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Hepatitis C Virus and Nonalcoholic Fatty Liver Disease: Similar Risk Factors for Necroinflammation, Fibrosis, and Cirrhosis
CLINICAL GASTROENTEROLOGY AND HEPATOLOGY 2010;8:97–99
LETTERS TO THE EDITOR Readers are encouraged to write letters to the editor concerning articles that have been published in CLINICAL GASTROENTEROLOGY AND HEPATOLOGY. Short, general comments are also considered, but use of the Letters to the Editor section for publication of original data in preliminary form is not encouraged. Letters should be typewritten and submitted electronically to http://www.editorialmanager.com/cgh.
Hepatitis C Virus and Nonalcoholic Fatty Liver Disease: Similar Risk Factors for Necroinflammation, Fibrosis, and Cirrhosis Dear Editor: We read with great interest the recent article by Kallwitz et al,1 recently published in Clinical Gastroenterology and Hepatology. In their article, the investigators showed that both ethnicity and body mass index (BMI) were associated strongly with the severity of liver damage in patients with hepatitis C virus (HCV) infection. The investigators showed that the key predictors of steatosis, necroinflammation, fibrosis, and cirrhosis are as follows: ethnicity (in Hispanics the fibrosis index is higher than in non-Hispanic whites and African Americans) and increased BMI. In another recent work in this journal, Hanouneh et al,2 using a logistic regression analysis, found that ethnicity, higher BMI, high viral load, genotype 1, higher fibrosis stage, and metabolic syndrome, were significantly associated with a lack of sustained virologic response. Thus, HCV infection needs to be viewed not only as a chronic liver disease but also as a metabolic disease. Interestingly, the same risk factors lead to steatosis, necroinflammation, fibrosis, and cirrhosis during nonalcoholic fatty liver disease (NAFLD). In addition, HCV chronic infection resembles NAFLD in numerous features including the presence of steatosis, necroinflammation, and fibrosis, as well as insulin resistance and oxidative stress in the liver.3 These findings reinforce the idea that the pathways involved in the pathogenesis of hepatic steatosis, inflammation, and fibrosis could be quite similar regardless of etiology. Furthermore, the clinical impact of these results is remarkable because it significantly could influence the management of patients with both HCV- and NAFLD-associated liver damage, suggesting that lifestyle intervention and treatments directed against metabolic syndrome also could improve hepatitis C presentation and progression. DONATELLA COMPARCOLA, MD ANNA ALISI, PHD VALERIO NOBILI, MD Liver Unit Bambino Gesù Children’s Hospital and Research Institute Rome, Italy 1. Kallwitz ER, Layden-Almer J, Dhamija M, et al. Ethnicity and body mass index are associated with hepatitis C presentation and progression. Clin Gastroenterol Hepatol 2010;8;xxx–xxx. 2. Hanouneh IA, Feldstein AE, Lopez R, et al. Clinical significance of metabolic syndrome in the setting of chronic hepatitis C virus infection. Clin Gastroenterol Hepatol 2008;6:584 –589. 3. Balsano C, Alisi A, Nobili V. Liver fibrosis and therapeutic strategies: the goal for improving metabolism. Curr Drug Targets 2009; 10:505–512.
Conflicts of interest The authors disclose no conflicts. doi:10.1016/j.cgh.2009.09.005
Reply. Thank you for your interest in our work. As your correspondence mentions, the metabolic syndrome impacts the disease course of the hepatitis C virus (HCV) in multiple ways. When the histologic lesion of both nonalcoholic steatohepatitis and chronic HCV occurred in the same biopsy, fibrosis tended to be more advanced than those with HCV and bland steatosis.1 In addition, the effect that HCV exerts on metabolic disease is important. This effect recently was highlighted by a study that associated HCV with both peripheral and hepatic insulin resistance in chronically infected individuals without any components of the metabolic syndrome.2 Clearly, the relationship between chronic HCV and the metabolic syndrome is complex, and the end result appears to be more significant liver disease. It is likely that further examination of important disparities occurring in diverse populations with HCV will shed further light on the impact of metabolic disease on hepatic disease progression. As an example, recent research in fatty liver disease highlighted the importance of ethnic differences in intraperitoneal fat distribution,3 which also could impact on HCV. Multidisciplinary treatment, as in metabolic liver disease,4 also could impact HCV natural history and treatment outcomes favorably. Although further data are needed to examine the effects of lifestyle modifications on HCV, we agree that HCV needs to be viewed in context of the interplay between the virus and metabolic factors. ERIC R. KALLWITZ, MD Section of Hepatology University of Illinois Chicago, Illinois 1. Bedossa P, Moucari R, Chelbi E, et al. Evidence for a role of nonalcoholic steatohepatitis in hepatitis C: a prospective study. Hepatology 2007;46:380 –387. 2. Vanni E, Abate ML, Gentilcore E, et al. Sites and mechanisms of insulin resistance in nonobese, nondiabetic patients with chronic hepatitis C. Hepatology 2009;50:697–706. 3. Guerrero R, Vega GL, Grundy SM, et al. Ethnic differences in hepatic steatosis: an insulin resistance paradox? Hepatology 2009;49:791– 801. 4. Bellentani S, Dalle Grave R, Suppini A, et al. Behavior therapy for nonalcoholic fatty liver disease: the need for a multidisciplinary approach. Hepatology 2008;47:746 –754.
