Department of Liver, Ziv Medical Center, Safed 13100, Israel.
World J Gastroenterol. 2012 Feb 28;18(8):800-5. doi: 10.3748/wjg.v18.i8.800.
To examine whether vitamin D improved viral response and predicted treatment outcome in patients with hepatitis C virus (HCV) genotype 2-3.
Fifty patients with chronic HCV genotype 2-3 were randomized consecutively into two groups: Treatment group [20 subjects, age 48 ± 14 years, body mass index (BMI) 30 ± 6, 65% male], who received 180 μg pegylated α-interferon-2a plus oral ribavirin 800 mg/d (Peg/RBV), together with oral vitamin D3 (Vitamidyne D drops; 2000 IU/d, 10 drops/d, normal serum level > 32 ng/mL) for 24 wk; and control group (30 subjects, age 45 ± 10 years, BMI 26 ± 3, 60% male), who received identical therapy without vitamin D. HCV RNA was assessed by reverse transcription polymerase chain reaction. Undetectable HCV RNA at 4, 12 and 24 wk after treatment was considered as rapid virological response, complete early virological response, and sustained virological response (SVR), respectively. Biomarkers of inflammation were measured.
The treatment group with vitamin D had higher BMI (30 ± 6 vs. 26 ± 3, P < 0.02), and high viral load (> 400,000 IU/mL, 65% vs. 40%, P < 0.01) than controls. Ninety-five percent of treated patients were HCV RNA negative at week 4 and 12. At 24 wk after treatment (SVR), 19/20 (95%) treated patients and 23/30 (77%) controls were HCV RNA negative (P < 0.001). Baseline serum vitamin D levels were lower at baseline (20 ± 8 ng/mL) and increased after 12 wk vitamin D treatment, to a mean level of (34 ± 11 ng/mL). Logistic regression analysis identified vitamin D supplement [odds ratio (OR) 3.0, 95% CI 2.0-4.9, P < 0.001], serum vitamin D levels (< 15 or > 15 ng/mL, OR 2.2, P < 0.01), and BMI (< 30 or > 30, OR 2.6, P < 0.01) as independent predictors of viral response. Adverse events were mild and typical of Peg/RBV.
Low vitamin D levels predicts negative treatment outcome, and adding vitamin D to conventional Peg/RBV therapy for patients with HCV genotype 2-3 significantly improves viral response.
观察维生素 D 是否能改善丙型肝炎病毒(HCV)基因型 2-3 患者的病毒应答,并预测治疗结果。
连续将 50 例慢性 HCV 基因型 2-3 患者随机分为两组:治疗组[20 例,年龄 48 ± 14 岁,体重指数(BMI)30 ± 6,65%为男性],接受 180μg 聚乙二醇干扰素-α-2a 联合口服利巴韦林 800mg/d(Peg/RBV)治疗,同时口服维生素 D3(Vitamidyne D 滴剂;2000IU/d,10 滴/d,正常血清水平>32ng/mL)24 周;对照组(30 例,年龄 45 ± 10 岁,BMI 26 ± 3,60%为男性),接受相同的治疗但不给予维生素 D。采用逆转录聚合酶链反应检测 HCV RNA。治疗后 4、12 和 24 周时 HCV RNA 不可检测定义为快速病毒学应答、完全早期病毒学应答和持续病毒学应答(SVR)。检测炎症生物标志物。
与对照组相比,维生素 D 治疗组患者的 BMI(30 ± 6 与 26 ± 3,P < 0.02)和高病毒载量(> 400,000IU/mL,65%与 40%,P < 0.01)更高。95%的治疗患者在第 4 周和第 12 周时 HCV RNA 阴性。治疗后 24 周(SVR)时,20/20(95%)治疗患者和 30/30(77%)对照组 HCV RNA 阴性(P < 0.001)。基线时血清维生素 D 水平较低(20 ± 8ng/mL),经 12 周维生素 D 治疗后升高,平均水平为(34 ± 11ng/mL)。Logistic 回归分析发现维生素 D 补充[比值比(OR)3.0,95%置信区间(CI)2.0-4.9,P < 0.001]、血清维生素 D 水平(< 15 或> 15ng/mL,OR 2.2,P < 0.01)和 BMI(< 30 或> 30,OR 2.6,P < 0.01)是病毒应答的独立预测因素。不良反应轻微,与 Peg/RBV 治疗典型相关。
低维生素 D 水平预示着治疗结果不佳,在常规 Peg/RBV 治疗基础上加用维生素 D 可显著提高 HCV 基因型 2-3 患者的病毒应答。