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For: Campo JAD, Romero-Gómez M. Steatosis and insulin resistance in hepatitis C: A way out for the virus? World J Gastroenterol 2009; 15(40): 5014-5019 [PMID: 19859993 DOI: 10.3748/wjg.15.5014] [Citation(s) in RCA: 48] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] Open

For:	Campo JAD, Romero-Gómez M. Steatosis and insulin resistance in hepatitis C: A way out for the virus? World J Gastroenterol 2009; 15(40): 5014-5019 [PMID: 19859993 DOI: 10.3748/wjg.15.5014] [Citation(s) in RCA: 48] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] Open

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Cited by Other Article(s)

Hasanoglu I, Rivero-Juárez A, Özkaya Şahin G, ESCMID Study Group for Viral Hepatitis (ESGVH). When Metabolic Dysfunction-Associated Steatotic Liver Disease Meets Viral Hepatitis. J Clin Med 2025;14:3422. [PMID: 40429417 PMCID: PMC12112634 DOI: 10.3390/jcm14103422] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/06/2025] [Revised: 04/04/2025] [Accepted: 04/23/2025] [Indexed: 05/29/2025] Open

Abstract

The interplay between Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) and viral hepatitis, primarily hepatitis B virus (HBV) and hepatitis C virus (HCV), presents a complex challenge in managing chronic liver diseases. Recent epidemiological insights suggest an escalating prevalence of MASLD globally, attributed mainly to the obesity epidemic and associated metabolic disorders. Concurrently, chronic viral hepatitis remains a significant contributor to liver disease morbidity and mortality worldwide, despite advances in antiviral therapies. According to the World Health Organization (WHO) 2023 data, approximately 296 million people are living with chronic HBV infection (about 3.8% of the global population), and 58 million people with HCV infection (about 0.7%), together accounting for over 1.1 million deaths annually. The coexistence of MASLD and viral hepatitis presents a complex scenario in clinical outcomes, where the effects on liver health can vary. Although many studies highlight the potential for additive or synergistic worsening of liver conditions, leading to complications such as cirrhosis, liver failure, and HCC, the impact of HBV on MASLD is not consistent. Managing patients with dual MASLD and viral hepatitis is complex due to the interplay of metabolic and viral factors. Lifestyle modifications, including weight loss, dietary changes, and physical activity, are fundamental to MASLD management and help reduce fibrosis risk in viral hepatitis. This review examines the dual impact of MASLD and viral hepatitis on liver pathology and delineates shared pathophysiological mechanisms, including the influence on hepatic steatosis, inflammation, and fibrogenesis. It also discusses therapeutic strategies tailored to manage this comorbidity, emphasizing the need for an integrated care approach that addresses both metabolic dysfunctions and viral infection to optimize patient outcomes.

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Jeremiah SS, Moin ASM, Butler AE. Virus-induced diabetes mellitus: revisiting infection etiology in light of SARS-CoV-2. Metabolism 2024;156:155917. [PMID: 38642828 DOI: 10.1016/j.metabol.2024.155917] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/30/2024] [Revised: 04/14/2024] [Accepted: 04/14/2024] [Indexed: 04/22/2024]

Yu YF, Hu G, Tong KK, Yang XY, Wu JY, Yu R. Effect of viral hepatitis on type 2 diabetes: A Mendelian randomization study. World J Diabetes 2024;15:220-231. [PMID: 38464364 PMCID: PMC10921171 DOI: 10.4239/wjd.v15.i2.220] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/11/2023] [Revised: 12/13/2023] [Accepted: 01/17/2024] [Indexed: 02/04/2024] Open

Burden, Outcome, and Comorbidities of Extrahepatic Manifestations in Hepatitis C Virus Infection. BIOLOGY 2022;12:biology12010023. [PMID: 36671716 PMCID: PMC9855523 DOI: 10.3390/biology12010023] [Citation(s) in RCA: 9] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Subscribe] [Scholar Register] [Received: 10/06/2022] [Revised: 12/06/2022] [Accepted: 12/20/2022] [Indexed: 12/24/2022]

Increased Insulin Resistance in Hepatitis-C Infection-Association with Altered Hepatic Function Testing. PATHOPHYSIOLOGY 2022;29:326-332. [PMID: 35893594 PMCID: PMC9326586 DOI: 10.3390/pathophysiology29030024] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/28/2022] [Revised: 06/14/2022] [Accepted: 06/17/2022] [Indexed: 12/15/2022] Open

Abstract

Introduction: Hepatitis C virus (HCV) infection is a serious global public health problem. It is estimated that 2% to 3% of the world’s population is infected with the virus. It was found that chronic hepatitis C is an independent predictor of the development of type 2 diabetes mellitus. Infection with HCV or the inflammatory response to HCV infection likely contributes to the development of insulin resistance (IR), which increases the risk of developing type 2 diabetes in the long term. This study aimed to assess the insulin resistance in hepatitis C and its correlation with various metabolic parameters. Materials and Methods: This cross-sectional observational study was conducted at a tertiary care hospital in North India in the Department of Internal Medicine with hepatitis C-positive patients attending an out-patient or in-patient department. We took a total of 100 patients aged > 18 years and divided them into two groups: Group A with hepatitis C (cases) and Group B without hepatitis C (controls). There were a total of 50 hepatitis C patients and 50 patients without hepatitis C. Results: A total of 100 patients were included in the present study after obtaining informed consent. There was a significantly higher level of serum ferritin and insulin in group A patients than group B patients. There was a positive correlation of insulin resistance with the serum insulin, ferritin levels, cholesterol, LDL and triglyceride level and a negative correlation with the serum HDL level. The incidence of insulin resistance was positively correlated with changes in fibrosis in the liver due to the hepatitis C infection. Conclusions: From our study, we found that there is an increased incidence of insulin resistance in the patients with hepatitis-C infection, and insulin resistance is associated with the presence of altered hepatic function test results.

