聚乙二醇干扰素和利巴韦林治疗基因1型HCV的病毒学应答伴有血红蛋白浓度下降
2011-01-14
来源：医脉通
贫血可能增加聚乙二醇干扰素和利巴韦林治疗丙型肝炎病毒（HCV）感染期间获得持续病毒学应答（SVR）的可能性。但若出现严重贫血可能需要药物减量，某些情况治疗效果欠佳尚需停药。该研究于2011年1月10日发表在《Hepatology》网络版上。
为了确定血红蛋白下降是否与SVR有关，我们回顾性评估了CHARIOT研究中 871名初治基因1型HCV患者。137名（16％）患者有贫血（血红蛋白<100g/L），其中只有14例（10％）接受了促红细胞生成素治疗。76％的患者血红蛋白较基线下降> 30g/L，其中526例没有出现贫血。贫血患者与未发生贫血的患者相比，病毒学反应率更高（治疗结束时，ETR 80％比65％，p= 0.003; SVR 61％比50％，p= 0.02）; 将接受促红细胞生成素的患者排除在分析之外，这些差异依然具有统计学意义。血红蛋白下降>30g/L与没有相似下降者相比，SVR率更高。分析治疗组和基线特征的多元logistic回归显示，贫血的SVR比值比为1.97（95％CI 1.08，3.62），血红蛋白下降>30 g / L的SVR比值比为2.17（95％CI为1.31，3.62）。在5~12周和13~48周首次发生血红蛋白下降> 30g/L者比0 – 4周首次发生这一改变或从未出现血红蛋白下降> 30g/L者更有可能取得SVR。结论：接受聚乙二醇干扰素和利巴韦林治疗的基因1型HCV感染患者，在治疗5 – 48周发生贫血或血红蛋白下降> 30g/L者的病毒学反应率更高，且与使用促红细胞生成素无关。慢性HCV患者接受聚乙二醇干扰素和利巴韦林抗病毒治疗时，通常发生贫血，可累及高达30％的患者。血红蛋白水平低可能是利巴韦林导致溶血或干扰素导致骨髓抑制所致。造血生长因子如促红细胞生成素已被用于抗病毒治疗过程中维持血红蛋白浓度，并证实其可改善患者生活质量，但没有改善持续病毒学应答（SVR）率。
医脉通推荐英文摘要：
Hepatology 2011.1.10 DOI: 10.1002/hep.24180
Virological response is associated with decline in hemoglobin concentration during pegylated interferon and ribavirin therapy in HCV genotype 1
William Sievert, Gregory J. Dore, Geoffrey W. McCaughan, Motoko Yoshihara, Darrell H
Anemia may increase the likelihood of achieving a sustained virological response (SVR) during pegylated interferon and ribavirin treatment of hepatitis C virus (HCV) infection. To determine whether hemoglobin decline is associated with SVR, we retrospectively evaluated the CHARIOT study of 871 treatment-naïve HCV genotype 1 patients. Anemia (serum hemoglobin <100 g/L) occurred in 137 (16%) patients of whom only 14 (10%) received erythropoietin. Hemoglobin decline >30g/L from baseline occurred in 76% of patients overall including 526 patients who did not become anemic. Virological responses were higher in anemic patients compared to those who did not develop anemia (end of treatment, ETR 80% vs. 65%, p=0.003; SVR 61% vs. 50%, p=0.02); these differences remained significant when patients receiving erythropoietin were excluded from analysis. SVR was also higher in patients with hemoglobin decline >30 g/L compared to those without a similar decline. In multiple logistic regression analyses with treatment group and baseline characteristics, the odds ratio for SVR was 1.97 (95% CI 1.08, 3.62) for anemia and 2.17 (95% CI 1.31, 3.62) for hemoglobin decline >30 g/L. Patients who first developed a hemoglobin decline >30 g/L during weeks 5 – 12 and 13 – 48 were more likely to achieve SVR than those who first developed such changes in weeks 0 – 4 or who never experienced them. Conclusion: patients with HCV genotype 1 infection who develop anemia or experience a hemoglobin decline >30 g/L during weeks 5 – 48 of therapy achieve higher virological responses to pegylated interferon and ribavirin therapy that are unrelated to erythropoietin use. Anemia frequently develops during antiviral therapy with pegylated interferon and ribavirin for chronic hepatitis C infection, affecting up to 30% of patients. Low hemoglobin levels may result from ribavirin-induced hemolysis or from interferon- induced bone marrow suppression. Significant anemia may lead to dosage reduction and, in some cases, treatment discontinuation resulting in sub-optimal treatment outcomes. Hematopoietic growth factors such as erythropoietin have been used to maintain hemoglobin concentrations during antiviral therapy and have been shown to improve quality of life but not sustained virological response (SVR) rates.
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