CROI 2016 Abstract eBook

Abstract Listing

Poster Abstracts

634 Real-Life ExperienceWith Sorafenib for the Treatment of HCC in HIV-Infected Patients

Nicolás Merchante 1 ; Esperanza Merino 2 ; Boris Revollo 3 ; Francisco Rodríguez-Arrondo 4 ; Marcial Delgado-Fernández 5 ; José López-Aldeguer 6 ; FranciscoTéllez 7 ; María J. Galindo 8 ; Koldo Aguirrebengoa 9 ; Juan A. Pineda 1 ; for the Grupo de Estudio de HepatitisVíricas de la Sociedad Española de Enfermedades Infecciosas y Microbiología Clínica: GEHEP-SEIMC 1 Hosp Universitario de Valme, Sevilla, Spain; 2 Hosp General Universitario de Alicante, Alicante, Spain; 3 Hosp German Trias i Pujol, Badalona, Spain; 4 Hosp Universitario de Donostia, San Sebastián, Spain; 5 Hosp Regional de Málaga, Málaga, Spain; 6 Hosp Universitari i Politècnic La Fe, Valencia, Spain; 7 Hosp La Línea de la Concepción (AGS Campo de Gibraltar), La Línea de la Concepción, Spain; 8 Hosp Clínico Universitario de Valencia, Valencia, Spain; 9 Hosp de Cruces, Baracaldo, Spain Background: Sorafenib is an oral multikinase inhibitor that has shown a survival benefit in patients with advanced hepatocellular carcinoma (HCC). To date, there is little information regarding the efficacy and safety of sorafenib in HIV-infected patients. Our objective was to report the experience with the use of sorafenib in a cohort of HIV-infected patients with HCC. Methods: The GEHEP-002 cohort recruits HCC cases diagnosed in HIV-infected patients from 32 centers from Spain. For this analysis, HCC cases receiving at least one dose of sorafenib were included. Tumor response was evaluated according to the Response Evaluation Criteria in Solid Tumors (RECIST). The overall survival after the start of treatment (OSaT) was defined as the time from sorafenib treatment initiation to the date of death from any cause or the date of the patient’s last follow-up visit. Results: 281 HCC cases have been diagnosed in HIV-infected patients in the participant centers. In 49 (17%) patients, treatment with sorafenib was started. Reasons for sorafenib use were: HCC recurrence with previous curative therapy (n=7), progression following transartherial chemoembolization (n=4), first treatment against HCC (n=38). Complete information regarding sorafenib therapy was available in 36 patients at the moment of the present analysis. The median (IRQ) elapsed time between HCC diagnosis and sorafenib initiation was 45 (19-218) days. BCLC stage at sorafenib initiation: A 3 (9%), B 2 (6%), C 26 (71%) and D 5 (14%). Median (IQR) duration of sorafenib was 60 (27-127) days. Any grade AE occurred in 21 (58%) patients. Diarrhea was the most common AE occurring in 12 (33%) patients. 15 (42%) patients developed a liver decompensation. The probability of decompensation during sorafenib was 12.5%, 50% and 90% in patients with CTP stage A, B and C, respectively (p=0.001). Antiretroviral therapy had to be modified before sorafenib initiation in 2 patients. The median CD4 cell count at sorafenib initiation and at the last clinical visit was 326 (199-623) and 305 (170-567) cells/mL, respectively (p=0.2). HIV viral load remained undetectable during therapy in all cases. Thirty (83%) patients have died at the end of the study. The median (RIQ) OSaT was 3.5 (2.1-7.1) months. Conclusions: The efficacy and tolerability of sorafenib in HIV-infected patients in real-life conditions is significantly lower than figures reported in the registration clinical trial. On the contrary, sorafenib does not seem to interfere with antiretroviral therapy. 635 Decreased Helicobacter pylori Prevalence in HIV-Infected Subjects Christian Schulz 1 ; Michael Selgrad 2 ; Peter Malfertheiner 1 1 Univ of Magdeburg, Magdeburg, Germany; 2 Univ of Regensburg, Regensburg, Germany Background: HIV infected individuals are at increased risk of malignancies including gastric cancer (GC). Due to its indisputable role in gastric cancer development H. pylori was recognized as a ‘definite carcinogen’ by the World Health Organization in 1994. In the Western world about 30% of individuals are infected with H. pylori . Several studies have reported inconsistent data on the prevalence of H. pylori in HIV infected subjects.The transmission routes, risk factors and the prevalent time of infection for the two infections are substantially different. The aim of the study was to determine the prevalence of H. pylori and CagA as relevant virulence factor in HIV-infected subjects. As a control we used an age matched group from a previous study with healthy randomly assigned subjects that were treated in our emergency department. Methods: We prospectively analyzed the serological H. pylori and CagA status of 203 HIV positive subjects (51 female) with a mean age of 40.8 years (±10.79 years SD). The control group of HIV-negative subjects consisted of 453 patients. Results: The overall prevalence of H. pylori was 35% (71/203) in HIV-infected patients, compared to 43.5% in non-HIV-infected controls. CagA was detectable in 47.9% of the H. pylori positive patients. H. pylori prevalence decreased with increasing CDC stadium of the HIV patients. Patients in CDC stadium C (n=54) had a significant lower H. pylori prevalence (25.9%) compared to patients in the CDC-A (n=128) (39.1%) and B (n=21) (33.3%) (p=0.052). The current immune status of the HIV patients did not show a correlation with H. pylori prevalence. Patients with a low (< 200) (33.3%), medium (200-400) (37.2%) and a high (> 400) (32.1%) CD4 cell count did not differ in H. pylori infection status (p=0.496). In patients receiving antiretroviral therapy (84.7%), the H. pylori prevalence (34.3%) did not differ from patients without treatment (38.7%) (p=0.389). African, Asian and Hispanic patients (n=44) had an expected higher H.pylori prevalence (65.9%)

Poster Abstracts

258

CROI 2016