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Trifan A, Stratina E, Rotaru A, Stafie R, Zenovia S, Nastasa R, Huiban L, Sfarti C, Cojocariu C, Cuciureanu T, Muzica C, Chiriac S, Girleanu I, Singeap AM, Stanciu C. Changes in Liver Steatosis Using Controlled Attenuation Parameter among Patients with Chronic Hepatitis C Infection Treated with Direct-Acting Antivirals Therapy Who Achieved Sustained Virological Response. Diagnostics (Basel) 2022;12:702. [PMID: 35328255 PMCID: PMC8947513 DOI: 10.3390/diagnostics12030702] [Citation(s) in RCA: 15] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/24/2022] [Revised: 03/09/2022] [Accepted: 03/11/2022] [Indexed: 02/06/2023] Open

Abstract

Chronic hepatitis C virus (HCV) infection induces hepatic steatosis due to viral and host factors. However, information regarding the effects of direct-acting antivirals (DAAs) therapy on liver steatosis and fibrosis is limited. Vibration-controlled transient elastography (VCTE) with a controlled attenuation parameter (CAP) represents a non-invasive method, which has been used in the last few years for the detection of hepatic steatosis and fibrosis before and at a sustained virological response at 12 weeks (SVR12). The aim of this study was to assess the modifications of liver steatosis and fibrosis in HCV-infected patients who achieved SVR12. Consecutive patients with chronic HCV infection that were treated with DAAs in a tertiary gastroenterology center from Romania were included. Demographics, laboratory data, and VCTE evaluation were recorded in all patients. Patients with previous hepatic decompensation and those who did not achieve SVR were excluded. Two hundred and eighty patients (67.1% females) who achieved SVR12 were included. Regarding the changes in biological parameters, including liver enzymes such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST), reduced to normal levels at SVR12 compared to the baseline (28.72 ± 24.71 U/L vs. 40.72 ± 27.34 U/L for ALT, p < 0.013 and 27.21 ± 11.15 U/L vs. 33.35 ± 23.37 U/L for AST, p = 0.029). On the contrary, the levels of triglycerides increased significantly from the baseline to SVR12 (124.03 ± 113.49 mg/dL to 153.78 ± 94.53, p = 0.004). Regarding hepatic steatosis by CAP evaluation, at SVR12, 186 (66.4%) of the individuals had a CAP score of ≥248 dB/m, an increase of 4.6% from the baseline. After viral eradication with DAAs, we observed an increase in hepatic steatosis. Hence, a long-term follow-up is mandatory to identify HCV-infected patients with hepatic steatosis post-SVR and the risk factors for more severe outcomes.

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Affiliation(s)

Anca Trifan Department of Gastroenterology, Grigore T. Popa University of Medicine and Pharmacy, 700111 Iasi, Romania; (A.T.); (A.R.); (R.S.); (S.Z.); (L.H.); (C.S.); (C.C.); (T.C.); (C.M.); (S.C.); (I.G.); (A.-M.S.); (C.S.) Department of Gastroenterology and Hepatology, “St. Spiridon” University Hospital, 700115 Iasi, Romania
Ermina Stratina Department of Gastroenterology, Grigore T. Popa University of Medicine and Pharmacy, 700111 Iasi, Romania; (A.T.); (A.R.); (R.S.); (S.Z.); (L.H.); (C.S.); (C.C.); (T.C.); (C.M.); (S.C.); (I.G.); (A.-M.S.); (C.S.) Department of Gastroenterology and Hepatology, “St. Spiridon” University Hospital, 700115 Iasi, Romania
Adrian Rotaru Department of Gastroenterology, Grigore T. Popa University of Medicine and Pharmacy, 700111 Iasi, Romania; (A.T.); (A.R.); (R.S.); (S.Z.); (L.H.); (C.S.); (C.C.); (T.C.); (C.M.); (S.C.); (I.G.); (A.-M.S.); (C.S.) Department of Gastroenterology and Hepatology, “St. Spiridon” University Hospital, 700115 Iasi, Romania
Remus Stafie Department of Gastroenterology, Grigore T. Popa University of Medicine and Pharmacy, 700111 Iasi, Romania; (A.T.); (A.R.); (R.S.); (S.Z.); (L.H.); (C.S.); (C.C.); (T.C.); (C.M.); (S.C.); (I.G.); (A.-M.S.); (C.S.) Department of Gastroenterology and Hepatology, “St. Spiridon” University Hospital, 700115 Iasi, Romania
Sebastian Zenovia Department of Gastroenterology, Grigore T. Popa University of Medicine and Pharmacy, 700111 Iasi, Romania; (A.T.); (A.R.); (R.S.); (S.Z.); (L.H.); (C.S.); (C.C.); (T.C.); (C.M.); (S.C.); (I.G.); (A.-M.S.); (C.S.) Department of Gastroenterology and Hepatology, “St. Spiridon” University Hospital, 700115 Iasi, Romania
Robert Nastasa Department of Gastroenterology, Grigore T. Popa University of Medicine and Pharmacy, 700111 Iasi, Romania; (A.T.); (A.R.); (R.S.); (S.Z.); (L.H.); (C.S.); (C.C.); (T.C.); (C.M.); (S.C.); (I.G.); (A.-M.S.); (C.S.) Department of Gastroenterology and Hepatology, “St. Spiridon” University Hospital, 700115 Iasi, Romania
Laura Huiban Department of Gastroenterology, Grigore T. Popa University of Medicine and Pharmacy, 700111 Iasi, Romania; (A.T.); (A.R.); (R.S.); (S.Z.); (L.H.); (C.S.); (C.C.); (T.C.); (C.M.); (S.C.); (I.G.); (A.-M.S.); (C.S.) Department of Gastroenterology and Hepatology, “St. Spiridon” University Hospital, 700115 Iasi, Romania
Catalin Sfarti Department of Gastroenterology, Grigore T. Popa University of Medicine and Pharmacy, 700111 Iasi, Romania; (A.T.); (A.R.); (R.S.); (S.Z.); (L.H.); (C.S.); (C.C.); (T.C.); (C.M.); (S.C.); (I.G.); (A.-M.S.); (C.S.) Department of Gastroenterology and Hepatology, “St. Spiridon” University Hospital, 700115 Iasi, Romania
Camelia Cojocariu Department of Gastroenterology, Grigore T. Popa University of Medicine and Pharmacy, 700111 Iasi, Romania; (A.T.); (A.R.); (R.S.); (S.Z.); (L.H.); (C.S.); (C.C.); (T.C.); (C.M.); (S.C.); (I.G.); (A.-M.S.); (C.S.) Department of Gastroenterology and Hepatology, “St. Spiridon” University Hospital, 700115 Iasi, Romania
Tudor Cuciureanu Department of Gastroenterology, Grigore T. Popa University of Medicine and Pharmacy, 700111 Iasi, Romania; (A.T.); (A.R.); (R.S.); (S.Z.); (L.H.); (C.S.); (C.C.); (T.C.); (C.M.); (S.C.); (I.G.); (A.-M.S.); (C.S.) Department of Gastroenterology and Hepatology, “St. Spiridon” University Hospital, 700115 Iasi, Romania
Cristina Muzica Department of Gastroenterology, Grigore T. Popa University of Medicine and Pharmacy, 700111 Iasi, Romania; (A.T.); (A.R.); (R.S.); (S.Z.); (L.H.); (C.S.); (C.C.); (T.C.); (C.M.); (S.C.); (I.G.); (A.-M.S.); (C.S.) Department of Gastroenterology and Hepatology, “St. Spiridon” University Hospital, 700115 Iasi, Romania
Stefan Chiriac Department of Gastroenterology, Grigore T. Popa University of Medicine and Pharmacy, 700111 Iasi, Romania; (A.T.); (A.R.); (R.S.); (S.Z.); (L.H.); (C.S.); (C.C.); (T.C.); (C.M.); (S.C.); (I.G.); (A.-M.S.); (C.S.) Department of Gastroenterology and Hepatology, “St. Spiridon” University Hospital, 700115 Iasi, Romania
Irina Girleanu Department of Gastroenterology, Grigore T. Popa University of Medicine and Pharmacy, 700111 Iasi, Romania; (A.T.); (A.R.); (R.S.); (S.Z.); (L.H.); (C.S.); (C.C.); (T.C.); (C.M.); (S.C.); (I.G.); (A.-M.S.); (C.S.) Department of Gastroenterology and Hepatology, “St. Spiridon” University Hospital, 700115 Iasi, Romania
Ana-Maria Singeap Department of Gastroenterology, Grigore T. Popa University of Medicine and Pharmacy, 700111 Iasi, Romania; (A.T.); (A.R.); (R.S.); (S.Z.); (L.H.); (C.S.); (C.C.); (T.C.); (C.M.); (S.C.); (I.G.); (A.-M.S.); (C.S.) Department of Gastroenterology and Hepatology, “St. Spiridon” University Hospital, 700115 Iasi, Romania
Carol Stanciu Department of Gastroenterology, Grigore T. Popa University of Medicine and Pharmacy, 700111 Iasi, Romania; (A.T.); (A.R.); (R.S.); (S.Z.); (L.H.); (C.S.); (C.C.); (T.C.); (C.M.); (S.C.); (I.G.); (A.-M.S.); (C.S.) Department of Gastroenterology and Hepatology, “St. Spiridon” University Hospital, 700115 Iasi, Romania

