Bipolar Disorders Program & INCT Translational Medicine, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
Neurosci Lett. 2013 Jun 7;544:80-4. doi: 10.1016/j.neulet.2013.03.045. Epub 2013 Apr 15.
A growing body of evidence suggests that crack cocaine misuse has widespread systemic and cognitive consequences, but little attention has been given to its systemic pathophysiology. We report here changes in inflammation markers, oxidative damage and brain derived neurotrophic factor in a sample of outpatients with crack cocaine use disorders. Fifty-three outpatients were recruited for this cross-sectional study and matched with fifty control subjects. The focus of this report is in between group differences in cytokines, oxidative damage and brain-derived neurotrophic factor (BDNF). Crack cocaine use was associated with higher BDNF levels when compared to controls, present only in those who used crack cocaine in the last month. Patients also had higher circulating levels of IL-1β, TNF-α and IL-10 when compared to controls. There were no significant differences in oxidative damage between patients and controls. These results represent a first demonstration that crack cocaine use disorders entail an activation of the reward, immune and inflammatory systems.
越来越多的证据表明,滥用可卡因会对全身系统和认知产生广泛影响,但人们对其全身病理生理学的关注甚少。我们在此报告了一批可卡因使用障碍门诊患者的炎症标志物、氧化损伤和脑源性神经营养因子的变化。本横断面研究共招募了 53 名门诊患者,并与 50 名对照匹配。本报告的重点是细胞因子、氧化损伤和脑源性神经营养因子 (BDNF) 组间差异。与对照组相比,最近一个月使用可卡因的患者 BDNF 水平更高,与对照组相比,患者的循环 IL-1β、TNF-α 和 IL-10 水平也更高。患者和对照组之间的氧化损伤没有显著差异。这些结果首次表明,可卡因使用障碍会导致奖励、免疫和炎症系统的激活。