Abstract
SummaryBackgroundLiver 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.MethodsPatients 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.ResultsAcross 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).ConclusionLiver 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.Electronic supplementary materialThe online version of this article (10.1007/s00508-019-01544-5) contains supplementary material, which is available to authorized users.
Highlights
Dyslipidemia, among other factors, is a major risk factor for cardiovascular disease (CVD) development and progression [1] and guidelines recommend lipid-lowering therapy in patients at increased risk for CVD
A vast body of literature exists on the effect of chronic liver disease (CLD) on lipid profiles in several etiologies, state of the art assessment of CLD severity by, e.g. grading fibrosis severity is lacking in many studies and advanced CLD (ACLD)/ cirrhosis is usually classified as a distinct etiology [2]
Actual real-life data are warranted as treatment in chronic liver disease has evolved and most patients are exposed to an altered lipid profile for an extensive period of time as progression to ACLD can be halted in many cases
Summary
Dyslipidemia, among other factors, is a major risk factor for cardiovascular disease (CVD) development and progression [1] and guidelines recommend lipid-lowering therapy in patients at increased risk for CVD. A vast body of literature exists on the effect of CLD on lipid profiles in several etiologies, state of the art assessment of CLD severity by, e.g. grading fibrosis severity is lacking in many studies and advanced CLD (ACLD)/ cirrhosis is usually classified as a distinct etiology [2]. This classification is insufficient, as dyslipidemia patterns change during ACLD, and baseline values are strongly dependent on the underlying etiology. Cut-off levels for initiation of lipid-lowering treatment/statin treatment are well-established and stratified by clinical atherosclerotic cardiovascular disease risk, no specific guidelines for CLD and concomitant CVD are available
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