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Blood glucose regulation in context of infection. VITAMINS AND HORMONES 2021;117:253-318. [PMID: 34420584 DOI: 10.1016/bs.vh.2021.06.009] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]

Abstract

The immune and endocrine systems collectively control homeostasis in the body. The endocrine system ensures that values of essential factors and nutrients such as glucose, electrolytes and vitamins are maintained within threshold values. The immune system resolves local disruptions in tissue homeostasis, caused by pathogens or malfunctioning cells. The immediate goals of these two systems do not always align. The immune system benefits from optimal access to nutrients for itself and restriction of nutrient availability to all other organs to limit pathogen replication. The endocrine system aims to ensure optimal nutrient access for all organs, limited only by the nutrients stores that the body has available. The actual state of homeostatic parameters such as blood glucose levels represents a careful balance based on regulatory signals from the immune and endocrine systems. This state is not static but continuously adjusted in response to changes in the current metabolic needs of the body, the amount of resources it has available and the level of threats it encounters. This balance is maintained by the ability of the immune and endocrine systems to interact and co-regulate systemic metabolism. In context of metabolic disease, this system is disrupted, which impairs functionality of both systems. The failure of the endocrine system to retain levels of nutrients such as glucose within threshold values impairs functionality of the immune system. In addition, metabolic stress of organs in context of obesity is perceived by the immune system as a disruption in local homeostasis, which it tries to resolve by the excretion of factors which further disrupt normal metabolic control. In this chapter, we will discuss how the immune and endocrine systems interact under homeostatic conditions and during infection with a focus on blood glucose regulation. In addition, we will discuss how this system fails in the context of metabolic disease.

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Differential Expression of the Host Lipid Regulators ANGPTL-3 and ANGPTL-4 in HCV Infection and Treatment. Int J Mol Sci 2021;22:ijms22157961. [PMID: 34360721 PMCID: PMC8348577 DOI: 10.3390/ijms22157961] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/15/2021] [Revised: 07/20/2021] [Accepted: 07/22/2021] [Indexed: 11/29/2022] Open

Frías M, Rivero-Juárez A, Machuca I, Camacho Á, Rivero A. The outlook for precision medicine for the treatment of chronic hepatitis C infection: challenges and opportunities. EXPERT REVIEW OF PRECISION MEDICINE AND DRUG DEVELOPMENT 2020. [DOI: 10.1080/23808993.2020.1764346] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/24/2022]

Wang CC, Cheng PN, Kao JH. Systematic review: chronic viral hepatitis and metabolic derangement. Aliment Pharmacol Ther 2020;51:216-230. [PMID: 31746482 DOI: 10.1111/apt.15575] [Citation(s) in RCA: 78] [Impact Index Per Article: 15.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/30/2019] [Revised: 08/08/2019] [Accepted: 10/17/2019] [Indexed: 12/12/2022]

Visfatin serum concentration and hepatic mRNA expression in chronic hepatitis C. Clin Exp Hepatol 2019;5:147-154. [PMID: 31501791 PMCID: PMC6728865 DOI: 10.5114/ceh.2019.85074] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/09/2018] [Accepted: 12/26/2018] [Indexed: 12/15/2022] Open

Wójcik K, Piekarska A, Dąbrowicz A, Stasiak M, Gawryś K, Jabłonowska E. Hepatic Expression of Phosphorylated Kinase Akt and Glycogen Synthase Kinase-3 Isoforms in Patients with Chronic Hepatitis C. Viral Immunol 2019;32:179-185. [PMID: 31091179 DOI: 10.1089/vim.2018.0141] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/12/2022] Open

Cardoso AC, Perez RM, de Figueiredo-Mendes C, Carvalho Leite N, Moraes-Coelho HS, Villela-Nogueira CA. Prevalence and predictive factors of moderate/severe liver steatosis in chronic hepatitis C (CHC) infected patients evaluated with controlled attenuation parameter (CAP). J Viral Hepat 2018;25:1244-1250. [PMID: 29768686 DOI: 10.1111/jvh.12930] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/26/2017] [Accepted: 04/16/2018] [Indexed: 12/15/2022]

