CROI 2020 Abstract eBook
Abstract eBook
Poster Abstracts
in fibroscan reading (-0.40 vs. -0.70 kPa, P=0.83), and significantly higher incidence of CNS AEs (41.5% vs. 5.3%, P<0.001). Conclusion: This first pilot RCT showed that EFV was associated with higher risk of hepatotoxicity, lower reduction of fibroscan score, and significantly higher risk of CNS toxicity in HIV/HCV coinfected participants. Our study provides further support to 2019 WHO guidelines which recommends moving away from EFV-based as a preferred 1st-line ART.
liver stiffness measured by transition elastography (TE) and treated with RPV-based regimens showed any improvement. 1 Martí-Rodrigo A, Alegre F, Moragrega ÁB, et al. Gut epub ahead of print doi:10.1136/ gutjnl-2019-31837 Methods: From a 4009 HIV-infected patients cohort in stable follow-up, patients who had some degree of liver-stiffness measured by TE (> 5.2Kpa) and at least 2 TE measurements were selected. A case-control study of exposed and non-exposed subjects to RPV was designed. In cases the exposure to RPV should have started in the period between the two TE measures (baseline and final). Case and control groups were matched for chronic hepatitis C (CHC), sustained virological response (SVR), years of HIV diagnosis (+3 years) and time elapsed between TE measures (+6 months). A linear model of repeated measures (GLM-RM) of the TE was carried out, controlling for HCV coinfection, time of SVR, time of HIV-infection, time elapsed between TE and BMI measures. Results: 120 case and 120 control subjects were selected without significant differences in gender (84%male), UDVP transmission (43%), CDC C stage (28%), and undetectable HIV viral load (85%). The median time between TE measurements was 51 (29-68) months. Main variables related to liver stiffness at baseline and final moments are shown in table. In the GLM-RM analysis a significant decrease was found in the measure of TE in case group, (mean difference of -1.9Kpa [CI95% -3.0 - -0.8]; p <0.01) and not in control (mean difference of -0.5Kpa [CI95% -1.6 - 0.6]; p = 0.4). This difference in the case group was found only in subjects who had CHC, mean difference of -2.9Kpa ([CI95% -4.6 - -1.3]; p <0.01). Conclusion: In patients co-infected with HIV / HCV receiving an ART based on RPV, a significant reduction in liver stiffness measured by TE was observed. 551 ACCURACY OF FIBROSIS-4 FOR CIRRHOSIS IN HIV+ PATIENTS WITH HEPATOCELLULAR CARCINOMA Jessie Torgersen 1 , Michael J. Kallan 1 , Dena M. Carbonari 1 , Lesley S. Park 2 , Rajni Mehta 3 , Kathryn D'Addeo 3 , Janet Tate 3 , Joseph Lim 4 , Matthew B. Goetz 5 , Maria Rodriguez-Barradas 6 , Norbert Bräu 7 , Sheldon T. Brown 7 , Tamar Taddei 3 , Amy C. Justice 3 , Vincent Lo Re 1 1 University of Pennsylvania, Philadelphia, PA, USA, 2 Stanford University, Stanford, CA, USA, 3 VA Connecticut Healthcare System, West Haven, CT, USA, 4 Yale University, New Haven, CT, USA, 5 VA Greater Los Angeles Health Care System, Los Angeles, CA, USA, 6 Michael E. DeBakey VA Medical Center, Houston, TX, USA, 7 James J. Peters VA Medical Center, Bronx, NY, USA Background: Hepatocellular carcinoma (HCC) may develop in the absence of cirrhosis in HIV, and determining how often this occurs can provide insights into mechanisms of carcinogenesis. Studies evaluating the prevalence of cirrhosis in the setting of HCC among HIV+ patients often rely on non-invasive markers, such as the Fibrosis-4 Index for Hepatic Fibrosis (FIB-4). However, the accuracy of FIB-4 for cirrhosis in the setting of HCC has not been determined among HIV+ patients. Methods: We conducted a cross-sectional study among HIV+ patients in the Veterans Aging Cohort Study with a HCC diagnosis from 1999-2015 and evaluated the accuracy of FIB-4 for medical record-confirmed cirrhosis. HCC diagnoses were identified in the VA cancer registry. FIB-4 was calculated using the age, alanine aminotransferase, aspartate aminotransferase, and platelet count obtained closest, but within one year prior, to the date of HCC diagnosis. Medical records were reviewed to abstract evidence of cirrhosis within one year prior to the date of HCC diagnosis. Cirrhosis was confirmed if: 1) liver histopathology report indicated cirrhosis (METAVIR stage F4 or Ishak fibrosis score ≥5); 2) abdominal imaging indicated cirrhosis (nodular contour of liver, splenomegaly with ascites, or esophageal varices); 3) endoscopy identified esophageal varices or portal gastropathy; 4) paracentesis was performed; or 5) clinician note reported ascites, spontaneous bacterial peritonitis, variceal hemorrhage, or hepatic encephalopathy. The diagnostic accuracy of FIB-4 was
