CROI 2019 Abstract eBook

Abstract eBook

Poster Abstracts

568 LIVER STIFFNESS AT SVR PREDICTS HEPATIC COMPLICATIONS IN HCV- INFECTED PATIENTS Anaïs Corma-Gómez 1 , María Iglesias 1 , Francisco Téllez 2 , Luis Morano 3 , Antonio Rivero-Juárez 4 , Maria J. Rios-Villegas 5 , Marta Santos 6 , Francisco Vera 7 , Jesus Santos 8 , Rafael Granados 9 , Dolores Merino 10 , Ignacio d. Santos Gil 11 , Juan Macías 1 , Juan A. Pineda 1 , for the Proyecto GEHEP-011 1 Hospital Universitario de Valme, Seville, Spain, 2 Hospital de la Línea de la Concepción, La Línea de la Concepción, Spain, 3 Hospital Universitario Alvaro Cunqueiro, Vigo, Spain, 4 Institutto Maimonides de Investigacion Biomedica de Cordoba, Córdoba, Spain, 5 Hospital Universitario Virgen Macarena, Sevilla, Spain, 6 Hospital de Jerez, Jerez de la Frontera, Spain, 7 Hospital General Universitario Santa Lucía, Cartagena, Spain, 8 Hospital Virgen de la Victoria, Málaga, Spain, 9 Hospital Universitario de Gran Canaria Dr Negrin, Las Palmas, Gran Canaria, 10 Complejo Hospitalario Universitario de Huelva, Huelva, Spain, 11 Hospital Universitario de La Princesa, Madrid, Spain Background: A minority of HCV-infected patients with sustained virological response (SVR) subsequently develops hepatic complications. Determining the factors that may identify patients with SVR at risk of poor clinical outcome are of the maximum interest. The objective of the study was to analyze the predictive ability of liver stiffness (LS) at the time of SVR for the emergence of liver complications in patients with advanced liver fibrosis treated with direct anting antiviral (DAA)-based therapy. Methods: Multicentric prospective cohort study. HCV-infected patients who met the following criteria were selected: 1) Achieved SVR with DAA-including regimens; 2) LS ≥9.5 kPa before starting therapy and; 3) LS measurement available at SVR. The primary end-point was the occurrence of a liver complication -hepatic decompensation or hepatocellular carcinoma (HCC)- or requiring liver transplant after SVR. The relationship between the time to the end-point and potential predictors of liver complications was assessed in a multivariate regression model for competitive risks. Results: 843 patients were included, 573 (68%) coinfected with HIV. 463 (55%) showed previous compensated cirrhosis. 50 (6%) had developed a liver decompensation prior to treatment and 787 (93%) had been treated with an interferon-free regimen. During a median (Q1-Q3) follow-up of 25.2 (15.8-30.6) months, 27 (3.2%) patients reached the primary end-point and 23 (2.7%) patients died. In the multivariate analysis, variables (subhazard ratio [SHR] [95% CI]) associated with developing a hepatic complication or requiring transplant were: pretreatment LS (1.03 [1.01-1.08] for 1 kPa increase), HCV genotype 3 (5.77 [2.33-14.33]), having achieved SVR with Peg-IFN-based therapy (3.70 [1.16-12.50]), prior hepatic decompensations (5.58 [1.95-15.99], CPT class B at SVR time (6.60 [2.02-21.50] and LS at the time of SVR (1.03 [1.01-1.01] for 1 kPa increase). Notably, none out of 482 patients with LS <14kPa at SVR time-point developed a liver complication or required hepatic transplant. 175 (34%) of the patients with LS>14 kPa prior to treatment had a value below this level at SVR-time point. Conclusion: LS at the time of SVR after DAA therapy predicts the clinical outcome of HCV-infected patients with advanced fibrosis, thus identifying candidates to be withdrawn from surveillance programs. Discontinuing HCC screening programs in patients with LS <14kPa at SVR may spare surveillance in over 30% of the patients currently undergoing it. 569 INFLAMMATION, ARTERIAL STIFFNESS, AND DIRECTLY ACTING ANTIVIRALS IN HCV AND HIV/HCV Sonika Malik 1 , Ruchi Bisen 1 , Melissa Osborn 1 , Sanjay Gandhi 1 , Grace A. McComsey 2 , Corrilynn O. Hileman 1 1 MetroHealth Medical Center, Cleveland, OH, USA, 2 University Hospitals Cleveland Medical Center, Cleveland, OH, USA Background: Coinfection with HCV increases cardiovascular disease (CVD) risk in HIV. Insulin resistance and heightened inflammation may contribute. While directly-acting antivirals (DAAs) improve glucose homeostasis and CVD risk in HCV-infected persons, the effect in HIV/HCV coinfection is less clear. Methods: This is a 24-week prospective, cohort study to compare baseline and changes in aortic pulse wave velocity (PWV), glucose homeostasis (HOMA-IR), systemic inflammation [interleukin-6 (IL6), soluble tumor necrosis factor α receptors 1 and 2 (sTNF-R1 and -R2)], monocyte activation (soluble CD14 and CD163), and gut integrity [intestinal fatty acid binding protein (IFAB)] among adults with HIV, HCV, HIV/HCV or neither infection (controls) and after HCV treatment in HCV and HIV/HCV. Adults without CVD or diabetes and on stable antiretroviral therapy (HIV and HIV/HCV) were included. Pairwise comparisons