Tsao YC, Chen JY, Yeh WC, Peng YS, Li WC. Association between visceral obesity and hepatitis C infection stratified by gender: a cross-sectional study in Taiwan. BMJ Open 2017;7:e017117. [PMID: 29133317 PMCID: PMC5695385 DOI: 10.1136/bmjopen-2017-017117] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/13/2022] Open

Riaz S, Bashir MF, Haider S, Rahid N. Association of genotypes with viral load and biochemical markers in HCV-infected Sindhi patients. Braz J Microbiol 2016;47:980-986. [PMID: 27528079 PMCID: PMC5052380 DOI: 10.1016/j.bjm.2016.07.014] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/09/2015] [Accepted: 04/05/2016] [Indexed: 12/16/2022] Open

Stevenson HL, Utay NS. Hepatic steatosis in HCV-infected persons in the direct-acting antiviral era. Trop Dis Travel Med Vaccines 2016;2:21. [PMID: 28883965 PMCID: PMC5530934 DOI: 10.1186/s40794-016-0038-5] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/18/2016] [Accepted: 09/22/2016] [Indexed: 02/07/2023] Open

Rojas Á, Del Campo JA, Clement S, Lemasson M, García-Valdecasas M, Gil-Gómez A, Ranchal I, Bartosch B, Bautista JD, Rosenberg AR, Negro F, Romero-Gómez M. Effect of Quercetin on Hepatitis C Virus Life Cycle: From Viral to Host Targets. Sci Rep 2016;6:31777. [PMID: 27546480 PMCID: PMC4992894 DOI: 10.1038/srep31777] [Citation(s) in RCA: 71] [Impact Index Per Article: 7.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/17/2016] [Accepted: 07/26/2016] [Indexed: 12/13/2022] Open

Affiliation(s)

Ángela Rojas UCM Digestive Diseases, Virgen Macarena-Virgen del Rocío University Hospitals and CIBERehd, Institute of Biomedicine, University of Sevilla, Sevilla, Spain.,Unit for the Clinical Management of Digestive Diseases, Hospital Universitario Valme de Sevilla, Sevilla, Spain
Jose A Del Campo Unit for the Clinical Management of Digestive Diseases, Hospital Universitario Valme de Sevilla, Sevilla, Spain
Sophie Clement Division of Clinical Pathology, University Hospital, Geneva, Switzerland
Matthieu Lemasson University Paris Descartes, EA 4474 "Hepatitis C Virology", France
Marta García-Valdecasas UCM Digestive Diseases, Virgen Macarena-Virgen del Rocío University Hospitals and CIBERehd, Institute of Biomedicine, University of Sevilla, Sevilla, Spain.,Unit for the Clinical Management of Digestive Diseases, Hospital Universitario Valme de Sevilla, Sevilla, Spain
Antonio Gil-Gómez UCM Digestive Diseases, Virgen Macarena-Virgen del Rocío University Hospitals and CIBERehd, Institute of Biomedicine, University of Sevilla, Sevilla, Spain.,Unit for the Clinical Management of Digestive Diseases, Hospital Universitario Valme de Sevilla, Sevilla, Spain
Isidora Ranchal Unit for the Clinical Management of Digestive Diseases, Hospital Universitario Valme de Sevilla, Sevilla, Spain
Birke Bartosch Inserm U1052, Cancer Research Centre, University of Lyon, France DevWeCan Laboratories of Excellence Network (Labex), Lyon, France
Juan D Bautista Biochemistry and Molecular Biology, Faculty of Pharmacy, University of Sevilla, Spain
Arielle R Rosenberg University Paris Descartes, EA 4474 "Hepatitis C Virology", France
Francesco Negro Division of Clinical Pathology, University Hospital, Geneva, Switzerland.,Division of Gastroenterology and Hepatology, University Hospital, Geneva, Switzerland
Manuel Romero-Gómez UCM Digestive Diseases, Virgen Macarena-Virgen del Rocío University Hospitals and CIBERehd, Institute of Biomedicine, University of Sevilla, Sevilla, Spain

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Desrochers GF, Sherratt AR, Blais DR, Nasheri N, Ning Z, Figeys D, Goto NK, Pezacki JP. Profiling Kinase Activity during Hepatitis C Virus Replication Using a Wortmannin Probe. ACS Infect Dis 2015;1:443-52. [PMID: 27617927 DOI: 10.1021/acsinfecdis.5b00083] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]

Federico A, Masarone M, Romano M, Dallio M, Rosato V, Persico M. Rapid Virological Response Represents the Highest Prediction Factor of Response to Antiviral Treatment in HCV-Related Chronic Hepatitis: a Multicenter Retrospective Study. HEPATITIS MONTHLY 2015;15:e18640. [PMID: 26286149 PMCID: PMC4532787 DOI: 10.5812/hepatmon.15(6)2015.18640] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Subscribe] [Scholar Register] [Received: 02/28/2014] [Revised: 05/26/2014] [Accepted: 06/22/2014] [Indexed: 12/11/2022]

Abstract

BACKGROUND

Standard [i.e. pegylated interferon (Peg-IFN) + ribavirin] treatment of hepatitis C virus (HCV)-related chronic hepatitis is associated with a sustained virological response (SVR) in 50 - 90% of patients. A rapid virological response (RVR) (i.e. negative HCV-RNA after 4 weeks of treatment) predicts SVR in almost 90% of patients.

OBJECTIVES

The main aim of this study was to assess the strength of RVR, as a predictive factor of antiviral treatment response.

PATIENTS AND METHODS

Using univariate and multivariate analysis, we retrospectively evaluated biochemical, metabolic, genetic and viral variables that might affect both RVR and SVR to Peg-IFN plus ribavirin, in 315 consecutive outpatients affected by HCV-related chronic hepatitis.

RESULTS

At univariate analysis, staging, body mass index, RVR, genotype and viral load were significantly related to SVR (P < 0.001). At multivariate analysis, RVR and genotype remained significant (P < 0.00001). The RVR had a predictive value of 83%. At univariate and multivariate analyses, diabetes (P = 0.003), genotype 2 (P = 0.000) and HCV-RNA values (P = 0.016) were independent predictors of RVR, even though at multivariate analyses, only genotype 2 was significantly related to RVR. When we stratified patients, according to genotype, no laboratory or clinical factors were predictive of RVR in genotype 1 patients at either univariate or multivariate analysis. In genotype 2 patients, staging (P = 0.029) and diabetes (P = 0.001) were the only significant predictors of RVR at univariate analyses, whereas no factor was independently related to RVR, at multivariate analysis.

