title: Acute hepatitis C infection lowers serum lipid levels.
abstract: Chronic hepatitis C infection is associated with hypolipidaemia that resolves with viral clearance. Lipid levels in a subgroup of patients rebound to levels that may increase the risk of coronary heart disease. The impact of acute hepatitis C infection and its clearance on lipid levels is unknown. We undertook a retrospective evaluation of subjects with acute hepatitis C infection evaluating lipid levels before, during and following acute infection. Thirty-eight subjects with acute hepatitis C infection had lipid levels available. Twelve patients had pre-infection and intra-infection lipid levels available. Cholesterol (197.8-152.4 mg/dL, P = 0.025), low-density lipoprotein (LDL) (116.1-76.3 mg/dL, P = 0.001) and non-high-density lipoprotein (non-HDL) cholesterol (164.0-122.7 mg/dL, P = 0.007) decreased dramatically during acute hepatitis C virus infection. Nineteen patients who achieved viral clearance had lipid levels available during infection and following resolution of infection. In these patients, cholesterol (145.0-176.0 mg/dL, P = 0.01), LDL (87.0-110.1 P = 0.0046) and non-HDL cholesterol (108.6-133.6 mg/dL, P = 0.008) increased significantly. No change was seen in patients who developed chronic infection. Four patients had lipid levels before, during and following resolution of infections and had increased postinfection LDL, cholesterol and non-HDL cholesterol from pre-infection levels, indicating acute infection may be associated with an increase in postinfection lipid levels and may confer an increased risk of coronary heart disease. Acute hepatitis C infection results in hypolipidaemia with decreased LDL, cholesterol and non-HDL cholesterol levels that increase following infection resolution. Levels may increase above pre-infection baseline lipid levels and should be monitored.
authors.affiliation: Gastrointestinal Unit, Massachusetts General Hospital, Boston, MA 02114, USA.
authors.forename: K E
authors.initials: KE
authors.lastname: Corey
authors.forename: J
authors.initials: J
authors.lastname: Mendez-Navarro
authors.forename: L L
authors.initials: LL
authors.lastname: Barlow
authors.forename: V
authors.initials: V
authors.lastname: Patwardhan
authors.forename: H
authors.initials: H
authors.lastname: Zheng
authors.forename: A Y
authors.initials: AY
authors.lastname: Kim
authors.forename: G M
authors.initials: GM
authors.lastname: Lauer
authors.forename: R T
authors.initials: RT
authors.lastname: Chung
mesh_terms: D000208:Acute Disease; D000328:Adult; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003327:Coronary Disease / Q000097:blood; D005260:Female; D016174:Hepacivirus / Q000235:genetics; D006526:Hepatitis C / Q000097:blood*; D006801:Humans; D008055:Lipids / Q000097:blood*; D008075:Lipoproteins, HDL / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000097:blood; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D008055:Lipids; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D012367:RNA, Viral; D014280:Triglycerides