Hepatic steatosis, hepatitis C, and human immunodeficiency viruses: A complex interplay
Authors: Thomas Pembroke, Giada Sebastiani
Journal: Hepatology (2017)

Potential conflict of interest: Dr. Sebastiani consults, is on the speakers' bureau, and received grants from Merck. She is on the speakers' bureau for AbbVie and Gilead. The study was not funded. T.P. holds a Starter Grant for Clinical Lecturers from the Academy of Medical Sciences/Wellcome Trust (UK) and a Canadian Association of the Study of the Liver Clinical Hepatology Fellowship. G.S. holds a Chercheur‐Boursier career award from the Fonds de recherche du Québec–Santé (FRQ‐S). TO THE EDITOR: We read with great interest the detailed article from Price et al. about the prevalence of hepatic steatosis (HS) measured by magnetic resonance imaging (MRI) and spectroscopy in 356 adults with various serological status, as regards hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infection.1 Surprisingly, the researchers found that HS prevalence was highest in the uninfected (33%) and HIV monoinfected cases (28%), followed by the HCV monoinfected (19%) and HIV/HCV coinfected (11%). We feel that this article deserves several comments. First, Price et al. report a significant lower prevalence of HS in both HIV monoinfected and HIV/HCV coinfected patients than previous studies (Table 1). This may be reflective of specific characteristics of the included populations. In the study by Price et al., infected patients had significantly lower proportions of male sex and alcohol intake compared to uninfected controls and to previous studies. Body mass index (BMI) was also significantly lower in infected patients than uninfected subjects, particularly in those HIV/HCV coinfected. Studies adopting different diagnostic techniques, including liver biopsy, ultrasound, and controlled attenuation parameter (CAP), have consistently reported BMI as a cofactor of HS in both HIV monoinfected and HIV/HCV coinfected patients.2 Moreover, the significant variations in race in this study, with higher prevalence of black ethnicity in HIV/HCV coinfected patients, are likely to be inferring a lower risk profile. Second, a lower HS prevalence could be partly explained by fat loss attributed to higher proportions of advanced liver fibrosis in infected versus uninfected subjects, particularly in HIV/HCV coinfected patients. However, Price et al. adopted simple biomarkers to diagnose liver fibrosis, which have inferior accuracy to other noninvasive techniques.3 Third, although the whole study population was comprised of 356 study participants, the sample size of the four study groups was relatively small, particularly for HCV monoinfected (n = 57) and HIV/HCV coinfected (n = 70) groups. Although MRI and spectroscopy is an accurate technique allowing a quantitative estimation of liver fat, it is expensive and not recommended for routine use in the clinical setting, which can prevent implementation of large‐scale studies.4 Table 1 - Prevalence of HS in HIV Monoinfected and HIV/HCV Coinfected Individuals in Selected Studies Author/Journal/Year Design/Method N Patients HCV+ (%) Males (%) Alcohol Excess (%) Ethnicity (%) Prevalence of HS (%) Sulkowski AIDS 2005 Prospective/biopsy 112 100 64.3 46.4 Black (94) 40 Bani‐Sadr AIDS 2006 Retrospective/biopsy 395 100 73.4 0 White (75.7) 61 Macias Hepatology 2012 Retrospective/biopsy 146 100 73 25 White (100) 60 Morse Clin Infect Dis 2015 Prospective/biopsy 62 0 94 0 White (65) 73 Guaraldi Clin Infect Dis 2008 Prospective/CT scan 341 0 72.4 0 NA 36.9 Li Vecchi Int J Infect Dis 2012 Prospective/ultrasound 57 0 67 11 NA 53 61 100 79 10 NA 54 Macias AIDS 2014 Prospective/FibroScan with CAP 505 50 69 11 White (95) 40 Vuille‐Lessard AIDS 2016 Prospective/FibroScan with CAP 300 0 70 0 White (42), Black (40) 48 Lombardi Dig Liver Dis 2016 Prospective/FibroScan with CAP 125 0 91 4 NA 55 Lui ATP 2016 Prospective/MRI spectroscopy 80 0 93 2 Asian (100) 28.7 Price Hepatology 2017 Prospective/MRI spectroscopy 122 0 53 4 White (53) 28 70 100 39 7 Black (59) 11 Abbreviations: CT, computed tomography; NA, not available. We conclude that the complex interaction and relative contribution of HIV, HCV, and HS need to be elucidated. The characteristics of the study population are likely to play a major role in dictating the prevalence of the disease. Given that HS is a dynamic condition, cross‐sectional studies may fail to reflect the true burden of disease. Longitudinal studies aimed to investigate incidence of HS, its effect on liver fibrosis, and identify risk factors where interventions can be targeted are warranted.