Plenary and Parallel Sessions (Abstracts 1–258)

Abstract

Male, n (%) 424 (51) 584 (54) Race, n (%) White 688 (83) 825 (77) Asian 81 (10) 163 (15) Black 41 (5) 61 (6) Age, median (range), years 53 (19-84) 53 (20-83) BMI, median (range), kg/m 2 25.6 (17.3-65.7) 25.3 (17.4-54.1) Genotype, n (%) 1 387 (47) 401 (37) Subtype 1a 178 (21) 168 (16) Subtype 1b 208 (25) 230 (21) Other 1 (0.1) 3 (0.3) 2 197 (24) 234 (22) 3 186 (22) 270 (25) 4 46 (6) 112 (10) 5 2 (0.2) 28 (3) 6 10 (1) 31 (3) IL28B non-CC genotype, n (%) 534 (64) 723 (67) HCV treatment-naïve, n (%) 657 (79) 801 (74) HCV treatment-experienced, n (%)* 171 (21) 275 (26) IFN-based 164 (96) 266 (97) SOF-based 7 (4) 9 (3) HCV RNA, median (range), log 10 IU/mL 6.2 (0.7-7.6) 6.2 (2.5-7.8) Baseline HCV RNA level, IU/mL, n (%) <1000000 338 (41) 446 (41) ≥1000000 490 (59) 630 (59) <6000000 623 (75) 850 (79) ≥6000000 205 (25) 226 (21) Fibrosis stage, n/N (%) † F0-F1 678/825 (82) 870/1075 (81) F2 56/825 (7) 87/1075 (8) F3 91/825 (11) 118/1075 (11) HIV-1 co-infected, n (%) 15 (2) 18 (2) Concomitant PPI use, n (%) 61 (7) 125 (12) On stable opiate substitution, n (%) 62 (7) 63 (6) >80% treatment compliant, n (%) 735 (89) 979 (91) APRI, n (%) <1 686 (83) 881 (82) ≥1 142 (17) 195 (18) Fibroscan, n/N (%) ‡ <9.6 kPa 501/579 (87) 703/801 (88) ≥9.6 kPa 78/579 (13) 98/801 (12) Fibrotest n/N (%) ‡ <0.59 279/347 (80) 292/367 (80) ≥0.59 68/347 (20) 75/367 (20) G/P, glecaprevir/pibrentasvir; BMI, body mass index; HCV, hepati ti s C virus; HIV, human immunodefi ciency virus; IFN, interferon; SOF, sofosbuvir; PPI, proton pump inhibitor; APRI, aspartate aminotransferase to platelet rati o. *IFN-based: IFN or pegIFN ± RBV; SOF-based: SOF + RBV ± pegIFN; SOF + RBV ± pegIFN pati ents counted as SOF-experienced only. † N adjusted for pati ents missing data. ‡ N adjusted for pati ents with fi brosis status assessed by FibroScan or Fibrotest. • Pati ent baseline demographics and disease characteristi cs were similar across the 8 and 12 week treatment arms 95% confi dence intervals are shown. *Indicates variable that was included in the logisti c regression analysis (also included in logisti c regression: presence of baseline polymorphisms at a key subset of positi ons, treatment durati on, and HCV genotype). LOGISTIC REGRESSION ANALYSIS • A multi variate stepwise logisti c regression analysis revealed that neither treatment durati on (8-week or 12-week) nor genotype (1-6) was associated with achievement of SVR12 • Presence of baseline polymorphisms in key NS3 positi ons (155, 156, or 168) or in NS5A had no impact on SVR12 • Presence of baseline polymorphisms in key NS3 positi ons (155, 156, or 168) combined with NS5A polymorphisms had a stati sti cally signifi cant impact on SVR12 (odds rati o = 0.017 [95% CI 0.003-0.098], P-value <0.1) AE leading to D/C 1 (0.1) 9 (0.8) DAA-related AE leading to D/C 0 3 (0.3) Laboratory Abnormalities, n/N (%) ALT, grade ≥3 (>5 × ULN) 0 1/1075 (<0.1)* Total bilirubin, grade ≥3 (>3 × ULN) 4/827 (0.5) † 2/1075 (0.2) † AE, adverse event; DAA, direct-acti ng anti viral; D/C, disconti nuati on; ALT, alanine aminotransferase. *Grade 3 ALT elevati on associated with grade 2 bilirubin and grade 3 AST and alkaline phosphatase elevati ons at Week 12 in the context of cholelithiasis (multi ple gallstones); pati ent achieved SVR12. †All pati ents had bilirubin elevati ons at baseline; the grade 3 elevati ons were primarily indirect, with no associated post-nadir ALT elevati ons by grade.