT is more effective than either drug alone or placebo, in reducing alcohol use in non-treatment seeking alcohol dependent subjects in a laboratory based alcohol self-administration experiment (ASAE) 2. examine a hypothesized dose-response for three doses of APZ (0, 7.5 mg/d and 15 mg/d) along with three doses of TPMT (0, 100mg/d and 200mg/d) 3. examine the putative mechanisms of action of APZ, TPMT alone and together on craving, subjective stimulation, candidate gene influences and other behavioral effects associated with alcohol consumption 4. establish the safety of giving APZ and TPMT together. Non-treatment seeking, alcohol dependent Participants (N=216) will be recruited from the community and randomly assigned to one of the 9 cells. Subjects drinking and safety is monitored over a 5-week titration to their target dose, leading to an in-laboratory alcohol self administration session, during which clinical and behavioral effects are assessed during access to alcohol. A 1 month follow-up assesses adverse events and drinking.