Researchers elucidate the prevalence of hepatic steatosis in patients infected with HIV, as well as in patients coinfected with HIV and HCV.
Hepatic steatosis, also known as fatty liver disease, is characterized by excessive fat being stored in liver cells. This condition elicits liver inflammation, and often progresses to liver cirrhosis and liver failure. Hepatic steatosis is the most common form of liver disease in the United States, affecting between 80 to 100 million individuals. Traditionally, to diagnose fatty liver disease, liver biopsies, in which a sample of liver tissue is examined for scarring and inflammation, were performed. However, liver biopsies are oftentimes painful and are associated with some risks. As a consequence, the invasiveness of traditional diagnostic procedures has hindered epidemiological studies concentering the prevalence of fatty liver disease in patient populations.
In a new study published in the Journal of Hepatology, lead investigator, Giada Sebastiani, MD, and her colleagues, sought to elucidate the prevalence of hepatic steatosis in patients infected with human immunodeficiency virus (HIV), as well as in patients coinfected with HIV and hepatitis C virus (HCV). This work stems from earlier studies which determined that between 30 to 70% of patients coinfected with HIV and HCV have fatty liver disease. However, contradictory studies exist, thus prompting Dr. Sebastiani and her colleagues to further investigate. In addition, the introduction of non-invasive tools, such as transient elastography (TE) and the controlled attenuation parameter (CAP), for the diagnosis of hepatic steatosis makes this undertaking possible. Briefly, TE measures liver stiffness and can be correlated to liver fibrosis while CAP relies on ultrasound attenuation by fat in the liver to diagnose hepatitis steatosis.
The authors began a screening program, called LIVEHIV, for hepatic steatosis and live fibrosis at McGill University in Canada in 2013. Patients in the study had to be at least 18-years-old and had to be HIV-positive. Patients were excluded if they presented evidence of other liver diseases, had evidence of liver cancer, or have had a liver transplant. After applying exclusion criteria, 726 HIV-infected patients were included in the study; of the 726 patients, approximately 23% were coinfected with HCV. The authors determined that HIV mono-infected patients had higher rates of hepatic steatosis progression (37.8 per 100 patients) than patients coinfected with HIV and HCV (21. 9 per 100 patients). The authors found that in HIV mono-infected patients, diagnosis of hepatic steatosis was a predictor of fibrosis progression. However, this was not the case in HIV/HCV coinfected patients. In addition, Dr. Sebastiani and her colleagues found that body mass index (BMI) was a major predictor of hepatic steatosis in HIV mono-infected patients.
This study represents the first prospective study to assess prevalence of hepatic steatosis and show that it is correlated with worsened fibrosis progression in HIV mono-infected patients. However, as acknowledged by the authors, several limitations of the study exist, such as the lack of controls from the general population as well as lack of histological and MRI spectroscopy to confirm the diagnosis of hepatic steatosis. Overall, this work shed light on hepatic steatosis dynamics in HIV mono-infected as well as patients co-infected with HIV/HCV. The authors conclude that hepatic steatosis is more common in mono-infected patients and is associated with progression of liver fibrosis. In addition, patients with higher BMI were found to be at increased risk of developing hepatic steatosis and future prophylactic efforts need to address this issue.
Samar Mahmoud graduated from Drew University in 2011 with a BA in Biochemistry and Molecular Biology. After two years of working in industry as a Quality Control Technician for a blood bank, she went back to school and graduated from Montclair State University in 2016 with an MS in Pharmaceutical Biochemistry. She is currently pursuing her PhD in Molecular and Cellular Biology at the University of Massachusetts at Amherst.