[ 摘要 ]

根據歷年三十個山地鄉及台灣地區的死亡資料比較顯示，在同一死因的比較下，無論是男性或是女性，山地鄉居民的死亡率均較台灣地區居民的死亡率高，其中尤其以罹患慢性肝病及肝硬化的死亡率差異最大。因此本研究的主要目的在於釐清東部地區原住民肝炎病毒感染及物質濫用習慣上與慢性肝疾（chronic liver disease, CLD）發生的相關性。 本研究是以醫院病例對照研究設計，以經醫院腸胃內科專科醫師診斷為慢性肝炎及肝硬化或經臨床檢驗結果為肝功能異常（AST＞40 IU/L 且 ALT＞45 IU/L）者共109名為病例組，其餘共302名非慢性肝疾之原住民病患為對照組。以結構式問卷訪談的方式來獲得研究對象菸煙、酒精、檳榔的暴露情形以及輸血和注射等健康行為。另以酵素免疫分析法及自動分析儀和商用試劑，測定B型肝炎病毒（hepatitis B virus, HBV）與C型肝炎病毒（hepatitis C virus, HCV）的慢性感染情形及aspartate aminotransferase/alanine aminotransferase等肝功能指數，對於C型肝炎病毒抗體（antibody against HCV, anti-HCV）陽性者則以反轉錄酵素-聚合酵素鏈反應（reverse transcriptase-polymerase chain reaction, RT-PCR）及ABI 377自動定序分析儀（ABI 377 autosequencer），進行C型肝炎病毒5¢端非轉譯區（5¢-untranslated region, 5¢UTR）之變異性（heterogeneity）分析。 研究結果顯示在經調整性別、年齡、HBsAg帶原狀態以及anti-HCV血清狀態的作用後，有抽菸、酒精攝取以及嚼食檳榔習慣者之危險對比值分別為2.5（95% CI：1.5-4.2）、3.0（95% CI：1.7-5.4）、3.0（95% CI：1.8-5.2），且均有顯著偏高的慢性肝疾危險性。此外，C型肝炎病毒陽性抗體效價、物質濫用習慣數及5¢UTR第100-240核?酸序列變異量與慢性肝疾危險性之間呈現顯著的劑量效應（test for trend, p<0.0001）。交互作用分析指出，C型肝炎病毒感染與嚼食檳榔及飲酒習慣者，或是B肝炎病毒帶原與菸煙及檳榔暴露之間均有顯著的相乘交互作用。 東部地區原住民無論是感染C型肝炎病毒者或是有飲酒及嚼食檳榔習慣者，均有顯著偏高之慢性肝疾危險估計值。另外，肝炎病毒慢性感染且有任一物質濫用習慣者比起單一病毒慢性感染及物質濫用習慣者有較高的慢性肝疾危險性。



[ 英文摘要 ]

According to the vital statistics of Taiwan, the mortality ratios for chronic hepatitis and cirrhosis of aboriginal townships were higher than residents of the Province of Taiwan for both sexes. Therefore, chronic liver disease (CLD) was one of the most important causes of death for aboriginal townships. For this reason, this study examined the effects of viral infections and substance abuse habits on risk of chronic liver disease in eastern aborigines. We conducted a hospital-based case-control study on 109 patients with chronic hepatitis, liver cirrhosis or liver dysfunction (AST>40 IU/L and ALT>45 IU/L) and 302 hospital controls. Information associated with exposure of cigarette smoking, alcohol drinking and betel quid chewing, health behavior, and history of blood transfusion and injection were obtained via structured-questionnaire interviews. Hepatitis B virus (HBV) and hepatitis C virus (HCV) infections were detected by enzyme immunoassay, and liver function markers (aspartate aminotransferase/alanine aminotransferase) were detected by autoanalyzer and commercial kits. In addition, we used reverse transcription-polymerase chain reaction (RT-PCR) and ABI 377 auto-sequencer to analyze the heterogeneity in the 5¢-untranslated region (5¢UTR) of HCV for subjects with anti-HCV seropositivity. After adjustment for sex-, age-, anti-HCV- and HBsAg- serostatus, the authors found that habitual cigarette smoking (odds ratio (OR) 2.5; 95% confidence interval (CI): 1.5-4.2), alcohol drinking (OR 3.0; 95% CI：1.7-5.4), and betel quit chewing (OR 3.0; 95% CI：1.8-5.2) were associated with significantly elevated CLD risks. Additionally, there were significant dose-response relationships between CLD risk and either level of anti-HCV titer or the number of substance abuse habit. There also was a liner trend of CLD risk for increasing number of variability in nucleotides 100-240 of HCV 5¢UTR. There was a significant multiplicative interaction between HCV seropositivity and either betel quit chewing or alcohol drinking and between HBsAg seropositivity and either betel quit chewing or cigarette smoking. Habitual alcohol drinking, betel quid chewing and chronic infections of HCV were associated with the developing of chronic liver disease in eastern aborigines. Moreover, hepatotropic virus chronic infected substance abusers had a higher CLD risk than others.