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標題: | B型肝炎病毒之病毒量、基因型及BCP突變在早發肝細胞癌所扮演的角色:手足配對之病例對照研究 Role of Hepatitis B Virus Load, Genotype, and Basal Core Promoter Mutations in Young-Onset Hepatocellular Carcinoma before Age 50: A Sibling Matched Case-Control Study |
作者: | Meng-Yin Yeh 葉孟瑩 |
指導教授: | 于明暉(Ming-Whei Yu) |
關鍵字: | BCP雙突變,早發肝癌,HBV相關病毒因子,HBV基因型,HBV病毒量,手足配對病例對照研究, basal core promoter double mutation,early-onset HCC,hepatitis B viral factor,HBV genotype,HBV viral load,sibling-matched case control study, |
出版年 : | 2013 |
學位: | 碩士 |
摘要: | 摘要
研究背景: 文獻指出,HBeAg、病毒量、基因型和BCP(basal core promoter)雙突變等B型肝炎病毒因子皆與增加罹患肝細胞癌(HCC)之危險有關,然而,鮮有學者探討HBV病毒因子對於早發肝癌(小於50歲發病)之間的關係,此外,在HBV帶原家庭中,病毒因子所影響手足間罹患HCC危險性差異的原因仍不清楚。因此,本研究利用配對病例與未發病手足對照研究來探討此議題。 材料方法: 本研究的個案來自多醫學中心之合作研究計畫。50歲以前即被診斷出肝細胞癌的病例有150位,其中小於40歲之個案有80位。對照組為病例個案之未發病手足,其性別必須與病例個案相同,且年齡差異需小於5歲。共有184位個案符合條件並收為對照組。抽菸情況與飲酒習慣的資料是透過採訪員之問卷所取得,HBV病毒資料來自血液樣本,血清中HBeAg狀態是利用SD BIOLINE HBeAg test kit所測得,另外HBV病毒量、基因型及BCP雙突變的部分則是透過聚合鏈鎖反應(PCR)或即時聚合鏈鎖反應(Real-time PCR)測得。配對之相對危險性(OR)與其95%信賴區間是使用條件式邏輯斯迴歸估計。 結果: HBV相關之病毒因子在經過年齡、抽菸情況、喝酒習慣、HBeAg狀態、病毒量、基因型和BCP雙突變的調整後,只有BCP雙突變有達到統計上之顯著水準。BCP雙突變在經過其他變項調整後之OR為4.01 (95% CI=1.84~8.75,p=0.0005)。其中,發病年齡小於40歲之配對,經過調整後之OR為5.93 (95% CI=2.13~16.49),而40~50歲發病之配對,經調整後之OR為2.43(95% CI=0.79~7.51)。 結論: 本研究在調整家族內HBV病毒感染來源後,證明BCP雙突變對於早發肝癌的發展與HBV帶原家庭中罹患HCC危險性之差異,皆是一個重要的因子。 Abstract Background: Hepatitis B viral factors, including HBeAg positivity, viral load, genotype, and basal core promoter (BCP) double mutations, have been associated with increased risk of hepatocellular carcinoma (HCC). However, few studies have been carried out to explore their role in the development of early-onset HCC diagnosed before age 50. In addition, the effects of these viral factors on the intra-familial difference in the risk of HCC in HBV carriers’s families are unclear. Therefore, we conducted a case-unaffected sibling matched case-control study to address these issues. Materials and Methods: All study subjects were recruited from a multi-center collaboration program on the risk of HCC. Case patients included 150 (80 of whom were diagnosed at equal to or less than 40 years of age) patients with HCC diagnosed at <50 years. All case patients’ unaffected same-sex siblings, who were born within 5 years of the birth of the cases in the same family, were included as control subjects. Totally 184 control subjects were included. Data on smoking status and alcohol consumption were collected from questionnaire by well-trained research assistants at enrollment. Serum HBeAg status was determined by SD BIOLINE HBeAg test kit, while HBV viral load, genotype, and BCP double mutations were assayed by PCR or real-time PCR. Matched odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by using conditional logistic regression. Results: Among HBV-related viral factors, only BCP double mutations reached statistical significance after adjustment for age, smoking status, alcohol consumption, HBeAg positivity, viral load, genotype, and BCP double mutations. Overall, the adjusted OR for individuals carrying BCP double mutations was 4.01 (95% CI=1.84~8.75, p=0.0005). The adjusted OR was 5.93 (95% CI=2.13~16.49) for case patients diagnosed 40 years and 2.43(95% CI=0.79~7.51) for case patients diagnosed 40-50 years. Conclusion: We demonstrated that BCP double mutation is a significant determinant for developing early-onset HCC and intrafamilial difference in the risk of HCC in HBV carriers’ families after controlling intrafamilial transmission of HBV. |
URI: | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/17560 |
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顯示於系所單位: | 流行病學與預防醫學研究所 |
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