丙型肝炎与结肠癌和直肠癌的不同代谢关联：一项为期 9 年的全国人群队列研究。

IF 3.3 3区医学 Q2 ONCOLOGY

Clinical colorectal cancer Pub Date : 2024-09-06 DOI:10.1016/j.clcc.2024.08.005

Chun-Wei Chen , Jur- Shan Cheng , Tsung-Hsing Chen , Chia-Jung Kuo , Hsin-Ping Ku , Rong-Nan Chien , Ming-Ling Chang

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引用次数: 0

摘要

背景：HCV 感染是否与结直肠癌（CRC）的发生有关，目前尚无定论：HCV感染是否与结直肠癌（CRC）的发生有关，目前尚无定论：结果从2003年到2012年，1:2:2倾向得分匹配的HCV治疗[干扰素治疗≥6个月，调查CRC（n = 9017）、结肠癌（CC）（n = 9022）和直肠癌（RC）（n = 9033），HCV未治疗和HCV未感染队列CRC（n = 18034）、CC（n = 18044）和RC（n = 18066）。HCV未感染队列的 CRC 累计发病率最低（0.117%；95% CI：0.062%-0.207%），而HCV治疗队列（0.966%；0.375%-2.122%）和HCV未治疗队列（0.807%；0.485%-1.280%）的发病率相似（P = .0662）；HCV感染[参考值：0.966%；0.375%-2.122%]：HCV感染[参考：HCV未治疗队列，HCV治疗：危险比（HR）：0.598；95% CI HR：0.337-1.059；HCV未感染：0.250；0.138-0.456]和年龄≥49岁（3.128;1.751-5.59）与CRC发病相关。HCV未治疗队列的CC累积发病率最高（0.883%; 0.371-1.839%），而HCV治疗队列（0.478%; 0.110-1.518%）和HCV未感染队列（0.147%; 0.071-0.284%）的发病率相似（P = .4853）；HCV 感染（HCV 治疗：0.474；0.232-0.971；HCV 未感染：0.338；0.184-0.62）、男性（2.18；1.301-3.654）、年龄≥ 49 岁（4.818；2.123-10.936）和糖尿病（1.983；1.205-3.262）与 CC 的发生有关。未接受 HCV 治疗的队列（0.332%；0.151-0.664%）的 RC 累积发病率高于未感染 HCV 的队列（0.116%；0.054-0.232%）（P = .0352）；HCV 感染（HCV 治疗：0.691；0.295-1.617；HCV-未感染：0.424；0.207-0.867）、年龄≥49岁（3.745，1.576-8.898）和中风（3.162；1.366-7.322）与RC发生相关：结论：HCV感染和年龄≥49岁与CRC、男性和糖尿病与CC、中风与RC的基线相关。抗HCV治疗可能会逆转HCV相关CC的风险，但不会逆转RC的风险。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Different Metabolic Associations of Hepatitis C With Colon and Rectal Cancers: A 9-Year Nationwide Population-Based Cohort Study

Background

Whether HCV infection is associated with colorectal cancer (CRC) development remains inconclusive.

Methods

A nationwide population-based cohort study of the Taiwan National Health Insurance Research Database was conducted.

Results

From 2003 to 2012, 1:2:2 propensity score-matched HCV-treated [interferon-based therapy ≥ 6 months, surveys for CRC (n = 9017), colon cancer (CC) (n = 9,022) and rectal cancer (RC) (n = 9,033), HCV-untreated and HCV-uninfected cohorts CRC (n = 18034), CC (n = 18,044) and RC (n = 18,066) were enrolled. The HCV-uninfected cohort had the lowest cumulative incidence of CRC (0.117%; 95% CI: 0.062%-0.207%), whereas the HCV-treated (0.966%; 0.375-2.122%) and HCV-untreated (0.807%; 0.485%-1.280%) cohorts had similar incidences (P = .0662); HCV infection [reference: HCV-untreated cohort, HCV-treated: hazard ratio (HR): 0.598; 95% CI HR: 0.337-1.059; HCV-uninfected: 0.250; 0.138-0.456] and age ≥ 49 years (3.128;1.751-5.59) were associated with CRC development. The HCV-untreated cohort had the highest cumulative incidence of CC (0.883%; 0.371-1.839%), while HCV-treated (0.478%; 0.110-1.518%) and HCV-uninfected cohorts (0.147%; 0.071-0.284%) had similar incidences (P = .4853); HCV infection (HCV-treated: 0.474; 0.232-0.971; HCV-uninfected: 0.338; 0.184-0.62), male sex (2.18; 1.301-3.654), age≥ 49 years (4.818; 2.123-10.936) and diabetes (1.983; 1.205-3.262) were associated with CC development. A higher RC cumulative incidence was noted in the HCV-untreated cohort (0.332%; 0.151-0.664%) than in the HCV-uninfected cohort (0.116%; 0.054-0.232%) (P = .0352); HCV infection (HCV-treated: 0.691; 0.295-1.617; HCV-uninfected: 0.424; 0.207-0.867), age ≥ 49 years (3.745, 1.576-8.898) and stroke (3.162; 1.366-7.322) were associated with RC development.

Conclusions

The baseline associations were HCV infection and age ≥ 49 years with CRC; male sex and diabetes with CC; and stroke with RC. Anti-HCV therapy might reverse the risk of HCV-related CC but not RC.

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来源期刊

Clinical colorectal cancer 医学-肿瘤学

CiteScore

5.50

自引率

2.90%

发文量

审稿时长

27 days

期刊介绍： Clinical Colorectal Cancer is a peer-reviewed, quarterly journal that publishes original articles describing various aspects of clinical and translational research of gastrointestinal cancers. Clinical Colorectal Cancer is devoted to articles on detection, diagnosis, prevention, and treatment of colorectal, pancreatic, liver, and other gastrointestinal cancers. The main emphasis is on recent scientific developments in all areas related to gastrointestinal cancers. Specific areas of interest include clinical research and mechanistic approaches; drug sensitivity and resistance; gene and antisense therapy; pathology, markers, and prognostic indicators; chemoprevention strategies; multimodality therapy; and integration of various approaches.