Hepatitis C and risk of lymphoma:: Results of the European Multicenter Case-Control Study EPILYMPH
Hepatitis C and risk of lymphoma:: Results of the European Multicenter Case-Control Study EPILYMPH
复制标题
DOI：
10.1053/j.gastro.2006.09.019
复制
发表时间：
2006-12-01
期刊：
影响因子：
29.4
通讯作者：
De Sanjose, Silvia
中科院分区：
文献类型：
--
作者：
Nieters, Alexandra;Kallinowski, Birgit;De Sanjose, Silvia
背景与目的：越来越多的证据表明丙型肝炎病毒（HCV）感染在恶性淋巴瘤的病因学中发挥着重要作用。然而，之前的流行病学研究规模有限，无法确定 HCV 感染与特定淋巴瘤亚型之间的关联。我们进行了一项大型、多中心病例对照研究来解决这个问题。方法：该研究涵盖 5 个欧洲国家，纳入 1998 年至 2004 年间招募的任何淋巴恶性肿瘤新诊断病例。对照病例按 5 岁年龄组、性别和研究中心进行匹配。进行面对面访谈以收集有关人口、医疗和家族史以及环境暴露的数据。采用酶联免疫分析法对 1807 例病例和 1788 例对照者（不包括人类免疫缺陷病毒阳性和器官移植受试者）的血清样本进行 HCV 感染筛查。对阳性样品和随机选择的阴性样品进行HCV RNA检测和HCV基因分型。结果：53 例 (2.9%) 淋巴瘤病例和 41 例 (2.3%) 对照受试者中检测到 HCV 感染（比值比 [OR]，1.42；95% 置信区间 [CI]：0.93-2.15）。仅限于 HCV-RNA 检测呈阳性的个体（表明持续感染和活跃的病毒复制），OR 为 1.82（95% CI：1.13-2.91）。在亚型特异性分析中，HCV 患病率与弥漫性大 B 细胞淋巴瘤相关（OR，2.19；95% CI：1.23-3.91），但与慢性淋巴细胞白血病或滤泡性淋巴瘤、霍奇金淋巴瘤或 T 细胞淋巴瘤无关。样本量不足以得出罕见淋巴瘤实体（例如脾边缘区淋巴瘤）的任何结论。结论：这些结果支持慢性 HCV 复制有助于淋巴瘤发生的模型，并确立了 HCV 感染在弥漫性大 B 细胞淋巴瘤发病机制中的特定作用。
Background & Aims: Increasing evidence points toward a role of hepatitis C virus (HCV) infection in the etiology of malignant lymphomas. However, previous epidemiologic studies were limited in size to establish an association between HCV infection and specific lymphoma subtypes. We performed a large, multicenter, case-control study to address this question. Methods: The study comprised 5 European countries and included newly diagnosed cases of any lymphoid malignancy recruited between 1998 and 2004. Controls were matched to cases by 5-year age group, sex, and study center. In-person interviews were conducted to collect data on demographic, medical, and family history as well as environmental exposures. Serum samples of 1807 cases and 1788 controls (excluding human immunodeficiency virus-positive and organ-transplantation subjects) were screened for HCV infection using an enzyme immunoassay. Positive as well as randomly selected negative samples were subjected to HCV RNA detection and HCV genotyping. Results: HCV infection was detected in 53 (2.9%) lymphoma cases and in 41 (2.3%) control subjects (odds ratio [OR], 1.42; 95% confidence interval [CI]: 0.93-2.15). Restricted to individuals who tested positive for HCV-RNA (indicating persistent infection and active viral replication), the OR was 1.82 (95% CI: 1.13-2.91). In subtype-specific analyses, HCV prevalence was associated with diffuse large B-cell lymphoma (OR, 2.19; 95% CI: 1.23-3.91) but not with chronic lymphocytic leukemia or follicular, Hodgkin's, or T-cell lymphoma. The sample size was not sufficient to derive any conclusions for rare lymphoma entities such as splenic marginal zone lymphoma. Conclusions: These results support a model that chronic HCV replication contributes to lymphomagenesis and establish a specific role of HCV infection in the pathogenesis of diffuse large B-cell lymphoma.