Zusammenfassung
Objectives: Animal and clinical studies implicated opioid dysfunction in the pathogenesis of alcohol abuse and dependence. The pi-opioid antagonist naltrexone reduces craving, eventually modulated by hypothalamic-pituitary-adrenal axis. Altered cortisol response to opioid receptor blockade not only in alcohol dependent persons, but also in persons with a family history of alcohol dependency was ...
Zusammenfassung
Objectives: Animal and clinical studies implicated opioid dysfunction in the pathogenesis of alcohol abuse and dependence. The pi-opioid antagonist naltrexone reduces craving, eventually modulated by hypothalamic-pituitary-adrenal axis. Altered cortisol response to opioid receptor blockade not only in alcohol dependent persons, but also in persons with a family history of alcohol dependency was reported. Methods: Twenty patients with alcohol dependence who had undergone detoxification were recruited. Naloxone (3.2 mg/70 kg body weight) having a very similar receptor profile to naltrexone and placebo were administered in cross-over fashion on two separate days 48 h apart. Mood and craving was assessed with well-established instruments (Alcohol Craving Questionnaire (ACQ), Profile of Mood Scale (POMS)). Both patients and raters were blind to all treatments. Twelve patients were first treated with naloxone, eight were first treated with placebo. Results: No significant differences were found between the placebo and naloxone groups according to ACQ and POMS. Cortisol levels were significantly higher in naloxone group. Conclusions: We could not replicate the result, that blocking of the endogenous opioid system leads to reduced craving in alcohol-dependent individuals, while increase of cortisol after naloxone challenge is the expected biological effect of opioid receptor blockade on the hypothalamic-pituitary-adrenal (HPA) axis.
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