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研究生:林加進
研究生(外文):ChiaChin Lin
論文名稱:臺灣地區B型肝炎病毒、C型肝炎病毒與其他輔助因子致肝細胞癌危險性之社區性長期追蹤研究
論文名稱(外文):Hepatitis B virus, Hepatitis C virus, and Other Cofactors Associated with the Cumulative Risk of Hepatocellular Carcinoma in Taiwan: A Prospective Community-based Study
指導教授:孫建安孫建安引用關係
指導教授(外文):ChienAn Sun
學位類別:碩士
校院名稱:國防醫學院
系所名稱:公共衛生學研究所
學門:醫藥衛生學門
學類:公共衛生學類
論文種類:學術論文
論文出版年:2002
畢業學年度:90
語文別:中文
論文頁數:117
中文關鍵詞:肝細胞癌C型肝炎病毒B型肝炎表面抗原交互作用社區性長期追蹤研究臺灣
外文關鍵詞:hepatocellular carcinomahepatitis C virushepatitis B surface antigeninteractionprospective community-based studyTaiwan
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此一社區性長期追蹤研究之目的係評估B型和C型肝炎病毒慢性感染與其他輔助因子包括抽菸、飲酒和嚼食檳榔等生活習慣對於罹患肝細胞癌之風險的獨立和交互作用。本研究係以1990年所建立之社區性肝細胞癌篩檢世代為研究對象,有效樣本共12,010名男性及1,795名女性個案,平均每名個案追蹤9.21年,於基線收案時以結構式問卷獲得社會人口學特性、吸菸、飲酒及嚼食檳榔習慣、個人及家族成員健康疾病史等資料,並同時採集血液及尿液樣本,其中血液樣本用來分析B型肝炎表面抗原(HBsAg)陽性狀態、B型肝炎病毒e抗原(HBeAg)陽性狀態(HBsAg為陽性者才測)、C型肝炎病毒抗體(anti-HCV)陽性狀態、胺基丙酸轉胺(ALT)、天門冬酸轉胺(AST)和甲型胎兒蛋白(AFP)異常狀態。研究結果發現單獨HBsAg陽性者、單獨anti-HCV陽性者及HBsAg與anti-HCV同時陽性者之肝細胞癌10年累積發生率分別為3.4%、3.6%和4.5%,都要顯著高於HBsAg與anti-HCV同時為陰性者(0.1%)。多變項分析的結果顯示單獨HBsAg陽性與罹患肝細胞癌之相對危險性(RR)為27.1(95%信賴區間[CI]=12.8-57.5),而單獨anti-HCV陽性與罹患肝細胞癌之RR為22.6(95% CI=9.2-55.6),而同時感染B型和C型肝炎病毒與罹患肝細胞癌之RR為23.9(95% CI=7.1-81.1);此一研究結果顯示單獨B型和C型肝炎病毒慢性感染是罹患肝細胞癌的顯著危險因子,而B型和C型肝炎病毒共同感染,彼此之間在致肝細胞癌危險性方面則呈現拮抗之交互作用。另一方面,B型和C型肝炎病毒分別與抽菸、飲酒和嚼食檳榔等生活習慣之間在肝細胞癌化過程中存在有相加性之交互作用。同時,對於HBsAg帶原者和anti-HCV陽性者而言,若其ALT呈現間歇性或持續性異常的現象,其罹患肝細胞癌的風險比ALT持續正常者要顯著的提高。綜合言之,本研究結果顯示B型和C型肝炎病毒的慢性感染分別是罹患肝細胞癌的主要危險因子,而其所造成之肝細胞持續性的發炎壞死,則可能會使得肝細胞對於香菸、檳榔所含有之化學致癌物質或黃麴毒素以及酒精具有較高的易感受性,進而提高其罹患肝細胞癌的風險。

