CROI 2018 Abstract eBook

Abstract eBook

Poster Abstracts

632 RISK OF DIABETES IN HCV-HIV PATIENTS IS ASSOCIATED WITH CIRRHOSIS, NOT WITH HCV

Aurélien Provoost 1 , Moustapha Drame 1 , Laurent Cotte 2 , Lise Cuzin 3 , Rodolphe Garraffo 4 , David Rey 5 , François Raffi 6 , Isabelle Poizot-Martin 7 , Pascal Puglièse 8 , Firouze Bani-Sadr 1 1 CHU de Reims, Reims, France, 2 Hospices Civils de Lyon, Lyon, France, 3 CHU de Toulouse, Toulouse, France, 4 CHU de Nice, Nice, France, 5 Hôpitaux Universitaires de Strasbourg, Strasbourg, France, 6 CHU de Nantes, Nantes, France, 7 Assistance Publique–Hopitaux Marseille, Marseille, France, 8 Nice University Hospital, Nice, France Background: Both HIV and hepatitis C (HCV) infections have been reportedly associated with a higher risk of diabetes mellitus (DM) but results are conflicting. The aim of this study was to determine whether there is an association between chronic HCV and the incidence of DM, and to study the role of factors such as cirrhosis, IFN-based HCV therapy, sustained virologic response (SVR) and chronic hepatitis B (HBV) infection among patients living with HIV (PLHIV) followed in a large French multicenter cohort in the combination antiretroviral therapy (cART) era. Methods: All PLHIV followed up in the Dat’AIDS cohort were eligible. Patients with preexisting DM or a diagnosis of DMwithin six months following HIV diagnosis, patients with spontaneous HCV cure or with no HCV serology were excluded. Cox models for survival analysis were used to study the time to occurrence of DM. Results: Among 28,699 PLHIV, 4,004 patients had chronic HCV-infection. The mean duration of HIV and HCV follow-up was 12.4±7.9 and 12.5±8.1 years, respectively. DM occurred in 969 (3.4%) patients overall. By multivariate analysis, increasing age (>50 years, HR 9.9, 95% CI 7.94-12.34, p<0.0001), elevated body mass index, cirrhosis (HR 2.26, 95% CI 1.79-2.85; p <0.0001), AIDS status (HR 1.35 95% CI 1.17-1.56; p<0.0001), nadir CD4 cell count ≤ 200/mm 3 (HR 1.49, 95% CI 1.29-1.73; p <0.0001) and detectable HIV viral load (HR 1.32 95% CI 1.05-1.65; p=0.017) were predictors of DM, whereas longer cART duration was associated with a lower risk of DM (HR 0.84 95% CI 0.83-0.85 p<0.0001). Chronic HCV and HBV-infection, IFN-based HCV therapy and lipodystrophy were not associated with DM. In a subanalysis among HCV-infected patients, SVR was not related to DM (HR 1.09 (95% CI 0.76-1.57); p=0.65). Conclusion: Our study shows that in PLHIV, cirrhosis is associated with an increased risk of DM, but not chronic HCV infection or duration of HCV infection. Furthermore, in the late cART era, the duration of cART was no longer associated with a higher risk of DM. Apart from HIV factors related to immunodeficiency (AIDS status, low nadir CD4 cell count and detectable HIV viral load), PLHIV share the same traditional risk factors for DM, such as age and BMI, as compared to the general population Ilaria Mastrorosa , Carmela Pinnetti, Patrizia Lorenzini, Alessandra Vergori, Gabriele Fabbri, Pietro Balestra, Maria Maddalena Plazzi, Martina Ricottini 1 , Rita Bellagamba, Stefania Cicalini, Rita Maddaluno, Mauro Zaccarelli, Adriana Ammassari, Andrea Antinori Lazzaro Spallanzani National Institute for Infectious Diseases, Rome, Italy Background: HCV may be implicated in the pathogenesis of neurocognitive impairment (NCI), but its precise contribution in the setting of the HIV infected (HIV+) population is still controversial. HCV-mediated liver injury may itself contribute to NCI. We investigated the effect of HCV infection and liver function (Lf) on neurocognition. Methods: From a prospective, monocenter, observational study conducted from January 2000 to July 2017 on neuropsychological (NP) evaluations, we selected HIV+ patients (pts) with known HCV status: negative serology (HCV-), positive serology (HCV+), viremic (RNA+), aviremic (RNA-). A comprehensive battery of 14 tests on 5 different domains was used to classify HIV-associated neurocognitive disorders (HAND) according to Frascati’s criteria. NPZ8 was used as summary measure of z-scores of NP tests. Fibrosis 4 score (Fib4) was calculated as measure of Lf. Chi-square and K-Wallis tests were used for statistical comparisons. Stepwise backward multivariable logistic regression was employed to investigate predictors of HAND. Results: Excluding pts with confounding factors for HAND diagnosis, we analyzed 1,305 pts: 953 HCV-, 109 HCV+RNA-, 243 HCV+RNA+. Male 79%, median age 45 yrs (IQR 38-52), median education 13 yrs (IQR 8-13), IDUs 17%,

