Alimentary Pharmacology and Therapeutics
Invited Editorials Editorial: NAFLD in HIV infection – call for action N. Bulteel* & C. Leen† *MRC Centre for Virus Research, University of Glasgow, Glasgow, UK. † University of Edinburgh, Western General Hospital, Edinburgh, UK. E-mail: [email protected] doi:10.1111/apt.13077
Non-alcoholic fatty liver disease (NAFLD) in HIV-positive patients is associated with HIV specific factors, such as lipodystrophy and the use of antiretroviral therapy (ART), as well as traditional risk factors (including obesity, insulin resistance and the metabolic syndrome).1, 2 The risk of metabolic syndrome is doubled in HIV-positive patients compared to healthy controls, and this increased incidence is observed in both antiretroviralexperienced and antiretroviral-na€ıve patients.3 In addition, HIV infection is associated with a higher risk of insulin resistance.4 As a consequence, and given the ageing HIV population, NAFLD has been reported in up to 15–60% of HIV-infected individuals.1, 5, 6 Vodkin et al. report that patients with HIV-associated NAFLD had significantly elevated aminotransferases and serum triglycerides, higher scores for non-invasive markers of fibrosis, increased rates of non-alcoholic steatohepatitis (NASH) and more features of liver injury on biopsy when compared to age–sex-matched controls with similar metabolic characteristics.7 Longer duration of HIV infection was the only variable significantly associated with the presence of NASH. It would be interesting to see data on the duration of ART, which the authors speculate may explain this observation. The authors did not find an association between antiretroviral regimen and incidence of NASH although numbers in each group were small and few patients were on antiretrovirals classically linked with NAFLD. Despite its limitations, this study provides important information on the severity of HIV-associated NAFLD. Non-invasive assessment of liver steatosis using transient
elastography is now available.8 Diagnosing and assessing severity of NAFLD/NASH should form part of the monitoring of HIV-positive individuals particularly for those with metabolic syndrome, or lipodystrophy and/or abnormal LFTs. Presently, lifestyle modification and dietary advice represent the only interventions for HIV-associated NAFLD outwith the treatment of specific metabolic disorders, and should be implemented aggressively as part of a multi-disciplinary approach to patient care.9, 10
ACKNOWLEDGEMENT Declaration of personal and funding interests: None. REFERENCES 1. Crum-Cianflone N, Dilay A, Collins G, et al. Nonalcoholic Fatty Liver Disease Paper among HIV-infected persons. J Acquir Immune Defic Syndr 2009; 50: 464–73. 2. Lemoine M, Serfaty L, Capeau J. From nonalcoholic fatty liver to nonalcoholic steatohepatitis and cirrhosis in HIV-infected patients: diagnosis and management. Curr Opin Infect Dis 2012; 25: 10–6. 3. Bonfanti P, Giannattasio C, Ricci E, et al. HIV and metabolic syndrome: a comparison with the general population. J Acquir Immune Defic Syndr 2007; 45: 426–31. 4. Grunfeld C. Insulin resistance in HIV infection: drugs, host responses, or restoration to health? Top HIV Med 2008; 16: 89–93. 5. Ingiliz P, Valantin MA, Duvivier C, et al. Liver damage underlying unexplained transaminase elevation in human immunodeficiency virus-1 mono-infected patients on antiretroviral therapy. Hepatology 2009; 49: 436–42. 6. Price JC, Seaberg EC, Latanich R, et al. Risk factors for fatty liver in the multicenter AIDS cohort study. Am J Gastroenterol 2014; 109: 695–704. 7. Vodkin I, Valasek MA, Bettencourt R, Cachay E, Loomba R. Clinical, biochemical and histological differences between HIVassociated NAFLD and primary NAFLD: a case–control study. Aliment Pharmacol Ther 2015; 41: 368–78. 8. Recio E, Cifuentes C, Macias J, et al. Interobserver concordance in controlled attenuation parameter measurement, a novel tool for the assessment of hepatic steatosis on the basis of transient elastography. Eur J Gastroenterol Hepatol 2013; 25: 905–11. 9. Lindegaard B, Hansen T, Hvid T, et al. The effect of strength and endurance training on insulin sensitivity and fat distribution in human immunodeficiency virus-infected patients with lipodystrophy. J Clin Endocrinol Metab 2008; 93: 3860–9. 10. Nascimbeni F, Pais R, Bellentani S, et al. From NAFLD in clinical practice to answers from guidelines. J Hepatol 2013; 59: 859–71.
AP&T invited editorial columns are restricted to discussing papers that have been published in the journal. An editorial must have a maximum of 300 words, may contain one table or figure, and should have no more than 10 references. It should be submitted electronically to the Editors via http://mc.manuscriptcentral.com/apt.