549 HEPATIC STEATOSIS ASSOCIATED WITH EXPOSURE TO ELVITEGRAVIR AND RALTEGRAVIR Thomas Benfield 1 , Jens D. Lundgren 2 , Flemming Bendtsen 3 , Susanne D. Nielsen 4 , Ditte M. Kirkegaard-Klitbo 3 1 University of Copenhagen, Copenhagen, Denmark, 2 CHIP, Department of Infectious Diseases, Copenhagen, Denmark, 3 Hvidovre Hospital, Hvidovre, Denmark, 4 Copenhagen University Hospital, Copenhagen, Denmark Background: Treatment with integrase strand transfer inhibitors and nucleotide analogues may be associated with weight gain in people living with HIV (PLWH). Overweight is associated with fatty liver. Here we studied the association of antiretrovirals and moderate-severe hepatic steatosis. Methods: PLWH without prior or current viral hepatitis or alcohol intake above recommendations were included in 2015-16. Liver steatosis was assessed by unenhanced CT liver scan. Moderate-severe hepatic steatosis was defined by liver attenuation ≤ 48 Hounsfield units. Association with antiretroviral exposure was presented as odds ratio with 95% CI after adjustment for age, sex, body mass index and duration of HIV infection. Results: PLWH included in the study were predominantly male (86%), European (87%), MSM (73%) and with undetectable HIV RNA (97%). Of 516 PLWH, 37 (7.2%) had moderate-severe hepatic steatosis. The mean treatment duration was 11 years. Moderate-severe hepatic steatosis was associated with any (OR 3.67 (1.29;10.46)) and cumulative (OR 1.19 (1.01;1.41) per year) exposure to raltegravir (number exposed (Nexp) = 59) and with cumulative exposure to elvitegravir (OR 2.84 (1.58;5.10) per year) (Nexp = 63)). The association with cumulative exposure to elvitegravir with emtricitabine/tenofovir disoproxil fumarate (OR 3.06 (1.63;5.75)) or with emtricitabine/tenofovir alafenamide ((OR 3.62 (0.73;17.81)) were comparable. Further, moderate-severe hepatic steatosis was associated with cumulative exposure (OR 1.22 (1.02;1.47) per year) to stavudine (Nexp = 86). Test for interaction with stavudine and raltegravir or elvitegravir were statistically non-significant (P=0.79 and P=0.45). Any exposure (Nexp) to abacavir (268), didanosine (78), emtricitabine (263), lamivudine (424), tenofovir disoproxil fumarate (416), tenofovir alafenamide (33), zidovudine (262), efavirenz (338), etravirine (14), nevirapine (113), rilpivirine (25), atazanavir (137), darunavir (135), lopinavir (61) or dolutegravir (67) was not associated with moderate-severe steatosis. Conclusion: Moderate-severe hepatic steatosis in PLWH without viral hepatitis or excessive alcohol intake was associated with cumulative exposure to stavudine, elvitegravir and raltegravir. Prospective trials are required to establish a causal association. 550 BENEFITS OF RILPIVIRINE FOR LIVER FIBROSIS IN HIV/HCV COINFECTED SUBJECTS Maria Luisa Montes 1 , Carmen Busca 1 , Antonio Olveira 1 , Luz Martin-Carbonero 1 , Eulalia Valencia 1 , Victoria Moreno 1 , Jose I. Bernardino 1 , Ignacio Pérez-Valero 1 , Rocio Montejano 1 , Rafael Micán 1 , Rosa De Miguel 1 , Jose R. Arribas 1 , Juan González-García 1 1 Hospital La Paz Institute for Health Research, Madrid, Spain Background: Recent studies have described that treatment with rilpivirine (RPV) induces antifibrotic effects in various models of chronic liver disease1. Our objective was to analyse whether HIV-infected patients with some degree of
Poster Abstracts
CROI 2020 197
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