慢性乙型肝炎患者代谢异常对肝纤维化的影响

Influence of abnormal metabolism on liver fibrosis in patients with chronic hepatitis B

目的探讨慢性乙型肝炎患者代谢异常对肝纤维化的影响。方法分析110例慢性乙型肝炎患者HOMA-IR、HOMA-β、糖脂代谢异常以及脂肪肝对肝纤维化的影响。结果 HOMA-IR越高,肝脏弹性值(LSM)越高(F=5.559、P=0.005),各项肝功能指标、TBil水平亦随HOMA-IR增大而有所升高,但组间差异无统计学意义(P>0.05)。HOMA-β越差,LSM越高(t=-2.771、P=0.029),各项肝功能指标、TBil水平亦随HOMA-β降低而有所升高,但组间差异无统计学意义(P>0.05)。糖代谢状态越差,患者LSM、ALP、GGT水平越高,伴发脂肪肝的比例越高(F=4.663、10.171、11.331、6.482,P=0.033、0.002、0.001、0.039),其他肝功能指标、TBil水平亦随糖代谢的恶化而有所升高,但组间差异尚无统计学意义(P>0.05)。脂代谢异常组较脂代谢正常组及有脂肪肝组较无脂肪肝组肝功能指标、TBil、LSM水平亦有所升高,但组间差异无统计学意义(P>0.05)。结论慢性乙型肝炎患者胰岛素抵抗、胰岛β细胞功能减退、糖脂代谢状态的恶化可促进肝纤维化的进程。

Objective To analyze the influence of abnormal metabolism on liver fibrosis in patients with chronic hepatitis B. Methods The influence factors on liver fibrosis by abnormal metabolism including HOMA-IR, HOMA-β, abnormal glucose and lipid metabolism, fatty liver disease were analyzed in 110 cases with chronic hepatitis B by the prospective cross-section research. Results The liver stiffness mesurement(LSM) was higher(F = 5.559, P = 0.005) for patients with higher HOMA-IR. The levels of indicators of liver function and TBil also increased with HOMA-IR, but with no significant differences(P > 0.05). With worse HOMA-β, the LSM was higher(t =-2.771, P = 0.029). The levels of indicators of liver function and TBil also increased along with HOMA-β, but with no significant differences(P > 0.05). Along with worse glucose metabolism condition, the LSM, ALP, GGT were higher, the proportion of fatty liver disease was higher(F = 4.663, 10.171, 11.331, 6.482; P = 0.033, 0.002, 0.001, 0.039). The levels of other indicators of liver function and TBil also increased along with worse glucose metabolism condition, but with no significant differences(P > 0.05). The levels of indicators of liver function, TBil and LSM were higher in abnormal lipid group or fatty liver disease group than that in normal lipid group or nonfatty liver disease group, but with no significant differences(P > 0.05). Conclusions Among patient with chronic hepatitis B, the insulin resistance, worse island beta cell function, worse glucose and lipid metabolism condition could promote progress of the liver fibrosis.