590
ª 2015 John Wiley & Sons Ltd
Invited Editorials Editorial: NAFLD in HIV infection – call for action N. Bulteel* & C. Leen† *MRC Centre for Virus Research, University of Glasgow, Glasgow, UK. † University of Edinburgh, Western General Hospital, Edinburgh, UK. E-mail: [email protected] doi:10.1111/apt.13077
Non-alcoholic fatty liver disease (NAFLD) in HIV-positive patients is associated with HIV specific factors, such as lipodystrophy and the use of antiretroviral therapy (ART), as well as traditional risk factors (including obesity, insulin resistance and the metabolic syndrome).1, 2 The risk of metabolic syndrome is doubled in HIV-positive patients compared to healthy controls, and this increased incidence is observed in both antiretroviralexperienced and antiretroviral-na€ıve patients.3 In addition, HIV infection is associated with a higher risk of insulin resistance.4 As a consequence, and given the ageing HIV population, NAFLD has been reported in up to 15–60% of HIV-infected individuals.1, 5, 6 Vodkin et al. report that patients with HIV-associated NAFLD had significantly elevated aminotransferases and serum triglycerides, higher scores for non-invasive markers of fibrosis, increased rates of non-alcoholic steatohepatitis (NASH) and more features of liver injury on biopsy when compared to age–sex-matched controls with similar metabolic characteristics.7 Longer duration of HIV infection was the only variable significantly associated with the presence of NASH. It would be interesting to see data on the duration of ART, which the authors speculate may explain this observation. The authors did not find an association between antiretroviral regimen and incidence of NASH although numbers in each group were small and few patients were on antiretrovirals classically linked with NAFLD. Despite its limitations, this study provides important information on the severity of HIV-associated NAFLD. Non-invasive assessment of liver steatosis using transient
elastography is now available.8 Diagnosing and assessing severity of NAFLD/NASH should form part of the monitoring of HIV-positive individuals particularly for those with metabolic syndrome, or lipodystrophy and/or abnormal LFTs. Presently, lifestyle modification and dietary advice represent the only interventions for HIV-associated NAFLD outwith the treatment of specific metabolic disorders, and should be implemented aggressively as part of a multi-disciplinary approach to patient care.9, 10
ACKNOWLEDGEMENT Declaration of personal and funding interests: None. REFERENCES 1. Crum-Cianflone N, Dilay A, Collins G, et al. Nonalcoholic Fatty Liver Disease Paper among HIV-infected persons. J Acquir Immune Defic Syndr 2009; 50: 464–73. 2. Lemoine M, Serfaty L, Capeau J. From nonalcoholic fatty liver to nonalcoholic steatohepatitis and cirrhosis in HIV-infected patients: diagnosis and management. Curr Opin Infect Dis 2012; 25: 10–6. 3. Bonfanti P, Giannattasio C, Ricci E, et al. HIV and metabolic syndrome: a comparison with the general population. J Acquir Immune Defic Syndr 2007; 45: 426–31. 4. Grunfeld C. Insulin resistance in HIV infection: drugs, host responses, or restoration to health? Top HIV Med 2008; 16: 89–93. 5. Ingiliz P, Valantin MA, Duvivier C, et al. Liver damage underlying unexplained transaminase elevation in human immunodeficiency virus-1 mono-infected patients on antiretroviral therapy. Hepatology 2009; 49: 436–42. 6. Price JC, Seaberg EC, Latanich R, et al. Risk factors for fatty liver in the multicenter AIDS cohort study. Am J Gastroenterol 2014; 109: 695–704. 7. Vodkin I, Valasek MA, Bettencourt R, Cachay E, Loomba R. Clinical, biochemical and histological differences between HIVassociated NAFLD and primary NAFLD: a case–control study. Aliment Pharmacol Ther 2015; 41: 368–78. 8. Recio E, Cifuentes C, Macias J, et al. Interobserver concordance in controlled attenuation parameter measurement, a novel tool for the assessment of hepatic steatosis on the basis of transient elastography. Eur J Gastroenterol Hepatol 2013; 25: 905–11. 9. Lindegaard B, Hansen T, Hvid T, et al. The effect of strength and endurance training on insulin sensitivity and fat distribution in human immunodeficiency virus-infected patients with lipodystrophy. J Clin Endocrinol Metab 2008; 93: 3860–9. 10. Nascimbeni F, Pais R, Bellentani S, et al. From NAFLD in clinical practice to answers from guidelines. J Hepatol 2013; 59: 859–71.
AP&T invited editorial columns are restricted to discussing papers that have been published in the journal. An editorial must have a maximum of 300 words, may contain one table or figure, and should have no more than 10 references. It should be submitted electronically to the Editors via http://mc.manuscriptcentral.com/apt.
590
ª 2015 John Wiley & Sons Ltd
