Prevalence and Predictors of Hepatic Steatosis in Persons Living With HIV
|The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Know the risks and potential benefits of clinical studies and talk to your health care provider before participating. Read our disclaimer for details.|
|ClinicalTrials.gov Identifier: NCT04795219|
Recruitment Status : Recruiting
First Posted : March 12, 2021
Last Update Posted : August 12, 2021
|Condition or disease|
|NAFLD NAFLD-HIV Hiv|
NAFLD is the most prevalent of all liver disorders and is the most common cause of chronic aminotransferase elevations in the United States. NAFLD also represents a major health threat worldwide, with a substantial impact on healthcare expenditures in the US and Europe. With the availability of highly effective ART, chronic liver disease has become a leading cause of non-AIDS related morbidity and mortality in PLWH. NAFLD is projected to become the leading cause of liver disease in the aging HIV population. The reported prevalence of NAFLD in PLWH without viral hepatitis co-infection ranges from 15-54% when assessed by imaging modalities and vibration-controlled transient elastography (VCTE), and is up to 73% in studies including liver biopsy, exceeding the reported prevalence of NAFLD in the general population. These prevalence figures vary as different modalities [computed tomography (CT), ultrasound, or Controlled attenuation parameter (CAP)] and criteria to define NAFLD were used. Further, current reports of NAFLD prevalence in PLWH are largely limited to single centers with small numbers of participants, inclusion of patients with concurrent HCV or limiting the study population to single sex or military personnel and their dependents. Systematic characterization of NAFLD in PLWH requires a large, representative, multi-ethnic, multi-centric cohort, which is currently lacking.
While obesity, insulin resistance and other components of the metabolic syndrome have been reported in some studies to increase the risk for NAFLD in PLWH, they are not universally observed in all PLWH, as studies of men with HIV report lower incidence of hepatic steatosis and lower BMI compared to controls. The impact of HIV and ART on NAFLD risk has also been much debated, with some studies supporting a role for the duration of infection and ART agents used, and others showing no associations. Recent reports suggest a potential decrease in NAFLD/NASH frequency and severity with light to moderate alcohol consumption in the general population. While PLWH commonly report alcohol use, the effects of non-heavy alcohol consumption on NAFLD and NASH risk and severity have not been studied in this population. Similarly, while coffee consumption has reported benefits on NAFLD in the general population, this effect has not been explored in PLWH. Several genetic variants have been found to modulate the risk and severity of NAFLD in the general population (Primary NAFLD), such as PNPLA3, TM6SF2, FADS1, GCKR, MBOAT7, and HSD17B13. To date, only a few studies evaluated genetic variation as a risk for NAFLD and its severity in PLWH. Emerging studies suggest an important role for gut microbiome as well as circulating gut derived metabolites in modulating the severity of Primary NAFLD but similar studies are lacking in PLWH.
- To determine the prevalence of hepatic steatosis and NAFLD in a large, multicenter, and multiethnic cohort of PLWH.
- To enroll at least 1250 PLWH into a cross-sectional study. The presence of hepatic steatosis and NAFLD and advanced fibrosis will be defined based on clinical, diagnostic, and VCTE criteria. Core data collection will include clinical, demographic, behavioral, anthropometric and laboratory information.
- To evaluate the prevalence of alcoholic liver disease versus NAFLD and assess the effects of varying amounts of alcohol and other beverage consumption on the risk and severity of hepatic steatosis.
- To evaluate the relationship between host (age, sex/gender, race/ethnicity, obesity, genetic variants, gut microbiome, etc.), HIV disease (HIV-1 RNA level, CD4+ T cell count, HIV duration) and HIV treatment with ART (type and duration), and environmental (alcohol, coffee and other beverages, diet, physical activity, sleep, food insecurity) factors and the prevalence of hepatic steatosis and NAFLD in PLWH.
