Department of Psychiatry, University Hospital Eppendorf, Hamburg, Germany.
Addict Biol. 2000 Oct 1;5(4):437-41. doi: 10.1111/j.1369-1600.2000.tb00213.x.
Based on the hypothesis that β-carbolines are involved in the pathogenesis of alcohol-related mood disturbance, harman and norharman levels were assayed in the blood plasma of alcoholics and correlated to the Hamilton Depression (HAM-D) scores after 3 and 5 weeks post-admission. Tobacco smoking was co-evaluated since it is known to influence β-carboline levels. After a 3-week period, plasma harman but not norharman was increased in depressed alcoholics and positively related to the HAM-D sum-score (r = 0.47; p < 0.04) and to tobacco smoking (r = 0.56; p < 0.02). Since no correlation between depression and smoking was found, these data could account for the higher incidence of depressive symptoms in withdrawn alcoholics with increased harman levels. The partial correlations support this hypothesis.
基于β-咔啉参与酒精相关情绪障碍发病机制的假设，测定了酒精中毒患者血浆中的哈尔曼和去哈尔曼水平，并与入院后 3 周和 5 周后的汉密尔顿抑郁量表（HAM-D）评分相关。由于已知吸烟会影响β-咔啉水平，因此对其进行了共同评估。在 3 周的时间后，抑郁酒精中毒者的血浆哈尔曼而非去哈尔曼水平升高，并与 HAM-D 总分呈正相关（r = 0.47；p < 0.04），并与吸烟呈正相关（r = 0.56；p < 0.02）。由于在抑郁和吸烟之间未发现相关性，这些数据可以解释在去哈尔曼水平升高的戒断性酒精中毒者中，抑郁症状发生率较高的原因。部分相关分析支持这一假设。
