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Original Paper

Med Princ Pract

DOI: 10.1159/000339206

Lipid Serum Profile in Patients with ViralLiver Cirrhosis

Cristin Constantin Vere Costin Teodor Streba Liliana Streba Ion Rogoveanu

Departments of Internal Medicine and Gastroenterology, University of Medicine and Pharmacy of Craiova,

Craiova, Romania

ever, TG and VLDL cholesterol values of controls and cirrhosis

groups were similar (p 1 0.05). We did not register any differ-

ences between the two cirrhosis groups (p 1 0.05). Conclu-

sion: Our data showed that both HCV and HBV cirrhosis se-

verely impaired liver lipid metabolism. Late stages of the dis-

ease resulted in a pseudonormalization of VLDL cholesterol

and TG values. Copyright 2012 S. Karger AG, Basel

Introduction

The liver plays a central role in lipid metabolism, asseveral pathways are, at least in part, dependent to thissite [1]. Major metabolic processes take place at this level,involving the production, transportation and storage ofapoproteins and lipoproteins, as well as catabolism of

various lipids and excretion of cholesterol and phospho-lipids. An alteration in liver functions resulting from cel-lular injury leads to changes in the serum concentration

of cholesterol and lipoproteins [25].Infection with hepatitis C (HCV) or B (HBV) viruses

leads to hepatic damage, which in turn relates to changesin alterations of the lipid metabolism [610]. Differentmechanisms are involved, dependent on the stage of theliver disease and the metabolic state [1113]. Low levels ofplasma cholesterol and lipoproteins, as well as lower tri-glyceride (TG) values are usual in chronic liver diseases.However, the number of studies which included patients

Key Words

Serum lipids Cirrhosis Viral hepatitis

Abstract

Objective: Our main aim was to investigate the serum lipid

levels in a series of patients with liver cirrhosis of viral origin.

Subjects and Methods:The study comprised 90 patients, 60

with viral liver cirrhosis, equally divided between hepatitis

virus C (HCV) and B (HBV) etiologies, and 30 control patients

with no known liver pathology. Patients were investigated

during a 5-year period in the 1st Medical Clinic of the Emer-

gency County Hospital of Craiova, Romania. The following

series of serum lipid parameters were recorded: lipemia, to-

tal cholesterol and cholesteryl ester, high-density lipopro-

tein (HDL) cholesterol, low-density lipoprotein (LDL) choles-

terol, very-low-density lipoprotein (VLDL) cholesterol and

triglyceride (TG) values. Statistical analysis of these parame-

ters was performed using the ANOVA test followed by Tukey

multiple comparison tests to compare replicate means; p !

0.05 was considered statistically significant. Results: We ob-served significantly lower values for serum lipids (543.5 and

549.37 mg/dl in the HBV and HCV cirrhosis subgroups, com-

pared with 649.9 mg/dl in controls), total cholesterol (143.6

and 147.9 vs. 198.0 mg/dl, respectively), cholesteryl esters

(83.6 and 80, compared to 147.9 mg/dl, respectively), LDL

cholesterol (91.6 and 88.5 vs. 132.4 mg/dl) in both cirrhosis

groups when compared with controls (p ! 0.001), as well as

HDL cholesterol (32.1 and 36.9 vs. 47.3 mg/dl, p ! 0.05). How-

Received: October 24, 2011

Accepted: May 1, 2012

Published online: June 19, 2012

Dr. Costin Teodor StrebaSt. Petru Rares No. 2RO200349 Craiova, Dolj (Romania)Tel. +40 72 2389 906E-Mail costi nstreba @ gmail.com

2012 S. Karger AG, Basel10117571/12/00000000$38.00/0

Accessible online at:www.karger.com/mpp

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Vere/Streba/Streba/RogoveanuMed Princ Pract2

with advanced cirrhosis remains low. The present studycomparatively evaluated plasma levels of serum lipids,total cholesterol and cholesteryl ester, high-density lipo-protein (HDL) cholesterol, low-density lipoprotein (LDL)cholesterol, very-low-density lipoprotein (VLDL) choles-terol and TG in three age and gender-matched groups,

two with HCV or HBV cirrhosis and one control group.

Subjects and Methods

This study was conducted in the 1st Medical Clinic of theEmergency County Hospital, Craiova, Romania, from January2006 to January 2011. A total of 90 patients were selected, as fol-lows: 30 with hepatic cirrhosis of HCV origin, 30 with hepatic cir-rhosis of HBV origin and 30 patients with no known liver diseases.The diagnosis of cirrhosis was established on anamnestic, clinicaland laboratory findings, imaging (ultrasonography and upper en-doscopy) and liver biopsy. No patients underwent antiviral thera-py. All the patients live in the same geographic area, with similarbody mass indices and similar dietary habits. All the patients werein advanced stages of cirrhosis (Child B and C). Exclusion criteriawere primary disproteinemia or disproteinemia associated withother pathologies (diabetes mellitus, nephrotic syndrome, hypo-thyroidism or other metabolic syndromes); body mass index 130and alcohol consumption as well as prior treatments with estro-gens, -blockers, diuretics or cortisol medication.