This community-based prospective study examined the independent and interactive effects of viral infections and lifestyle habits on the incidence of hepatocellular carcinoma (HCC) in Taiwan. The study cohort was initially established for a cancer screening purpose. A baseline recruitment was conducted for 12,010 males and 1,795 females from July 1990 to June 1992 and evaluated hepatitis B surface antigen (HBsAg), second-generation hepatitis C virus (HCV) antibody (anti-HCV), conventional liver function tests including alanine aminotransferase (ALT) and aspartate aminotransferase (AST), as well as α-fetoprotein (AFP). From July 1990 to June 2001, 127 HCC cases were identified by data linkage with National Cancer Registry and National Death Certificate systems. A total of 105 HCC cases occurred one year after enrollment were included for the incidence study. The 10-year cumulative incidence for subjects who were seropositive for HBsAg alone, seropositive for anti-HCV alone, and positive for both HBsAg and anti-HCV was 3.4%, 3.6%, and 4.5%, respectively. These cumulative risks of HCC were significantly higher than the cumulative incidence of 0.1% in subjects with seronegativity for both HBsAg and anti-HCV. Results of multivariate analysis revealed, as compared with those who were seronegative for both HBsAg and anti-HCV, that the relative risk (RR) of developing HCC associated with HBsAg-positive alone, anti-HCV alone, and seropositive for both HBsAg and anti-HCV was 27.1 (95% confidence interval [CI]=12.8-57.5) and 22.6 (95% CI=9.2-55.6), and 23.9 (95% CI=7.1-81.1), respectively. These results indicate that the presence of chronic HBV or HCV infection was the main risk determinant of HCC, while the combined effect of chronic HBV and HCV infections on the risk of development of HCC tend to be antagonistically interactive. Furthermore, there were additively synergistic effects of HBV and HCV infections with lifestyle factors including cigarette smoking, alcohol drinking, and betel quid chewing on the occurrence of HCC. Moreover, HBsAg carriers or anti-HCV-positive individuals who had intermittent or persistent ALT elevation had significantly increased risk of HCC as compared with those who had persistently normal ALT levels. The data suggest that chronic HBV or HCV infection causes chronic necroinflammation and regenerative proliferation in the liver. The sustained hepatocellular proliferation may render HBsAg or HCV carriers more susceptible to the effects of environmental carcinogens in the hepatocarcinogenesis.

第一章 前言
第二章 文獻探討
第一節 肝細胞癌描述流行病學
(一) 年齡
(二) 性別差異
(三) 國際間比較
(四) 種族間差異和移民研究
第二節 肝細胞癌危險因子
(一) B型肝炎病毒
(二) C型肝炎病毒
(三) 黃麴毒素
(四) 吸菸
(五) 喝酒
(六) 雄性賀爾蒙
(七) 家族史
(八) 其他因子
(九) 危險因子致肝細胞癌的交互作用
第三章 研究目的
第四章 研究材料與方法
第一節 『臺灣地區社區性肝細胞癌早期篩檢』計劃簡介
(一) 研究世代
(二) 兩階段篩檢方法
(三) 基礎收案結果
第二節 本研究之實施方法及進行步驟
(一) 研究設計及研究對象
(二) 資料收集及分析
1. 問卷資料
2. 實驗室檢驗資料
3. 腹部超音波檢查
4. 資料連鎖檢索
5. 資料處理與統計分析
第五章 結果
第一節 研究世代之基線收案特徵
第二節 研究世代於追蹤期間之癌症別發生情形與死因別分布情形
第三節 肝細胞癌新發病例之基本人口學與生化值特徵
第四節 罹患肝細胞癌之危險因子分析
(一) 基本人口學危險因子之單變項分析
(二) 肝炎病毒感染標記、肝功能指標、甲型胎兒蛋白、個人與家族
病史等危險因子之單變項分析
(三) 抽菸、飲酒和嚼檳榔習慣等危險因子之單變項分析
(四) 飲食習慣危險因子之單變項分析
(五) 危險因子間交互作用之分析
(六) 基線收案時為肝硬化個案之罹患肝細胞癌風險的危險因子分析
(七) 肝炎病毒感染與肝功能指標之變化對於罹患肝細胞癌風險之相

(八) 罹患肝細胞癌危險因子之多變項分析
第六章 討論
第一節 B型肝炎病毒感染與罹患肝細胞癌危險性之探討
第二節 C型肝炎病毒感染與罹患肝細胞癌危險性之探討
第三節 B型肝炎病毒與C型肝炎病毒慢性感染在肝細胞癌病因學特徵之
比較及彼此之間交互作用的探討
第四節 黃麴毒素與罹患肝細胞癌危險性之探討
第五節 抽菸、飲酒和嚼檳榔習慣之致肝細胞癌的獨立作用以及與B型和
C型肝炎病毒之間之交互作用的探討
第六節 研究限制
第七章 結論
第八章 參考文獻

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