CONCLUSIONS

The RVR is the strongest factor of SVR and infection with HCV genotype 2 is significantly associated with RVR. Neither biochemical and/or metabolic factors seem to exert influence on RVR.

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González-Reimers E, Quintero-Platt G, Rodríguez-Gaspar M, Alemán-Valls R, Pérez-Hernández O, Santolaria-Fernández F. Liver steatosis in hepatitis C patients. World J Hepatol 2015;7:1337-1346. [PMID: 26052379 PMCID: PMC4450197 DOI: 10.4254/wjh.v7.i10.1337] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/31/2014] [Revised: 01/31/2015] [Accepted: 03/09/2015] [Indexed: 02/06/2023] Open

Abenavoli L, Masarone M, Peta V, Milic N, Kobyliak N, Rouabhia S, Persico M. Insulin resistance and liver steatosis in chronic hepatitis C infection genotype 3. World J Gastroenterol 2014;20:15233-15240. [PMID: 25386071 PMCID: PMC4223256 DOI: 10.3748/wjg.v20.i41.15233] [Citation(s) in RCA: 43] [Impact Index Per Article: 3.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/18/2014] [Revised: 04/28/2014] [Accepted: 06/13/2014] [Indexed: 02/06/2023] Open

Statins and Hepatitis C Virus Infection: An Old Therapy With New Scope. Am J Med Sci 2014;348:426-30. [DOI: 10.1097/maj.0000000000000291] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/18/2022]

Perticone M, Miceli S, Maio R, Caroleo B, Sciacqua A, Tassone EJ, Greco L, Staltari O, Sesti G, Perticone F. Chronic HCV infection increases cardiac left ventricular mass index in normotensive patients. J Hepatol 2014;61:755-60. [PMID: 24882051 DOI: 10.1016/j.jhep.2014.05.032] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/10/2014] [Revised: 05/19/2014] [Accepted: 05/20/2014] [Indexed: 12/13/2022]

Abstract

BACKGROUND & AIMS

Left ventricular hypertrophy (LVH), is an independent predictor for cardiovascular events. We investigated if chronic hepatitis C virus (HCV) infection and the related insulin resistance (IR)/hyperinsulinemia could influence the increase of left ventricular mass (LVM).

METHODS

We enrolled 260 outpatients matched for age, body mass index, gender, ethnicity: 52 with never-treated uncomplicated chronic HCV infection (HCV(+)), 104 never-treated hypertensives (HT) and 104 healthy subjects (NT). LVM was calculated according to the Devereux formula and indexed for body surface area. The following laboratory parameters were measured: fasting plasma glucose and insulin, total, LDL- and HDL-cholesterol, triglyceride, creatinine, e-GFR-EPI, HOMA. Quantitative HCV-RNA was assessed by PCR.

RESULTS

HCV(+) patients with respect to healthy normotensive subjects had an increased LVMI (100 ± 23 vs. 83 ± 15 g/m(2); p < 0.0001), similar to that observed in HT group (103 ± 25 g/m(2)). Regarding biochemical variables, HCV(+) patients, in comparison with normotensive healthy subjects, had higher triglyceride, creatinine, fasting insulin and HOMA (3.2 ± 1.3 vs. 2.5 ± 1.0; p < 0.0001). At linear regression analysis, the correlation between LVMI and HOMA was similar in HT (r = 0.528, p < 0.0001) and HCV(+) (r = 0.489, p < 0.0001) groups. At multiple regression analysis, HOMA resulted the major determinant of LMVI in all groups, explaining respectively 21.8%, 27.8%, and 23.9% of its variation in NT, HT and HCV(+). At correlational analysis HCV-RNA and HOMA demonstrated a strong and linear relationship between them, explaining the 72.4% of their variation (p = 0.022).

CONCLUSIONS

We demonstrated a significant and direct correlation between HOMA and LVMI in patients with chronic HCV infection, similar to that observed in hypertensives.

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The role of suppressors of cytokine signalling in human neoplasms. Mol Biol Int 2014;2014:630797. [PMID: 24757565 PMCID: PMC3976820 DOI: 10.1155/2014/630797] [Citation(s) in RCA: 46] [Impact Index Per Article: 4.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/11/2013] [Revised: 02/02/2014] [Accepted: 02/04/2014] [Indexed: 12/28/2022] Open

Rojas Á, del Campo JA, Maraver M, Aparcero R, García-Valdecasas M, Diago M, Carmona I, Andrade RJ, Solà R, Romero-Gómez M. Hepatitis C virus infection alters lipid metabolism depending on IL28B polymorphism and viral genotype and modulates gene expression in vivo and in vitro. J Viral Hepat 2014;21:19-24. [PMID: 24188401 DOI: 10.1111/jvh.12209] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/18/2013] [Accepted: 10/15/2013] [Indexed: 02/06/2023]

Abstract

Hepatitis C virus (HCV) interacts with lipid receptors to enter the cell, circulates as lipoviroparticle and is secreted as VLDL. We aimed to investigate the role of the rs12979860 polymorphism in the IL28B gene in 143 with chronic hepatitis C genotype 1, 144 infected with genotype 3, 90 genotype 4 and 413 noninfected individuals on lipid profile and to test the impact of HCV infection in an in vitro model on VLDL biosynthesis-related gene expression rs12979860 polymorphism was analysed using real-time PCR coupled to Fluorescence Resonance Energy Transfer (FRET). Huh7.5 (rs12979860 CT) and Huh7 (genotype CC) cells were infected with JFH-1 particles and serum from patients infected with genotypes 1 and 3. Gene expression of apolipoprotein B (apoB), microsomal triglyceride transfer protein (MTP), acetyl CoA carboxylase (ACC), diacylglycerol acyltransferase 2 (DGAT2), diacylglycerol acyltransferase 1 (DGAT1) and low-density lipoprotein receptor (LDLr) genes were determined by semiquantitative RT-PCR in vivo and in vitro. Genotype CC rs12979860 polymorphism was associated with significantly higher serum LDL and total cholesterol levels in patients with hepatitis C genotype 1 but not in patients with hepatitis C genotype 3, genotype 4 and control (noninfected) population. Genotype CC was more often seen in genotype 3 and healthy people in comparison with genotype 1; P = 0.001. In vitro results showed that HCV infection promotes lipid metabolism gene expression induction depending on viral genotype, but to a lesser extent in cells with CT genotype. These results demonstrate that IL28B genotype influences lipid metabolism in patients with hepatitis C but not in noninfected and it seems to be viral genotype-mediated. HCV infection modifies lipid-related genes expression (DGAT1 and DGAT2) in cultured cells based on viral genotype and IL28 polymorphism.

