Mikram Jafri

838 Pegylated Interferon Alfa, Nitazoxanide, Telapravir, Ribavirin, in Genotype 1 Undergoing Prior Experienced Chronic Hepatitis C Patients-a Randomized Placebo Control Clinical Pilot Trial (I N T R I G U E C) Interim

Introduction Chronic hepatitis C is a global challenge with end stage liver disease and rising Hepatocellular Carcinoma. Peg Interferon α and Ribavirin was the backbone of therapy. Recently introduced Directly Acting Antivirals -protease inhibitor has a promising role in escalating Sustained Viral Response in Response guided therapy in non-responders, partial and relapses. This study utilised Nitazoxanide (NTZ) and Telapravir, with SOC for 24 weeks in treatment experienced patients. Methods 50 (n=50) patients were divided into Group A (n=12) NTZ 500 mg three times for 12 weeks, Group B (n=12) NTZ 500 mg twice daily for 24 weeks Group C (n=26) control. All received Peg Interferon α 2a 180 μg SQ QOW with fixed dose of Ribavirin 1200 mg daily for 24 weeks with Telapravir 750 mg three times daily for 12 weeks. Viral load was obtained at day 0, 7th day, 14th day, 4 weeks, 12th week and 24 weeks. Viral kinetics was analysed. In Group A: 5/12 (42%) Non-Responder, 6/12 (50%) partial responder, 2/12 (16%) relapsers. In Group B: 5/12 (42%) Non-responders, 6/12 (50%) partial responder, 1/12 relapsers (8%). In Group C: 10/26 (38%) non-responder, 10/26 (38%) partial responder, 4/26 (15%) relapsers, 2/26 (8%) unknown. Exclusion: Decompensated Cirrhotic, HCC, poor DM, Haemolytic Anaemia, Severe Coronary artery disease, major depression, renal failure, Prior severe skin rash, active drug and alcohol abuse. Side Effects: Anaemia 28/50 (56%), Neutropenia 14/50 (28%), Thrombocytopaenia 8/50 (16%), Fatigue 34/50 (68%), Depression 10/50 (20%), Mild skin rash 22/50 (44%), Severe skin rash 1/50 (2%). Use of Growth factors: Epogen 12/50 (24%) Neupogen 8/50 (16%) Elthrombopag 5/50 (10%). Results Conclusion This quadruple truncated regimen has excelled the RVR, ETVR over SOC with Directly Acting Antivirals over 13%, without any difference between 24 weeks of NTZ over 12. Needs a larger trial for validation. Competing interests None declared.

PWE-271 Ratio of IL 10 over IL 12 is a novel surrogate to evaluate the severity of non-alcoholic steatohapatitis (NASH)—a prospective clinical pilot study

Introduction Non-alcoholic steatohepatitis (NASH) is a growing global epidemic progressing to cirrhosis, liver failure, HCC, warrants liver transplant. The natural history is still not well defined, inflammatory cytokines, intrahepatic immune traffic, degree of apoptosis and path of fibrogenesis are the sequel of the disease process. This study evaluates a novel inflammatory cytokines (IL 10 and IL 12) ratio to predict NAFLD to NASH and its severity index. Methods Ninety (n=90) patients, mean age of 45 (28–54) were divided into Group A (n=30) BMI (mean) <25% with normal lipids, healthy control. Group B NAFL D (n=30) BMI >29% with NAFLD (hepatic steatosis, Waist/Hip ratio >0.9, high lipids, HOMA >1.8, mean normal ALT, AST, RBP 4, 2.5, Leptin, Adiponectin, TNF α, serum NASH score <0.8, mean fibrotic score <0.1, mean IL 10/IL 12 ratio <0.9. NASH C (n=30), BMI >30, W/H ratio >1.1, high lipids, HOMA >2.2, high AST, ALT, RBP >4.5, high leptin, low adiponectin, high TNF α, IL10/IL12 ratio >2.5. Serums NASH score >0.6, fibrotic score over 0.2. Liver biopsy in NASH group, macrovascular fat 18/30 (60%), balloning 12/30 (40%), Mallory body 7/30 (23%), METAVIR score F2 12/30 (40%), F3 9/30 (30%), F4 3/30 (10%). Exclusion Criteria: Diabetes, viral hepatitis, autoimmune liver disease, alcohol consumption over 20 g daily, steatogenic medications including herbs. Results Characteristic Group A Group B Group C Serum NASH score NA <0.8 >0.6 Mean Fibrotic score NA <0.4 >0.2 Macrovascular fat NA NA 18/30 (60%) Mallory body NA NA 7/30 (23%) Ballooning NA NA 12/30 (40%) F2 NA NA 12/30 (40%) F3 NA NA 9/30 (30%) F4 NA NA 3/30 (10%) Conclusion IL 10/12 ratio correlated positively with the progression of NAFLD to NASH. IL 10/12 ratio >2.5 has NASH with high steatosis and fibrotic state and elevated inflammatory cytokines. Larger study will establish the predictive index of IL10/IL 12 NASH severity and prognosis. Competing interests None declared.