of log-transformed outcome variables were made at baseline and absolute changes over 24 weeks were compared within and between groups that underwent HCV treatment. Analysis of covariance (ANCOVA) was used for adjustment. Results: 126 subjects (25 HIV, 35 HCV, 39 HIV/HCV, 27 controls) were included. 54 (30 HCV, 24 HIV/HCV) received DAAs and attained sustained virologic response (SVR). Groups were similar except HCV subjects were older (56 vs 51 years) and more likely to have HTN (51 vs 23%); controls were more likely Caucasian (85 vs 48%) and non-smokers (81 vs 38%). Of those who underwent HCV treatment, 77% initiated ledipasvir/sofosbuvir. Baseline PWV was not different among groups and 0-24 week changes were not significant within or between groups treated for HCV (p=0.46 for between group test). Baseline HOMA-IR was higher in HIV/HCV than HIV and HCV trended to be higher than controls, but did not change after DAAs (p=0.89 for between group test). Baseline IFAB and sCD163 were greater in HIV/HCV than HCV and HIV, respectively. Most inflammatory markers were higher in HCV and HIV than controls. The figure shows 0-24 week changes in the markers tested. Most markers improved in HCV, while they did not change in HIV/HCV. Changes in sTNF-R1 and sCD14 tended to be different between groups with improvements in HCV group only. Conclusion: After DAA treatment, immune activation and gut markers improved in the HCV group; no change was observed in the HIV/HCV group. Further, PWV did not improve in either group. Cardiac risk may remain elevated in HIV/HCV despite SVR with DAAs.

Poster Abstracts

570 EFFECT OF LIVER FIBROSIS STAGE AND DAA TREATMENT ON RISK OF CVD EVENTS IN ERCHIVES Adeel A. Butt , Peng Yan, Samia Aslam, Obaid S. Shaikh VA Pittsburgh Healthcare System, Pittsburgh, PA, USA Background: Hepatitis C virus (HCV) infection is associated with a higher risk of cardiovascular disease (CVD) events. Treatment with directly acting antiviral (DAA) regimens has been shown to reduce this risk in most, but not all studies. How liver fibrosis stage affects risk of incidence CVD events after treatment with DAA regimens is unknown. We undertook this study to determine the effect of baseline liver fibrosis stage upon the risk of incident CVD events in DAA-treated HCV infected persons, and compare it with untreated and those treated with older pegylated interferon-based (PEG) regimens. Methods: Within ERCHIVES (Electronically Retrieved Cohort of HCV Infected Veterans), we identified all persons treated for HCV for >=7 weeks and propensity-score matched group who never received HCV treatment. We excluded those with HIV, HBV and previously diagnosed CVD. Incidence rate (per 1,000 person-years) and risk factors for CVD events (Cox proportional hazards analysis) were stratified by liver fibrosis stage. Liver fibrosis stage was determined by FIB-4 score. CVD events were identified using ICD-9CM/ICD-10 codes. Kaplan-Meier plots were generated to show and compare CVD-free survival by fibrosis stage and treatment regimen. Results: Among 32,575 treated and same number of propensity-score matched untreated persons in the final dataset, median age was 58 years, 27%were Black race and 96%were male. The incidence rate for CVD events/1,000 person- years (95% CI) among the treated was as follows: FIB-4<1.25: 19.3 (17.2,21.4); FIB-4 1.26-3.25: 19.9 (18.4,21.5); FIB-4>3.25: 24.5 (21.5,27.6). Rates among

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