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Eslam M, Booth DR, George J, Ahlenstiel G. Interaction of IFNL3 with insulin resistance, steatosis and lipid metabolism in chronic hepatitis C virus infection. World J Gastroenterol 2013;19:7055-7061. [PMID: 24222948 PMCID: PMC3819540 DOI: 10.3748/wjg.v19.i41.7055] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/27/2013] [Revised: 09/14/2013] [Accepted: 09/29/2013] [Indexed: 02/06/2023] Open

Laurito MP, Parise ER. Association between insulin resistance and sustained virologic response in hepatitis C treatment, genotypes 1 versus 2 and 3: systematic literature review and meta-analysis. Braz J Infect Dis 2013;17:555-63. [PMID: 24055394 PMCID: PMC9425142 DOI: 10.1016/j.bjid.2013.02.009] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/21/2012] [Accepted: 02/06/2013] [Indexed: 02/06/2023] Open

Abstract

Background/aims

Controversial results have been found in literature for the association between insulin resistance and sustained virologic response to standard chronic hepatitis C treatment. This study aims to provide a systematic literature review with meta-analysis, in order to evaluate if insulin resistance interferes with sustained virologic response in patients infected by the HCV genotype 1 versus HCV genotypes 2 and 3, undergoing treatment with interferon and ribavirin or pegylated interferon and ribavarin.

Methods

Systematic search was performed on main electronic databases until May 2012. Primary outcome was sustained virologic response, defined as undetectable levels of HCV-RNA six months after the end of treatment. Meta-analytic measure was estimated using Dersimonian and Laird's method, using Stata software.

Results

Thirteen studies involving 2238 infected patients were included. There was a statistically significant association between insulin resistance and lower sustained virologic response rate, and this difference occurred in HCV genotype G1 (OR: 2.23; 95% CI: 1.59–3.13) and G2/G3 (OR: 4.45; 95% CI: 1.59–12.49). In addition, a difference was seen in the cut-offs used for defining insulin resistance by Homeostasis Model Assessment of Insulin Resistance. To minimize this limitation, sub-analysis that excluded the studies that did not use 2 as a cut-off value was performed and the results still demonstrated association between insulin resistance and sustained virologic response, for both genotypic groups.

Conclusion

This meta-analysis provides evidence that elevated Homeostasis Model Assessment of Insulin Resistance is associated with a lower sustained virologic response rate in patients with hepatitis C treated with interferon and ribavirin or pegylated interferon and ribavarin, regardless of their genotype.

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Li WC, Lee YY, Chen IC, Sun C, Chiu FH, Chuang CH. Association between the hepatitis B and C viruses and metabolic diseases in patients stratified by age. Liver Int 2013;33:1194-202. [PMID: 23782533 DOI: 10.1111/liv.12224] [Citation(s) in RCA: 25] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/19/2012] [Accepted: 05/11/2013] [Indexed: 12/26/2022]

Tripathi LP, Kambara H, Chen YA, Nishimura Y, Moriishi K, Okamoto T, Morita E, Abe T, Mori Y, Matsuura Y, Mizuguchi K. Understanding the Biological Context of NS5A–Host Interactions in HCV Infection: A Network-Based Approach. J Proteome Res 2013;12:2537-51. [DOI: 10.1021/pr3011217] [Citation(s) in RCA: 25] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/08/2023]

Adinolfi LE, Restivo L, Marrone A. The predictive value of steatosis in hepatitis C virus infection. Expert Rev Gastroenterol Hepatol 2013;7:205-13. [PMID: 23445230 DOI: 10.1586/egh.13.7] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/18/2022]

Aghemo A, Prati GM, Rumi MG, Soffredini R, D'Ambrosio R, Orsi E, De Nicola S, Degasperi E, Grancini V, Colombo M. Sustained virological response prevents the development of insulin resistance in patients with chronic hepatitis C. Hepatology 2012;56:1681-7. [PMID: 22619107 DOI: 10.1002/hep.25867] [Citation(s) in RCA: 80] [Impact Index Per Article: 6.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/20/2012] [Accepted: 05/15/2012] [Indexed: 12/17/2022]

Abstract

UNLABELLED

Hepatitis C virus (HCV) infection is associated with insulin resistance (IR), which is a condition known to influence the progression of liver fibrosis and the response to pegylated interferon (PEG-IFN)/ribavirin (RBV) therapy. We aimed to assess whether a sustained virological response (SVR) after antiviral therapy prevents the development of IR in the long term. Members of the Milan Safety Tolerability study cohort, who received PEG-IFNα2a/RBV or PEG-IFNα2b/RBV, underwent a homeostasis model assessment (HOMA) at the baseline and 24 months after treatment completion. For all patients (n = 431), a liver biopsy sample was scored for grading, staging (Ishak), and steatosis. At the baseline, IR (HOMA value > 2) was detected in 48 patients (12%), and it was associated with body weight (P = 0.03), an HCV load < 0.6 × 10(6) IU/L (P = 0.006), fibrosis staging ≥ 4 (P = 0.01), and moderate to severe steatosis (P = 0.03). IR did not influence the rates of end-of-treatment response (75% versus 69%, P = 0.4), SVR (63% versus 60%, P = 0.8), or relapse (19% versus 24%, P = 0.5). After treatment, IR developed in 49 of the 384 nondiabetic patients (14%). Although the mean baseline and posttreatment HOMA values were similar in SVR patients (1.11 ± 0.8 versus 1.18 ± 1.1, P = 0.25), patients experiencing treatment failure showed a significant increase in the mean HOMA value at the follow-up visit (1.20 ± 0.85 versus 1.49 ± 1.3, P = 0.007), and there was an increased rate of de novo IR in non-SVR patients versus SVR patients (17% versus 7%, P = 0.007). According to a logistic regression analysis, treatment failure (odds ratio = 2.81, 95% confidence interval = 1.39-5.67, P = 0.004) and a 10% body mass index increase (odds ratio = 6.42, 95% confidence interval = 1.69-24.3, P = 0.006) were significantly associated with the development of de novo IR.