Sa1074 Effects of Lidocaine 3% Gel Delivered Rectally in Ano Rectal Dysfunction (ARD) Induced by Telaprevir Therapy in Chronic Hepatitis C-a Randomized Placebo Control Study

Introduction Telapravir is a Potent Protease Inhibitor, which causes anorectal dysfunction (ARD) comprising Proctalgia, Rectal Ulcers, Hemorrhoids and rectal bleeding. Conventional therapy is suboptimal causing treatment Failure. This study evaluates 3% Topical Lidocaine gel rectal delivery to abate the drug related ARD to avoid treatment failure. Methods 52 Patients (mean age 51) were recruited undergoing therapy with Telapravir, Peg Interferon and Ribaviran for CHC-C. 45/52 (86%), with Rectalgia, 8/52 (15%) rectal ulcers, Hemorrhoids 19/52 (36%) with bleeding 6/19 (31%) without Bleeding 13/19 (68%). Group A (n=17) placebo Group B (n=17) hydrocortisone 2.5% Cream and Group C (n=18) Lidocaine 3% Gel foam per rectally twice daily. All underwent Pre and post Proctoscopic evaluation and Ano-rectal manometry. Results Conclusion Results: Rectalgia resolved in 3/17 (17%), 8/17 (47%) and 7/18 (94%) for Group A, B and C respectively. Rectal ulcers healed in 0/2 (0%), 1/3 (33%) and 2/3 (66%) for all the above groups. Hemorrhoids resolved in 1/6 (16%), 2/6 (33%) and 5/7 (71%) in all groups. Pre/Post Proctoscopy revealed normal mucosal integrity 4/17 (23%), 7/17 (41%) and 17/18 (94%) above groups. Results of Pre/Post Rx mean scores for pain, Itching and Burning shown on (Abstract PMO-168 table 3). AR Manometry results showed Pre/Post treatment high sphincter tone >4 mm in Group A 2/15 (8%) and no differences in pre and post treatment, Group B 7/15 (41%), 4/15 (22%) and Group C 5/15 (20%), 2/15 (10%) respectively (Abstract PMO-168 table 4). Side events; Numbness, 4/17 (23%) in lidocaine. Conclusion: Rectally delivered Lidocaine 3% gel is efficacious, tolerable compared to the SOC and placebo for ARD causing treatment failure, retention and SVR. Larger trial needs to validate this finding. Competing interests None declared.

Mo1910 Prevalence of Hepatitis E in New York Among HIV Negative Chronic Liver Disease Population “Is it an Innocent Bystander”

Introduction Hepatitis E is essentially an oral fecal infection with high prevalence in developing countries. There is limited data available on its prevalence in Urban US. The study evaluates the prevalence of hepatitis E antibody IgG and IgM in New York in patients with chronic liver disease. Methods 440 (n=440) were divided into two groups: group A; control 140 patients without any stigmata of liver disease. Group B, 300 patients with history of liver disease including hepatitis B 125/300 (41%), Chronic hepatitis C 60/300 (20%), fatty liver 70/300 (23%), Alcoholic liver disease 29/300 (10%), HBV HCV co infection 9/300 (3%), auto immune hepatitis 2/300 (0.6%), PBC /PSC 5/300 (2%). HEV antibody IGM and IGG were measured with HEV genotyping. 22/300 (7%) patients were liver transplant recipients, 6/300 (2%) patients were kidney transplant recipients. 43/300 (14%) patients were Intra venous Drug Abuser. 20/300 (7%) received Blood products. Results History and genotypic characteristics Conclusion Results : Group (A) HEV IgG positive 13% (18/140), Group B HEV IgG positive 40.6% (122/300) including 3.7% (4/122) having both IgM and IgG positive. The prevalence of HEV IgG was 54% (12/22) in the liver transplant recipient group and 33% (2/6%) kidney transplant recipient group. The study demonstrates the prevalence of hepatitis E infection in New York and HEV antibody in CLD. Including transplant donors and recipients. Question remains the impact and progression of acute or chronic liver disease with concomitant HEV in pre, peri, and post liver transplant recipient. Larger study needs to validate. Competing interests None declared.

BISAP and CTSI Scores as Predictors of Clinical Outcomes in an African American Cohort

Sweat chloride performance parameters are shown (table); differences between the 2 clinical settings are due to differences in CF frequency in each population. Borderline sweat tests have a much greater predictability for CF in a GI-CF clinic patient population than in population screening. Sweat chloride ≥60mmol/L was diagnostic of CF in both settings. Conclusion: Sweat testing should be performed in PANC patients to diagnose CF (≥60mmol/ L) and identify patients with an equivocal result (40-59mmol/L) who require further evaluation for CF.