- To establish a robust specimen bank comprised of serum, plasma, genomic DNA as well as PBMC and stool at select sites.
|Study Type :||Observational|
|Estimated Enrollment :||1250 participants|
|Official Title:||Prevalence and Predictors of Hepatic Steatosis in Persons Living With HIV|
|Actual Study Start Date :||July 19, 2021|
|Estimated Primary Completion Date :||January 1, 2024|
|Estimated Study Completion Date :||June 1, 2024|
- Prevalence of hepatic steatosis in persons living with HIV (PLWH). [ Time Frame: Baseline ]Prevalence of hepatic steatosis in PLWH will be reported as the number of participants with hepatic steatosis, defined by controlled attenuation parameter (CAP) ≥263 dB/m, over the total number of participants assessed.
- Prevalence of nonalcoholic fatty liver disease (NAFLD) in PLWH [ Time Frame: Baseline ]Prevalence of NAFLD in PLWH will be reported as the number of participants with NAFLD, defined by CAP ≥263 dB/m and absence of significant alcohol consumption and other chronic liver diseases, over the total number of participants assessed.
- Prevalence of alcohol-related steatosis in PLWH. [ Time Frame: Baseline ]Prevalence of alcohol-related steatosis will be reported as the number of participants with CAP ≥263 dB/m and self-reported ≥3 drinks daily on average in men and ≥2 drinks daily on average in women over the total number of participants assessed.
- Prevalence of advanced fibrosis in PLWH. [ Time Frame: Baseline ]Prevalence of advanced fibrosis will be reported as the number of participants with liver stiffness measurement (LSM) of ≥12.1 kPa over the total number of participants assessed.
Biospecimen Retention: Samples With DNA
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT04795219
|Contact: Jennifer Price, MD, PhDemail@example.com|
|Contact: Tab Srisengfa, BSfirstname.lastname@example.org|
|United States, Alabama|
|University of Alabama||Not yet recruiting|
|Tuscaloosa, Alabama, United States, 35487|
|Contact: Olivia Hogue 205-975-4285 email@example.com|
|Principal Investigator: Turner Overton, MD|
|United States, California|
|University of California, San Diego||Recruiting|
|La Jolla, California, United States, 92037|
|Contact: Lori Edge 858-246-5333 firstname.lastname@example.org|
|Principal Investigator: Rohit Loomba, MD|
|University of California, San Francisco||Recruiting|
|San Francisco, California, United States, 94143|
|Contact: Tab Srisengfa 415-502-3725 email@example.com|
|Principal Investigator: Jennifer Price, MD, PhD|
|United States, Indiana|
|Indiana University School of Medicine||Recruiting|
|Indianapolis, Indiana, United States, 46202|
|Contact: Holly King 317-278-6200 firstname.lastname@example.org|
|Principal Investigator: Naga Chalasani, MD|
|United States, Maryland|
|John Hopkins University||Recruiting|
|Baltimore, Maryland, United States, 21287|
|Contact: Stephanie Katz 443-287-9605 email@example.com|
|Principal Investigator: Mark Sulkowski, MD|
|United States, North Carolina|
|Durham, North Carolina, United States, 27701|
|Contact: Mariko Kopping 919-684-4798 firstname.lastname@example.org|
|Principal Investigator: Susanna Naggie, MD|
|United States, Texas|
|University of Texas||Recruiting|
|Houston, Texas, United States, 77030|
|Contact: Ruda Mohaweche Ruda.Mohaweche@uth.tmc.edu|
|Principal Investigator: Jordan Lake, MD, MSc|
|United States, Virginia|
|Virginia Commonwealth University||Recruiting|
|Richmond, Virginia, United States, 23284|
|Contact: Paula Smith 804-828-2988 email@example.com|
|Principal Investigator: Richard Sterling, MD|
|Principal Investigator:||Jennifer Price, MD, PhD||University of California, San Francisco|
|Principal Investigator:||Jordan Lake, MD, MSc||University of Texas|