Daily cannabis smoking as a risk factor for progression of fibrosis in chronic hepatitis C

Daily cannabis smoking as a risk factor for progression of fibrosis in chronic hepatitis C
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DOI:
10.1002/hep.20733
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发表时间:
2005-07-01
期刊:
影响因子:
13.5
通讯作者:
Mallat, A
Mallat, A
中科院分区:
医学1区
文献类型:
--
作者:
Hézode, C;Roudot-Thoraval, F;Mallat, A

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大麻中存在的大麻素通过大麻素受体CB1和CB2发挥生物效应。我们最近证实CB1和CB2受体调控实验性肝纤维化的进展。因此,我们调查了吸食大麻对慢性丙型肝炎(CHC)患者纤维化进展率的影响。对270例持续时间已知的CHC患者进行了肝活检研究。记录了人口统计学、流行病学、代谢和病毒学数据,并获得了丙型肝炎病毒感染期间大麻、酒精和烟草使用的详细历史记录。根据Metavir系统对纤维化分期、脂肪变性和活动度分级进行评分。将患者分为非大麻使用者(52.2%)、偶尔吸食者(14.8%)和日常吸食者(33.0%),并评估大麻使用与纤维化进展率(FPR)或纤维化分期的关系。在多变量分析中,6个因素与大于0.074(队列的中位数)独立相关:每日吸食大麻(OR=3.4[1-5-7.4]),美托韦活动A2级或更高(OR=5.4[2.9-10.3]),染毒年龄>40岁(OR=10.5[3.0-37.1]),基因3(OR=3.4[1.5-7.7]),过量饮酒(OR=2.2[1.1-4.5]),脂肪变性(OR=2.0[1.0~4.1])。每日吸食大麻也是快速出现不良反应的独立预测因素(>0.15)(OR=3.6[1-5-7.5])。最后,每日吸食大麻(OR=2.5[1-1-5.6];P=.034)也可以预测严重的纤维化(>=F3),与Metavir活动分级、过量饮酒、肝脏活检年龄、脂肪变性和吸烟无关。综上所述,在慢性丙型肝炎期间,每日吸食大麻与纤维化进展显著相关。建议正在进行的慢性丙型肝炎患者避免定期使用大麻。
Cannabinoids present in Cannabis sativa (marijuana) exert biological effects via cannabinoid receptors CB1 and CB2. We recently demonstrated that CB1 and CB2 receptors regulate progression of experimental liver fibrosis. We therefore investigated the impact of cannabis smoking on fibrosis progression rate in patients with chronic hepatitis C (CHC). Two hundred seventy consecutive untreated patients with CHC of known duration undergoing liver biopsy were studied. Demographic, epidemiological, metabolic, and virological data were recorded, and detailed histories of cannabis, alcohol, and tobacco use over the span of hepatitis C virus infection were obtained. Fibrosis stage, steatosis, and activity grades were scored according to Metavir system. Patients were categorized as noncannabis users (52.2%), occasional users (14.8%), or daily users (33.0%), and the relationship between cannabis use and fibrosis progression rate (FPR) or fibrosis stage was assessed. On multivariate analysis, six factors were independently related to a FPR greater than 0.074 (median value of the cohort): daily cannabis use (OR = 3.4 [1-5-7.4]), Metavir activity grade A2 or higher (OR = 5.4 [2.9-10.3]), age at contamination of more than 40 years (OR = 10.5 [3.0-37.1]), genotype 3 (OR = 3.4 [1.5-7.7]), excessive alcohol intake (OR = 2.2 [1.1-4.5]), and steatosis (OR = 2.0 [1.0-4.1]). Daily cannabis use was also an independent predictor of a rapid FPR (> 0.15) (OR = 3.6 [1-5-7.5]). Finally, severe fibrosis (>= F3) was also predicted by daily cannabis use (OR = 2.5 [1-1-5.6]; P =.034), independently of Metavir activity grade, excessive alcohol intake, age at liver biopsy, steatosis, and tobacco smoking. In conclusion, daily cannabis smoking is significantly associated with fibrosis progression during CHC. Patients with ongoing CHC should be advised to refrain from regular cannabis use.