Alcoholism, clinical and experimental research
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Alcohol. Clin. Exp. Res. · Apr 2007
Randomized Controlled TrialOpioid receptor gene (OPRM1, OPRK1, and OPRD1) variants and response to naltrexone treatment for alcohol dependence: results from the VA Cooperative Study.
Pharmacotherapy of alcohol dependence (AD) is at an early stage of development; currently available medications have limited efficacy. It would be clinically valuable to identify, before initiation of a course of treatment, those patients who, based on genetic markers, are most likely to respond to a specific pharmacotherapy. A previous report suggested that a functional variant at the genetic locus encoding the mu opioid receptor (Asn40Asp) is such a marker, in short-term (3-month) treatment with the opioid-blocking drug naltrexone (NTX). ⋯ These results do not support association of the OPRM1 Asn40Asp polymorphism with NTX treatment response for AD.
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Alcohol. Clin. Exp. Res. · Apr 2007
Randomized Controlled TrialMultidimensionality of the Alcohol Withdrawal Symptom Checklist: a factor analysis of the Alcohol Withdrawal Symptom Checklist and CIWA-Ar.
This study evaluated the factor structure of 2 scales for measuring the severity of the alcohol withdrawal syndrome (AWS): a self-rated scale, the Alcohol Withdrawal Symptoms Checklist (AWSC), and an observer-rated scale, the Clinical Institute Withdrawal Assessment-Alcohol, Revised (CIWA-Ar). ⋯ Self-rated measures of AWS could play an important role in complementing observer-rated measures in clinical and research settings. In this sample, the AWSC appeared to identify multiple dimensions of AWS with face validity for clinical relevance.
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Alcohol. Clin. Exp. Res. · Apr 2007
Alcohol binge before trauma/hemorrhage impairs integrity of host defense mechanisms during recovery.
Alcohol abuse, both chronic and acute, is a known modulator of immune function and is associated with increased incidence of traumatic injury. Previously, we demonstrated that acute alcohol intoxication before hemorrhagic shock impairs hemodynamic and neuroendocrine counterregulation, suppresses early lung proinflammatory cytokine expression, and increases mortality from infection during recovery. In the present study, we examined the impact of a 3-day alcohol binge on host responses during trauma/hemorrhage (T x Hem) and following overnight recovery. ⋯ These results indicate that a 3-day alcohol binge results in hemodynamic instability associated with attenuated neuroendocrine activation and increased mortality during T x Hem as well as sustained suppression of the proinflammatory cytokine response of blood and pleural-derived cells to a "second-hit" inflammatory challenge. As a result, we speculate that the net shift toward an anti-inflammatory state may contribute to enhanced susceptibility to infection during the recovery period.
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Alcohol. Clin. Exp. Res. · Apr 2007
Effects of gangliosides on ethanol-induced neurodegeneration in the developing mouse brain.
Ethanol exposure induces apoptotic neurodegeneration in the developing rodent brain during synaptogenesis. This process has been studied as a model for fetal alcohol syndrome. Previously, we have shown that gangliosides and LIGA20 (a semisynthetic derivative of GM1 ganglioside) attenuate ethanol-induced apoptosis in cultured neurons. In the present study, the effects of GM1 and LIGA20 on ethanol-induced apoptotic neurodegeneration were examined using an in vivo neonatal mouse model. ⋯ These results indicate that GM1 and LIGA20, which have been shown to be neuroprotective against insults caused by various agents, partially attenuate ethanol-induced apoptotic neurodegeneration in the developing mouse brain.