631 ERADICATION OF HCV: EFFECTS ON CARDIOVASCULAR RISK AND PRECLINICAL ATHEROSCLEROSIS Ana Carrero 1 , Juan Berenguer 1 , Victor Hontanon 2 , Jordi Navarro 3 , José Hernández-Quero 4 , Maria J. Galindo 5 , Carmen Quereda 6 , Ignacio Santos 7 , María J. Téllez 8 , Enrique Ortega 9 , José Sanz 10 , Javier Bermejo 1 , José M. Bellón 1 , Juan González-García 2 1 General University Hospital Gregorio Marañón, Madrid, Spain, 2 La Paz University Hospital, Madrid, Spain, 3 Hospital Universitario de la Vall d’Hebron, Barcelona, Spain, 4 Hospital Universitario San Cecilio, Granada, Spain, 5 Hospital Clinic of Valencia, Valencia, Spain, 6 Hospital Ramon y Cajal, Madrid, Spain, 7 Hospital Universitario de La Princesa, Madrid, Spain, 8 Hospital Universitario Clínico San Carlos, Madrid, Spain, 9 Hospital General de Valencia, Valencia, Spain, 10 Hospital Universitario Príncipe de Asturias, Madrid, Spain Background: We previously showed that eradication of HCV in HIV/HCV- coinfected patients was associated a near-significant increase in the risk of cardiovascular events (Hepatology 2017; 66:344). We compared changes in 10-year Framingham cardiovascular risk (10y-CVR) and changes in noninvasive tests for preclinical atherosclerosis in coinfected patients with and without SVR receiving anti-HCV therapy (anti-HCV Rx). Methods: We performed a multicenter prospective study between February 2012 and March 2014. Serum lipids, 10y-CVR, arterial stiffness by carotid- femoral pulse wave velocity (PWV), and carotid intima-medial thickness (cIMT) by B-mode ultrasound were assessed at baseline and 96 wk after initiation of anti-HCV Rx. Age at baseline was computed for estimation of 10y-CVR at both time-points. Results: We recruited 262 patients. Median age, 48 yr; males, 77%; prior IDU, 78%; HCV genotype-1, 65%; median liver stiffness, 13 kPa; anti-HCV Rx, pegylated interferon and ribavirin (PR) plus 1 direct-acting antiviral (DAA) 54%, PR 33%; all-oral DAA, 13%; concomitant ART, 98%. A total of 163 (62%) patients achieved SVR. After the exclusion of patients who died or were lost to follow-up and of those initiating statin therapy during the study period, paired measurements (baseline and wk 96) were available from 227 patients for 10y-CVR, from 128 patients for PWV, and from 49 patients for cIMT. No significant differences were found at baseline in these variables between responders and nonresponders (Table). Significantly higher changes (∆) in LDL-C and 10y-CVR were observed in responders than in non-responders (Table). No significant differences were found in ∆-PWV or ∆-cIMT between responders and nonresponders (Table). Conclusion: We found that eradication of HCV in coinfected patients was associated with an increase in 10y-CVR. This change was driven by an increase in serum LDL-C. Eradication of HCV was not associated with improvements in noninvasive tests for preclinical atherosclerosis.

Poster Abstracts

633 HCV AND LIVER DISEASE INCREASE RISK OF NEUROCOGNITIVE IMPAIRMENT IN HIV+ INDIVIDUALS

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