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

Abstract

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。

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.