FULLTEXT: -DYSLIPIDEMIA IN ACUTE VIRAL HEPATITIS: -Impaired plasma lipid profiles in acute hepatitis

Abstract

The present study examined plasma lipid profiles in thirty patients suffered from acute viral hepatitis.

Patients' blood samples were collected at both the debut and recovery of diseases.

Thirty sex and age matched normal subjects were included as controls.

  • Plasma total triglycerides (TG),
  • total cholesterol,
  • high density lipoprotein cholesterol (HDL-C),
  • low density lipoprotein cholesterol (LDL-C),
  • apolipoprotein AI (ApoAI),
  • apolipoprotein B (ApoB),
  • lipoprotein (a) (Lp(a)),
  • blood coagulation status including prothrombin complex activity
  • and activated partial tromboplastin time (APTT),
  • and hepatic functions were determined by the automatic biochemical analytical instrument.

It demonstrated that plasma levels of total cholesterol, HDL-C and apoAI were significantly lower in the patients at the acute phase of hepatitis than those in normal subjects, whereas plasma levels of TG and LDL-C were obviously higher in the patients than in normal subjects (P < 0.05).

Moreover, we demonstrated that patients' plasma levels of total cholesterol, LDL-C, HDL-C and apoAI were lower at the active phase of the diseases than at the recovering phase, which indicating that acute liver damage could significant influence lipid metabolism in vivo.

No pathological changes of blood coagulation status occurred in these patients during the study as all selected patients had moderate hepatitis.

It may conclude that examinations of plasma lipid profile could be considered as a clinical index to reflect liver damage in the active phase of hepatitis.  


Introduction

Liver is the most important organ for the metabolism of lipids, lipoproteins and apolipoproteins.

Under normal circumstances, most plasma endogenous lipids and lipoproteins are synthesized in the liver and then are secreted into the blood circulation [1,2].

And plasma lipoproteins are also mainly catabolism by the liver to maintain the relative balance of lipid and lipoprotein metabolism in vivo [3].

It has been well documented that chronic liver dysfunction might interfere lipid metabolism in vivo and could change plasma lipid and lipoprotein patterns [4].

Acute hepatitis may be referred to an inflammatory process of the liver lasting less than six months.

In China, the most common etiology of acute hepatitis is viral infection, in which hepatitis A and hepatitis E are the most common causes.

In clinical, the courses of acute hepatitis may vary widely from mild symptom that does not require treatment to the fulminant hepatic failure that needs emergency liver transplantation.

Acute viral hepatitis is more likely to be asymptomatic in younger people.

In addition, acute hepatitis may occur less commonly with infections such as Epstein-Barr virus, cytomegalovirus, adenovirus, herpes simplex and Coxsackie virus or with other noninfectious reasons.

It has been demonstrated that in the acute and/or chronic liver diseases, hepatic function could be impaired and the circulating lipids and lipoproteins are not only present in abnormal amounts but they frequently also have abnormal composition including electrophoretic mobility and appearance [4].

Previous studies pay more emphasis on changes of lipid metabolisms under chronic hepatitis and cirrhosis with or without hepatocellular carcinoma [5-7].

In the present study we followed plasma lipid and lipoprotein patterns of patients suffered from acute hepatitis to further explore the changes of lipid and lipoprotein profiles of the patients.


Lipids Health Dis. 2010; 9: 5.

doi: 10.1186/1476-511X-9-5.  

Libo Luo,#1 Xiangke Pu,#2,3 Yongzhong Wang,2 and Ning Xucorresponding author4

1First People's Hospital of Changzhou, Jiangsu 213003, China 2Third People's Hospital of Changzhou, Jiangsu 213001, China 3School of Radiology and Public Health, Soochow University, Jiangsu 215123, China 4Department of Clinical Chemistry and Pharmacology, University Hospital of Lund, Lund S-22185, Sweden

corresponding authorCorresponding author. #Contributed equally.

distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Libo Luo,#1 Xiangke Pu,#2,3 Yongzhong Wang,2 and Ning Xucorresponding author4

1First People's Hospital of Changzhou, Jiangsu 213003, China 2Third People's Hospital of Changzhou, Jiangsu 213001, China 3School of Radiology and Public Health, Soochow University, Jiangsu 215123, China 4Department of Clinical Chemistry and Pharmacology, University Hospital of Lund, Lund S-22185, Sweden

corresponding authorCorresponding author. #Contributed equally.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.  

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NOTICIA SELECCIONADA POR E-MEDICUM
Prof. Dr. Mario I. CámeraDirector Médico
Prof. Dr. Mario I. Cámera

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824760/