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Hepatitis C virus-associated hypobetalipoproteinemia is correlated with plasma viral load, steatosis, and liver fibrosis.
Am J Gastroenterol. 2003 May; 98(5):1150-4.AJ

Abstract

OBJECTIVES

A relationship between chronic hepatitis C virus (HCV) infection and lipid metabolism has recently been suggested. The aim of this study was to determine the correlation between lipid profile and virology, histologic lesions, and response to alpha interferon therapy in noncirrhotic, nondiabetic patients with hepatitis C.

METHODS

A total of 109 consecutive untreated chronic hepatitis C patients were studied to assess the following: 1) the effects of HCV genotype, viral load, steatosis, hepatic fibrosis, and body mass index (BMI) on lipid profile; and 2) whether lipid parameters could predict response to antiviral therapy.

RESULTS

The control group showed a significantly higher apolipoprotein B (apoB) concentration compared with patients with chronic hepatitis C. Hypobetalipoproteinemia (apo B <0.7 g/L) was found in 27 (24.7%) chronic HCV patients and in five (5.3%) control subjects (p = 0.0002). Levels of apo B were negatively correlated with steatosis and HCV viral load (r = -0.22; p = 0.03). This last correlation was strong for non-1 genotype and genotype 3 (r = -0.48; p = 0.0005, and r = -0.47; p = 0.007, respectively) but was not found in genotype 1. In multivariate analysis, low apo B concentration was significantly associated with fibrosis grade 2 or 3 versus grade 0 or 1 (p < 0.001), steatosis >5% (p < 0.001), low body mass index (p < 0.001), and high HCV viral load (p < 0.014). No correlation was found in the 76 treated patients between apo B and response to interferon therapy.

CONCLUSIONS

In chronic HCV patients, hypobetalipoproteinemia occurs already in the early stages of HCV infection before the development of liver cirrhosis. The correlation between apo B levels and HCV viral load seems to confirm the interaction between hepatitis C infection and beta-lipoprotein metabolism.

Authors+Show Affiliations

Services de Diabétologie et Endocrinologie, Dijon cedex, France.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12809841

Citation

Petit, Jean Michel, et al. "Hepatitis C Virus-associated Hypobetalipoproteinemia Is Correlated With Plasma Viral Load, Steatosis, and Liver Fibrosis." The American Journal of Gastroenterology, vol. 98, no. 5, 2003, pp. 1150-4.
Petit JM, Benichou M, Duvillard L, et al. Hepatitis C virus-associated hypobetalipoproteinemia is correlated with plasma viral load, steatosis, and liver fibrosis. Am J Gastroenterol. 2003;98(5):1150-4.
Petit, J. M., Benichou, M., Duvillard, L., Jooste, V., Bour, J. B., Minello, A., Verges, B., Brun, J. M., Gambert, P., & Hillon, P. (2003). Hepatitis C virus-associated hypobetalipoproteinemia is correlated with plasma viral load, steatosis, and liver fibrosis. The American Journal of Gastroenterology, 98(5), 1150-4.
Petit JM, et al. Hepatitis C Virus-associated Hypobetalipoproteinemia Is Correlated With Plasma Viral Load, Steatosis, and Liver Fibrosis. Am J Gastroenterol. 2003;98(5):1150-4. PubMed PMID: 12809841.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hepatitis C virus-associated hypobetalipoproteinemia is correlated with plasma viral load, steatosis, and liver fibrosis. AU - Petit,Jean Michel, AU - Benichou,Muriel, AU - Duvillard,Laurence, AU - Jooste,Valerie, AU - Bour,Jean Baptiste, AU - Minello,Anne, AU - Verges,Bruno, AU - Brun,Jean Marcel, AU - Gambert,Philippe, AU - Hillon,Patrick, PY - 2003/6/18/pubmed PY - 2003/7/25/medline PY - 2003/6/18/entrez SP - 1150 EP - 4 JF - The American journal of gastroenterology JO - Am J Gastroenterol VL - 98 IS - 5 N2 - OBJECTIVES: A relationship between chronic hepatitis C virus (HCV) infection and lipid metabolism has recently been suggested. The aim of this study was to determine the correlation between lipid profile and virology, histologic lesions, and response to alpha interferon therapy in noncirrhotic, nondiabetic patients with hepatitis C. METHODS: A total of 109 consecutive untreated chronic hepatitis C patients were studied to assess the following: 1) the effects of HCV genotype, viral load, steatosis, hepatic fibrosis, and body mass index (BMI) on lipid profile; and 2) whether lipid parameters could predict response to antiviral therapy. RESULTS: The control group showed a significantly higher apolipoprotein B (apoB) concentration compared with patients with chronic hepatitis C. Hypobetalipoproteinemia (apo B <0.7 g/L) was found in 27 (24.7%) chronic HCV patients and in five (5.3%) control subjects (p = 0.0002). Levels of apo B were negatively correlated with steatosis and HCV viral load (r = -0.22; p = 0.03). This last correlation was strong for non-1 genotype and genotype 3 (r = -0.48; p = 0.0005, and r = -0.47; p = 0.007, respectively) but was not found in genotype 1. In multivariate analysis, low apo B concentration was significantly associated with fibrosis grade 2 or 3 versus grade 0 or 1 (p < 0.001), steatosis >5% (p < 0.001), low body mass index (p < 0.001), and high HCV viral load (p < 0.014). No correlation was found in the 76 treated patients between apo B and response to interferon therapy. CONCLUSIONS: In chronic HCV patients, hypobetalipoproteinemia occurs already in the early stages of HCV infection before the development of liver cirrhosis. The correlation between apo B levels and HCV viral load seems to confirm the interaction between hepatitis C infection and beta-lipoprotein metabolism. SN - 0002-9270 UR - https://www.unboundmedicine.com/medline/citation/12809841/Hepatitis_C_virus_associated_hypobetalipoproteinemia_is_correlated_with_plasma_viral_load_steatosis_and_liver_fibrosis_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&amp;sid=nlm:pubmed&amp;issn=0002-9270&amp;date=2003&amp;volume=98&amp;issue=5&amp;spage=1150 DB - PRIME DP - Unbound Medicine ER -