Martel-Laferrière Valérie, Nitulescu Roy, Cox Joseph, Cooper Curtis, Tyndall Mark, Rouleau Danielle, Walmsley Sharon, Wong Leo, Klein Marina B
Centre de Recherche du Centre hospitalier de l'Université de Montréal, 900 Saint-Denis, Montréal, Quebec, H2X 0A9, Canada.
McGill University Health Centre, 1001 Decarie Blvd, Montreal, Quebec, H4A 3J1, Canada.
BMC Infect Dis. 2017 Jan 17;17(1):80. doi: 10.1186/s12879-017-2196-0.
Cocaine and crack use has been associated with HIV and HCV infections, but its consequences on HCV progression have not been well established. We analyzed the impact of cocaine/crack use on liver fibrosis progression in a cohort of HIV-HCV co-infected patients.
A Canadian multicenter prospective cohort study followed 1238 HIV-HCV co-infected persons every 6 months between 2003 and 2013. Data were analyzed from 573 patients with positive HCV RNA, not on HCV treatment, without significant liver fibrosis (AST-to-Platelet Ratio Index (APRI) <1.5) or history of end-stage liver disease at baseline, and having at least two study visits. Recent cocaine/crack use was defined as use within 6 months of cohort entry. Incidence rates of progression to significant fibrosis (APRI ≥ 1.5) were determined according to recent cocaine/crack use. Cox Proportional Hazards models were used to assess the association between time-updated cocaine/crack use and progression to APRI ≥ 1.5 adjusting for age, sex, HCV duration, baseline ln(APRI), and time-updated alcohol abuse, history of other drug use and CD4+ cell count.
At baseline, 211 persons (37%) were recent cocaine/crack users and 501 (87%) ever used cocaine/crack. Recent users did not differ from non-recent users on gender, age, and CD4+ T-cell count. Over 1599 person-years of follow up (522 PY in recent users, 887 PY in previous users and 190 PY in never users),158 (28%) persons developed significant fibrosis (9.9/100 PY; 95% CI, 8.3-11.4); 56 (27%) recent users (10.7/100 PY; 7.9-13.5), 81 (28%) previous users (9.1/100 PY; 7.1-11.1), and 21 (29%) never users (11.1/100 PY; 6.3-15.8). There was no association between ever having used or time-updated cocaine/crack use and progression to APRI ≥ 1.5 (adjusted HR (95%CI): 0.96 (0.58, 1.57) and 0.88;(0.63-1.25), respectively).
We could not find evidence that cocaine/crack use is associated with progression to advanced liver fibrosis in our prospective study of HIV-HCV co-infected patients.
可卡因和快克可卡因的使用与艾滋病毒和丙型肝炎病毒感染有关,但其对丙型肝炎病毒进展的影响尚未完全明确。我们分析了可卡因/快克可卡因的使用对一组艾滋病毒-丙型肝炎病毒合并感染患者肝纤维化进展的影响。
一项加拿大多中心前瞻性队列研究在2003年至2013年期间每6个月对1238名艾滋病毒-丙型肝炎病毒合并感染患者进行随访。对573例丙型肝炎病毒核糖核酸(HCV RNA)阳性、未接受丙型肝炎治疗、基线时无明显肝纤维化(天冬氨酸转氨酶与血小板比值指数(APRI)<1.5)或终末期肝病病史且至少有两次研究访视的患者的数据进行分析。近期可卡因/快克可卡因使用定义为队列入组后6个月内使用。根据近期可卡因/快克可卡因使用情况确定进展为显著纤维化(APRI≥1.5)的发病率。采用Cox比例风险模型评估随时间更新的可卡因/快克可卡因使用与进展为APRI≥1.5之间的关联,并对年龄、性别、丙型肝炎病程、基线ln(APRI)以及随时间更新的酒精滥用、其他药物使用史和CD4+细胞计数进行校正。
在基线时,211人(37%)为近期可卡因/快克可卡因使用者,501人(87%)曾使用过可卡因/快克可卡因。近期使用者与非近期使用者在性别、年龄和CD4+T细胞计数方面无差异。在超过1599人年的随访中(近期使用者522人年,既往使用者887人年,从未使用者190人年),158人(28%)发生了显著纤维化(9.9/100人年;95%可信区间,8.3 - 11.4);56名(27%)近期使用者(10.7/100人年;7.9 - 13.5),81名(28%)既往使用者(9.1/100人年;7.1 - 11.1),21名(29%)从未使用者(11.1/100人年;6.3 - 15.8)。曾经使用或随时间更新的可卡因/快克可卡因使用与进展为APRI≥1.5之间无关联(校正风险比(95%可信区间)分别为0.96(0.58,1.57)和0.88(0.63 - 1.25))。
在我们对艾滋病毒-丙型肝炎病毒合并感染患者的前瞻性研究中,未发现证据表明可卡因/快克可卡因的使用与进展为晚期肝纤维化有关。