CONCLUSION

In nondiabetic patients with chronic HCV, the achievement of SVR with PEG-IFN and RBV prevents the development of de novo IR.

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Del Campo JA, Rojas &A, Romero-Gómez M. Entry of hepatitis C virus into the cell: a therapeutic target. World J Gastroenterol 2012;18:4481-5. [PMID: 22969220 PMCID: PMC3435772 DOI: 10.3748/wjg.v18.i33.4481] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/05/2012] [Revised: 08/13/2012] [Accepted: 08/16/2012] [Indexed: 02/06/2023] Open

Chung WJ. [Chronic hepatitis C and insulin resistance]. THE KOREAN JOURNAL OF GASTROENTEROLOGY 2012;59:268-74. [PMID: 22544023 DOI: 10.4166/kjg.2012.59.4.268] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/03/2022]

Chen W, Tomlinson G, Krahn M, Heathcote J. Immigrant patients with chronic hepatitis C and advanced fibrosis have a higher risk of hepatocellular carcinoma. J Viral Hepat 2012;19:574-80. [PMID: 22762142 DOI: 10.1111/j.1365-2893.2012.01583.x] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/16/2023]

Tripathi LP, Kambara H, Moriishi K, Morita E, Abe T, Mori Y, Chen YA, Matsuura Y, Mizuguchi K. Proteomic analysis of hepatitis C virus (HCV) core protein transfection and host regulator PA28γ knockout in HCV pathogenesis: a network-based study. J Proteome Res 2012;11:3664-79. [PMID: 22646850 DOI: 10.1021/pr300121a] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]

Oliveira LPM, Jesus RPD, Boulhosa RSSB, Mendes CMC, Gnoatto MC, Lemaire DC, Toralles MBP, Cavalcante LN, Lyra AC, Lyra LGC. Effect of soy protein supplementation in patients with chronic hepatitis C: a randomized clinical trial. World J Gastroenterol 2012;18:2203-11. [PMID: 22611313 PMCID: PMC3351770 DOI: 10.3748/wjg.v18.i18.2203] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/01/2011] [Revised: 09/09/2011] [Accepted: 03/28/2012] [Indexed: 02/06/2023] Open

Abstract

AIM

To evaluate the effects of soy supplementation on insulin resistance, fatty liver and alanine aminotransferase (ALT) levels in non-diabetic patients with chronic hepatitis C (CHC).

METHODS

In a prospective, randomized and single-blinded clinical trial, we compared patients with CHC who had casein as a supplement (n = 80) (control group), with patients who consumed a soy supplement diet (n = 80) [intervention group (IG)]. Both groups received 32 g/d of protein for 12 wk.

RESULTS

Patients' baseline features showed that 48.1% were overweight, 43.7% had abdominal fat accumulation, 34.7% had hepatic steatosis and 36.3% had an homeostasis model assessment index of insulin resistance (HOMA-IR) ≥ 3.0. Descriptive analysis showed that protein supplementation diet reduced hepatic steatosis in both groups; however, significant reductions in ALT levels occurred in the soy group. Multiple regression modeling indicated that in the presence of severe fibrosis (F3/F4), γ glutamyl transferase elevation and high density lipoprotein (HDL) reduction, the intervention group had 75% less chance of developing hepatic steatosis (OR= 0.25; 95% CI: 0.06-0.82) and 55% less chance of presenting with an ALT level ≥ 1.5 × the upper limit of normal (ULN) (OR = 0.45, 95% CI: 0.22-0.89). Soy treatment did not have any effect on insulin resistance (OR = 1.92; 95% CI: 0.80-4.83), which might be attributed to the fact that the HOMA-IR values at baseline in most of our patients were in the normal range. Advanced hepatic fibrosis, an ALT level > 1.5 × ULN and visceral fat were predictors of an HOMA-IR ≥ 3. The IG group had a reduced risk of an ALT level > 1.5 × ULN. An HOMA-IR ≥ 3.0 and HDL < 35 mg/dL were also risk factors for increased ALT.

CONCLUSION

Soy supplementation decreased ALT levels and thus may improve liver inflammation in hepatitis C virus (HCV) patients; it also reduced hepatic steatosis in a subgroup of patients but did not change insulin resistance. It should be considered in the nutritional care of HCV patients.

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El-Zayadi AR, Anis M. Hepatitis C virus induced insulin resistance impairs response to anti viral therapy. World J Gastroenterol 2012;18:212-24. [PMID: 22294824 PMCID: PMC3261538 DOI: 10.3748/wjg.v18.i3.212] [Citation(s) in RCA: 40] [Impact Index Per Article: 3.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/14/2011] [Revised: 06/20/2011] [Accepted: 06/21/2011] [Indexed: 02/06/2023] Open

IRS1 Expression in Hepatic Tissue and Leukocytes in Chronic Hepatitis C Virus Infected Patients: A Comparative Study. Int J Hepatol 2012;2012:698905. [PMID: 22830036 PMCID: PMC3398587 DOI: 10.1155/2012/698905] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/28/2012] [Revised: 04/18/2012] [Accepted: 05/04/2012] [Indexed: 02/07/2023] Open

Ivanyi-Nagy R, Darlix JL. Fuzziness in the Core of the Human Pathogenic Viruses HCV and HIV. ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY 2012;725:142-58. [DOI: 10.1007/978-1-4614-0659-4_9] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/04/2023]

Hübscher SG. Steatosis and fibrosis progression in patients with recurrent hepatitis C infection: complex interactions providing diagnostic and therapeutic challenges. Liver Transpl 2011;17:1374-9. [PMID: 22006866 DOI: 10.1002/lt.22452] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]

Lipid and carbohydrate parameters in children with chronic hepatitis C. Adv Med Sci 2011;56:180-5. [PMID: 22112430 DOI: 10.2478/v10039-011-0048-5] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]

Mohamed AA, Loutfy SA, Craik JD, Hashem AGM, Siam I. Chronic hepatitis c genotype-4 infection: role of insulin resistance in hepatocellular carcinoma. Virol J 2011;8:496. [PMID: 22044490 PMCID: PMC3218090 DOI: 10.1186/1743-422x-8-496] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/06/2011] [Accepted: 11/01/2011] [Indexed: 12/16/2022] Open

