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06.09.2019 | original article | Ausgabe 17-18/2019 Open Access

Wiener klinische Wochenschrift 17-18/2019

Patterns and prevalence of dyslipidemia in patients with different etiologies of chronic liver disease

Zeitschrift:
Wiener klinische Wochenschrift > Ausgabe 17-18/2019
Autoren:
Lukas W. Unger, Bernadette Forstner, Stephan Schneglberger, Moritz Muckenhuber, Ernst Eigenbauer, Bernhard Scheiner, Mattias Mandorfer, Michael Trauner, M.D. Thomas Reiberger
Wichtige Hinweise

Electronic supplementary material

The online version of this article (https://​doi.​org/​10.​1007/​s00508-019-01544-5) contains supplementary material, which is available to authorized users.

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Summary

Background

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.

Methods

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.

Results

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).

Conclusion

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.
Zusatzmaterial
The electronic supplementary material contains a scatter plot with vizualized linear regression for total cholesterol and liver stiffness.
508_2019_1544_MOESM1_ESM.docx
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