Division of General Surgery, Department of Surgery, Medical University of Vienna, Währinger Gürtel 18-20, Vienna, Austria.
Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Währinger Gürtel 18-20, Vienna, Austria.
Wien Klin Wochenschr. 2019 Sep;131(17-18):395-403. doi: 10.1007/s00508-019-01544-5. Epub 2019 Sep 6.
Liver disease impacts on hepatic synthesis of lipoproteins and lipogenesis but data on dyslipidemia during disease progression are limited. We assessed the patterns of dyslipidemia in (i) different liver disease etiologies and discriminated (ii) non-advanced (non-ACLD) from advanced chronic liver disease (ACLD) as it is unclear how progression to ACLD impacts on dyslipidemia-associated cardiovascular risk.
Patients with alcoholic liver disease (n = 121), hepatitis C (n = 1438), hepatitis B (n = 384), metabolic/fatty liver disease (n = 532), cholestatic liver disease (n = 119), and autoimmune hepatitis (n = 114) were included. Liver stiffness ≥15 kPa defined ACLD. Dyslipidemia was defined as total cholesterol >200 mg/dL, low-density lipoprotein (LDL)-cholesterol >130 mg/dL and triglycerides >200 mg/dL.
Across all etiologies, total cholesterol levels were significantly lower in ACLD, when compared to non-ACLD. Accordingly, LDL-cholesterol levels were significantly lower in ACLD due to hepatitis C, hepatitis B, metabolic/fatty liver disease and autoimmune hepatitis. Triglyceride levels did not differ due to disease severity in any etiology. Despite lower total and LDL cholesterol levels in ACLD, etiology-specific dyslipidemia patterns remained similar to non-ACLD. Contrary to this "improved" lipid status in ACLD, cardiovascular comorbidities were more prevalent in ACLD: arterial hypertension was present in 26.6% of non-ACLD and in 55.4% of ACLD patients (p < 0.001), and diabetes was present in 8.1% of non-ACLD and 25.6% of ACLD patients (p < 0.001).
Liver disease etiology is a major determinant of dyslipidemia patterns and prevalence. Progression to ACLD "improves" serum lipid levels while arterial hypertension and diabetes mellitus are more prevalent. Future studies should evaluate cardiovascular events after ACLD-induced "improvement" of dyslipidemia.
肝脏疾病会影响脂蛋白的肝合成和脂肪生成，但关于疾病进展过程中血脂异常的数据有限。我们评估了（i）不同肝脏疾病病因的血脂异常模式，并区分了（ii）非进展性慢性肝病（非 ACLD）与进展性慢性肝病（ACLD），因为尚不清楚进展为 ACLD 如何影响与血脂异常相关的心血管风险。
纳入了酒精性肝病（n=121）、丙型肝炎（n=1438）、乙型肝炎（n=384）、代谢/脂肪性肝病（n=532）、胆汁淤积性肝病（n=119）和自身免疫性肝炎（n=114）患者。肝脏硬度≥15kPa 定义为 ACLD。血脂异常定义为总胆固醇>200mg/dL、低密度脂蛋白（LDL）-胆固醇>130mg/dL 和甘油三酯>200mg/dL。
在所有病因中，与非 ACLD 相比，ACLD 的总胆固醇水平显著降低。因此，由于丙型肝炎、乙型肝炎、代谢/脂肪性肝病和自身免疫性肝炎，ACLD 的 LDL-胆固醇水平显著降低。由于疾病严重程度，任何病因的甘油三酯水平均无差异。尽管 ACLD 的总胆固醇和 LDL 胆固醇水平较低，但 ACLD 的病因特异性血脂异常模式仍与非 ACLD 相似。与 ACLD 中“改善”的脂质状态相反，ACLD 中更常见心血管合并症：非 ACLD 中高血压的患病率为 26.6%，而 ACLD 中高血压的患病率为 55.4%（p<0.001），非 ACLD 中糖尿病的患病率为 8.1%，而 ACLD 中糖尿病的患病率为 25.6%（p<0.001）。
肝脏疾病病因是血脂异常模式和患病率的主要决定因素。进展为 ACLD 可“改善”血清脂质水平，而高血压和糖尿病更为普遍。未来的研究应评估 ACLD 引起的血脂异常“改善”后心血管事件的发生情况。
