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  • 學位論文

代謝因子在慢性B型肝炎病毒感染中與B型肝炎病毒基因量之關係

The Relationship between Metabolic Factors and Hepatitis B Virus DNA Levels in Chronic Hepatitis B Virus Infection

指導教授 : 李蘭 黃國晉

摘要


目的:B型肝炎病毒基因量為不良肝病預後的重要決定因子,本研究針對慢性B型肝炎病毒感染者,探討代謝及生活型態因子與其B型肝炎病毒基因量的關係。 方法:本研究自北台灣某大學校園招募141名B型肝炎病毒表面抗原陽性,但不帶有C型肝炎病毒抗體,且未被診斷過肝硬化的B型肝炎病毒帶原者。每名研究樣本需完成自填式問卷、身體測量,並接受血液採集以檢驗B型肝炎病毒血清基因量及代謝因子。所有資料經整理建檔後進行統計分析,最後使用複羅吉斯迴歸分析,找出與有高B型肝炎病毒血清基因量(≥10000 copies/mL)有顯著關係之危險因子。 結果:在調整了相關因子包括年齡、性別、B型肝炎病毒e抗原血清型、高血清丙胺酸轉胺脢及胰島素阻抗性之影響後,肥胖者(身體質量指數≥25 kg/m2)及體重正常者(身體質量指數為18.5-22.9 kg/m2),相對於體重過重者(身體質量指數為23-24.9 kg/m2),皆有高B型肝炎病毒血清基因量的風險;相對危險性分別為3.84和5.27。即使限制在e抗原血清型陰性的B型肝炎病毒帶原者,此現象依然存在。此外,在控制了年齡、性別、B型肝炎病毒e抗原血清型、及高血清丙胺酸轉胺脢之影響後,同時有胰島素阻抗與肥胖兩項危險因子者,會大幅增加有高B型肝炎病毒血清基因量的風險(相對危險性=9.22)。 結論:本研究發現,身體質量指數與B型肝炎病毒血清基因量之間有V型關係,亦即相對於體型正常者或肥胖者,體重過重者反而有較低的B型肝炎病毒血清基因量。此結果顯示,藉由代謝因子來修飾B型肝炎病毒血清基因量的潛在可能性。但是,生活型態因子與B型肝炎血清基因量之間,本研究並未發現有顯著關係存在。

並列摘要


OBJECTIVES: This study aimed to investigate whether metabolic and lifestyle factors were independently associated with serum levels of deoxyribonucleic acid of hepatitis B virus (HBV DNA), a valuable predictor for advanced liver diseases. METHODS: Participants were hepatitis B virus (HBV) carriers in a university of Northern Taiwan. A total of 141 participants who had positive serum hepatitis B surface antigen, negative serum antibody to hepatitis C virus, and no liver cirrhosis received a structured questionnaire and underwent the anthropometric indices, serum HBV DNA levels and metabolic factors measurements. The odds ratios (ORs) and 95% confidence interval (CI) of high serum HBV DNA level (≥10000 copies/mL) were estimated by multiple logistic regression analyses. RESULTS: As compared to overweight (body mass index (BMI) 23-24.9 kg/m2), obesity (BMI ≥25 kg/m2) (OR=3.84, 95% CI=1.38-10.7, P=0.010) and normal weight (BMI 18.5-22.9 kg/m2) (OR=5.27, 95% CI=1.49-18.6, P=0.010) were at significant risk of high serum HBV DNA levels after adjustment for age, gender, hepatitis B e antigen (HBeAg) serostatus, high alanine aminotransferase (ALT) level, and insulin resistance defined as the homeostasis model assessment of insulin resistance ≥2.5. This effect kept consistent even in stepwise analysis restricted to HBeAg seronegatives. Furthermore, insulin resistance and obesity had additive effects on high HBV DNA levels (OR=9.22, 95% CI=1.73-49.1, P=0.009) after controlling for age, gender, HBeAg serostatus, and high ALT level. CONCLUSIONS: The V shape association that linking overweight with low HBV DNA levels suggests the potential modifiability of hepatitis B viral loads through metabolic factors. Further investigation is warranted for the causal temporality and early preventive strategies.

參考文獻


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