Patel K, Thompson AJ, Chuang WL, Lee CM, Peng CY, Shanmuganathan G, Thongsawat S, Tanwandee T, Mahachai V, Pramoolsinsap C, Cho M, Han KH, Shah SR, Foster GR, Clark PJ, Pulkstenis E, Subramanian GM, McHutchison JG. Insulin resistance is independently associated with significant hepatic fibrosis in Asian chronic hepatitis C genotype 2 or 3 patients. J Gastroenterol Hepatol 2011;26:1182-8. [PMID: 21410752 DOI: 10.1111/j.1440-1746.2011.06722.x] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]

Abstract

BACKGROUND AND AIM

The role of insulin resistance (IR) and hepatic steatosis in fibrogenesis in chronic hepatitis C infection (CHC) has yielded conflicting data and few studies have been performed in Asian-region populations. We retrospectively investigated the relationship between host metabolic variables, including IR and hepatic steatosis, to hepatic fibrosis in Asian-region CHC genotype 2/3 patients.

METHODS

A total of 303 treatment-naïve Asian-region patients with CHC genotype 2/3 were enrolled in a multicenter phase 3 study of albinterferon alfa-2b plus ribavirin for 24 weeks. IR was defined as Homeostasis Model for Assessment of IR (HOMA-IR) > 2. Baseline liver biopsy was evaluated by a single expert histopathologist. Post hoc subgroup logistic regression modeling selected for independent variables associated with significant fibrosis (METAVIR stage F2-F4).

RESULTS

Insulin resistance was available in 263 non-diabetic Asian-region patients (hepatitis C virus-2 [HCV-2] = 171, HCV-3 = 92), and 433 non-Asian region patients (407 "Caucasian"); METAVIR fibrosis prevalence F0-F1 (minimal fibrosis)= 201 (77%) and F2-F4 (significant fibrosis) = 59 (23%), and steatosis prevalence of grade 0 = 169 (65%), grade 1 = 64 (25%), grade 2/3 = 27 (10%). Median HOMA-IR was 1.8 (interquartile range: 1.2-2.7); 100 (38%) patients had HOMA-IR > 2. Factors independently associated with significant fibrosis included HOMA-IR (odds ratio [OR]= 8.42), necro-inflammatory grade (OR = 3.17), age (OR = 1.07) and serum total cholesterol levels (OR = 0.008). This was similar to non-Asian region patients, but steatosis was not associated with significant fibrosis in either cohort.

CONCLUSIONS

In this subgroup study of Asian-region HCV genotype 2 or 3 patients, insulin resistance, along with age, cholesterol levels and necro-inflammation, but not steatosis may be associated with significant hepatic fibrosis.

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Ahmed AM, Hassan MS, Abd-Elsayed A, Hassan H, Hasanain AF, Helmy A. Insulin resistance, steatosis, and fibrosis in Egyptian patients with chronic Hepatitis C virus infection. Saudi J Gastroenterol 2011;17:245-51. [PMID: 21727730 PMCID: PMC3133981 DOI: 10.4103/1319-3767.82578] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/26/2022] Open

Lamb P, Harrison S. Metabolic Syndrome and HCV: Where Do We Stand in 2010? ACTA ACUST UNITED AC 2010. [DOI: 10.1007/s11901-010-0044-4] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]

Palaniswamy C, Aronow WS, Sukhija R, Chugh T, Ramdeen N, Kalapatapu K, Weiss MB, Pucillo AL, Monsen CE. Major adverse cardiac events in patients with hepatitis C infection treated with bare-metal versus drug-eluting stents. Clin Cardiol 2010;33:367-370. [PMID: 20556808 PMCID: PMC6653466 DOI: 10.1002/clc.20764] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/03/2010] [Revised: 02/17/2010] [Indexed: 11/10/2022] Open

Kawaguchi T, Sata M. Importance of hepatitis C virus-associated insulin resistance: Therapeutic strategies for insulin sensitization. World J Gastroenterol 2010;16:1943-52. [PMID: 20419831 PMCID: PMC2860071 DOI: 10.3748/wjg.v16.i16.1943] [Citation(s) in RCA: 50] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open

Abstract

Insulin resistance is one of the pathological features in patients with hepatitis C virus (HCV) infection. Generally, persistence of insulin resistance leads to an increase in the risk of life-threatening complications such as cardiovascular diseases. However, these complications are not major causes of death in patients with HCV-associated insulin resistance. Indeed, insulin resistance plays a crucial role in the development of various complications and events associated with HCV infection. Mounting evidence indicates that HCV-associated insulin resistance may cause (1) hepatic steatosis; (2) resistance to anti-viral treatment; (3) hepatic fibrosis and esophageal varices; (4) hepatocarcinogenesis and proliferation of hepatocellular carcinoma; and (5) extrahepatic manifestations. Thus, HCV-associated insulin resistance is a therapeutic target at any stage of HCV infection. Although the risk of insulin resistance in HCV-infected patients has been documented, therapeutic guidelines for preventing the distinctive complications of HCV-associated insulin resistance have not yet been established. In addition, mechanisms for the development of HCV-associated insulin resistance differ from lifestyle-associated insulin resistance. In order to ameliorate HCV-associated insulin resistance and its complications, the efficacy of the following interventions is discussed: a late evening snack, coffee consumption, dietary iron restriction, phlebotomy, and zinc supplements. Little is known regarding the effect of anti-diabetic agents on HCV infection, however, a possible association between use of exogenous insulin or a sulfonylurea agent and the development of HCC has recently been reported. On the other hand, insulin-sensitizing agents are reported to improve sustained virologic response rates. In this review, we summarize distinctive complications of, and therapeutic strategies for, HCV-associated insulin resistance. Furthermore, we discuss supplementation with branched-chain amino acids as a unique insulin-sensitizing strategy for patients with HCV-associated insulin resistance.

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Insulin resistance, hepatic steatosis and hepatitis C: A complex relationship with relevant clinical implications. Ann Hepatol 2010. [DOI: 10.1016/s1665-2681(19)31735-1] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 03/26/2023]

Tripathi LP, Kataoka C, Taguwa S, Moriishi K, Mori Y, Matsuura Y, Mizuguchi K. Network based analysis of hepatitis C virus Core and NS4B protein interactions. MOLECULAR BIOSYSTEMS 2010;6:2539-53. [DOI: 10.1039/c0mb00103a] [Citation(s) in RCA: 44] [Impact Index Per Article: 2.9] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]