Conflicts of interest The authors disclose no conflicts. doi:10.1016/j.cgh.2009.10.030
LETTERS TO THE EDITOR Readers are encouraged to write letters to the editor concerning articles that have been published in CLINICAL GASTROENTEROLOGY AND HEPATOLOGY. Short, general comments are also considered, but use of the Letters to the Editor section for publication of original data in preliminary form is not encouraged. Letters should be typewritten and submitted electronically to http://www.editorialmanager.com/cgh.
Hepatitis C Virus and Nonalcoholic Fatty Liver Disease: Similar Risk Factors for Necroinflammation, Fibrosis, and Cirrhosis Dear Editor: We read with great interest the recent article by Kallwitz et al,1 recently published in Clinical Gastroenterology and Hepatology. In their article, the investigators showed that both ethnicity and body mass index (BMI) were associated strongly with the severity of liver damage in patients with hepatitis C virus (HCV) infection. The investigators showed that the key predictors of steatosis, necroinflammation, fibrosis, and cirrhosis are as follows: ethnicity (in Hispanics the fibrosis index is higher than in non-Hispanic whites and African Americans) and increased BMI. In another recent work in this journal, Hanouneh et al,2 using a logistic regression analysis, found that ethnicity, higher BMI, high viral load, genotype 1, higher fibrosis stage, and metabolic syndrome, were significantly associated with a lack of sustained virologic response. Thus, HCV infection needs to be viewed not only as a chronic liver disease but also as a metabolic disease. Interestingly, the same risk factors lead to steatosis, necroinflammation, fibrosis, and cirrhosis during nonalcoholic fatty liver disease (NAFLD). In addition, HCV chronic infection resembles NAFLD in numerous features including the presence of steatosis, necroinflammation, and fibrosis, as well as insulin resistance and oxidative stress in the liver.3 These findings reinforce the idea that the pathways involved in the pathogenesis of hepatic steatosis, inflammation, and fibrosis could be quite similar regardless of etiology. Furthermore, the clinical impact of these results is remarkable because it significantly could influence the management of patients with both HCV- and NAFLD-associated liver damage, suggesting that lifestyle intervention and treatments directed against metabolic syndrome also could improve hepatitis C presentation and progression. DONATELLA COMPARCOLA, MD ANNA ALISI, PHD VALERIO NOBILI, MD Liver Unit Bambino Gesù Children’s Hospital and Research Institute Rome, Italy 1. Kallwitz ER, Layden-Almer J, Dhamija M, et al. Ethnicity and body mass index are associated with hepatitis C presentation and progression. Clin Gastroenterol Hepatol 2010;8;xxx–xxx. 2. Hanouneh IA, Feldstein AE, Lopez R, et al. Clinical significance of metabolic syndrome in the setting of chronic hepatitis C virus infection. Clin Gastroenterol Hepatol 2008;6:584 –589. 3. Balsano C, Alisi A, Nobili V. Liver fibrosis and therapeutic strategies: the goal for improving metabolism. Curr Drug Targets 2009; 10:505–512.
Conflicts of interest The authors disclose no conflicts. doi:10.1016/j.cgh.2009.09.005
Reply. Thank you for your interest in our work. As your correspondence mentions, the metabolic syndrome impacts the disease course of the hepatitis C virus (HCV) in multiple ways. When the histologic lesion of both nonalcoholic steatohepatitis and chronic HCV occurred in the same biopsy, fibrosis tended to be more advanced than those with HCV and bland steatosis.1 In addition, the effect that HCV exerts on metabolic disease is important. This effect recently was highlighted by a study that associated HCV with both peripheral and hepatic insulin resistance in chronically infected individuals without any components of the metabolic syndrome.2 Clearly, the relationship between chronic HCV and the metabolic syndrome is complex, and the end result appears to be more significant liver disease. It is likely that further examination of important disparities occurring in diverse populations with HCV will shed further light on the impact of metabolic disease on hepatic disease progression. As an example, recent research in fatty liver disease highlighted the importance of ethnic differences in intraperitoneal fat distribution,3 which also could impact on HCV. Multidisciplinary treatment, as in metabolic liver disease,4 also could impact HCV natural history and treatment outcomes favorably. Although further data are needed to examine the effects of lifestyle modifications on HCV, we agree that HCV needs to be viewed in context of the interplay between the virus and metabolic factors. ERIC R. KALLWITZ, MD Section of Hepatology University of Illinois Chicago, Illinois 1. Bedossa P, Moucari R, Chelbi E, et al. Evidence for a role of nonalcoholic steatohepatitis in hepatitis C: a prospective study. Hepatology 2007;46:380 –387. 2. Vanni E, Abate ML, Gentilcore E, et al. Sites and mechanisms of insulin resistance in nonobese, nondiabetic patients with chronic hepatitis C. Hepatology 2009;50:697–706. 3. Guerrero R, Vega GL, Grundy SM, et al. Ethnic differences in hepatic steatosis: an insulin resistance paradox? Hepatology 2009;49:791– 801. 4. Bellentani S, Dalle Grave R, Suppini A, et al. Behavior therapy for nonalcoholic fatty liver disease: the need for a multidisciplinary approach. Hepatology 2008;47:746 –754.
Conflicts of interest The authors disclose no conflicts. doi:10.1016/j.cgh.2009.10.030