Serum lipids, total cholesterol and cholesteryl ester, HDL cho-lesterol, LDL cholesterol, VLDL cholesterol and TG values weremeasured using colorimetric enzyme methods (Kobas 6000 ana-lyzer; Roche Diagnostics, USA).

Statistical analysis of these parameters was performed usingthe ANOVA test followed by Tukey multiple comparison tests;Bartletts statistic was used to test for equal variances; p! 0.05 wasconsidered statistically significant. All statistical calculationswere performed using the Graph Pad Prism software (InStat,USA).

Results

Patients were similar in terms of gender and age (ta-ble 1). All three groups were similar in terms of age dis-tribution (median ages 50.87, 49.83 and 47.93 years, re-spectively), ranging between 30 and 70 years. The malepopulation was predominant in our cohort, with a totalof 57 men (63.3%) and a similar gender distribution in allthree groups. Bartletts statistic showed normal distribu-tion of the variances in all samples.

The comparisons of serum values for lipids, total cho-

lesterol, cholesteryl esters, HDL, LDL and VLDL choles-terol and TG for all three groups are given in table 2. Thedifferences between the controls and both cirrhoticgroups for serum lipids (p ! 0.001), total cholesterol (p !0.001), cholesteryl esters (p ! 0.001), HDL (p ! 0.05) andLDL cholesterol (p ! 0.001) were statistically significant.However, there was no statistically significant differencebetween TG and VLDL cholesterol values of controls andany of the two cirrhosis groups (p 1 0.05). Also, cirrhoticpatients had similar values for all serum parameters, ir-respective of the viral etiology (p 1 0.05).

Discussion

Our results indicated that serum levels of lipid, totalcholesterol and cholesteryl ester, as well as HDL and LDLcholesterol (but not VLDL cholesterol) were lower in pa-

Table 1. Gender and age distribution of study groups

Male Female Mean age8 SD (range)

HBV cirrhosis 20 10 50.8788.72 (3466)HCV cirrhosis 18 12 49.8385.84 (3856)Controls 19 11 47.93811.53 (3070)

Table 2. Serum values of all studied parameters

HBV cirrhosis HCV cirrhosis Controls p value

Serum lipids 543.5890.0 549.37876.1 642.9855.2 0.00082Total cholesterol 143.6831.8 147.9836.9 198.0824.3 0.00073Cholesteryl ester 83.60815.86 80.0822.0 147.9836.9 0.00077HDL cholesterol 32.185.5 36.986.9 47.384.3 0.0278LDL cholesterol 91.6824.9 88.5831.2 132.4827.3 0.00091VLDL cholesterol 20.884.5 18.987.0 20.783.5 0.069TG 104.8822.1 99.4835.7 104.8817.3 0.071

Results are shown as means8 standard deviation. All values are calculated in mil ligrams per deciliter.

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Lipid Serum Profile Med Princ Pract 3

tients with advanced stages of liver disease, irrespective oftheir viral etiology. No changes were observed in TG levelsof the three groups. No differences were observed betweenthe patients with HBV and HCV either, thereby provingthat the advanced stages of liver disease and subsequentorgan failure were similar, irrespective of the viral etiology.

As we had previously shown [9], cholesterol and TGlevels were influenced by the etiology and severity ofchronic viral hepatitis, being in direct relation with thehistological activity score and steatosis. The present studyhas taken the paradigm further, proving that the etio-logical differences that existed with the onset of cirrhosiswere leveled at the advanced stage due to the inherent he-patocyte damage.

Previous studies [2, 3, 5, 6, 14] had established a connec-tion between liver damage due to viral infection and a de-cline in cholesterol and apolipoprotein metabolism. Thisrelationship was further demonstrated by recent basic and

clinical research aimed at uncovering the mechanisms be-hind these alterations [7, 10, 13, 15]. While the interferencefrom viral infection is clearly established, only a limitednumber of studies further details how liver cirrhosis, espe-cially in advanced stages, alters lipid metabolism.

Our findings confirmed previous studies [7, 8, 10, 16,17] that revealed an alteration of lipid metabolism in ad-

vanced stages of viral liver cirrhosis principally becausehepatocyte alteration was already profound. Patientswere preselected in advanced disease stages, thus hepato-cyte alteration was already profound.

Several studies found lower TG levels in HCV- orHBV-infected patients without cirrhosis. In our study,however, TG levels were similar in all three groups. Thisis probably due to the fact that in late stages of hepaticdisease, the activity of TG lipase (the enzyme responsiblefor hydrolyzing ester linkages of TGs) is severely im-paired [6].

Conclusions

HCV and HBV cirrhosis severely impaired liver lipid

metabolism, thus resulting in low serum values of totalcholesterol, cholesteryl ester, HDL and LDL cholesterol.However, VLDL cholesterol and TG levels were not af-fected in late stages of liver disease.

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