obtained from random-effects meta-analyses. Risks of bias were determined to identify quality of the studies. Results: We identified 3,796 records by search strategy. A total of 41 eligible literatures were finally included. All had high-moderate quality. Of these, 9,718 adult participants from 13 countries were included in analyses, with 8,792 (90.1%) from Asia, 755 (7.8%) from Europe, 123 (1.3%) from US, and 82 (0.8%) from Africa. For each of the five phases, basic characteristics of participants and the estimated prevalence of NF, SF, AF, and cirrhosis were described inTable 1. Conclusion: Fibrosis risk persists through CHB natural course. The present data can be used as supportive reference for clinical practice, guidelines complement, and investigation of non-invasive diagnosis. FRI418 Estimating the clinical and economic burden of chronic hepatitis B (CHB) in the United States Zobair Younossi 1,2 , Radhika Tampi 1 , Leyla Deavila 1 , Rebecca Cable 1 , Fatema Nader 3 , Issah Younossi 3 , Andrei Racila 1,3 . 1 Inova Health System, Betty and Guy Beatty Center for Integrated Research, Falls Church, United States; 2 Inova Health System, Department of Medicine, Center for Liver Diseases; 3 Center for Outcomes Research in Liver Diseases, Washington, DC Email: zobair.younossi@inova.org Background and Aims: Hepatitis B virus (HBV) infection is a major cause of chronic liver disease and hepatocellular carcinoma world- wide. Over the past decade, new antiviral therapies have been developed which can lead to sustained HBV suppression, potentially improving clinical outcomes and patient-reported outcomes (PROs). Our aim was to estimate the clinical and economic burden of prevalent CHB in 10,000 50-year-old patients in the United States. Method: We used a decision tree combined with Markov model with 1-year cycles and 20-year horizon to estimate the burden of CHB when treated with nucleos(t)ide analogs (NAs). The cohort entered the model in one of four sub-states of CHB – E antigen positive/ negative (HBeAg +, −) and high and low serum HBV DNA. We included a recovered state (R), compensated and decompensated cirrhosis (CC & DCC), and hepatocellular carcinoma (HCC), first year post-liver transplant (oyPLT) and post-liver transplant (PLT). Patients could die from liver-related and background mortality (LRM & BM). Following AASLD 2018 treatment guidelines, we treated patients with high viral load, and assumed patients were treatment naïve, received monotherapy, with 100% adherence over model horizon. Transition probabilities were found through literature review. For treatment probability, we used the combined market share for the three major NAs utilized in HBV carewhich was 85% (Trio Health). We estimated health state costs by micro-costing and through literature review in 2019 USD with 3% annual discount. Average annual treatment costs and average reduction in HCC incidence were weighted by market share of the NAs. We conducted a univariate sensitivity analysis. Results: At 85% treatment probability, economic burden of CHB is $149.7 million over 20 years, or $884 per person-year, and 1.4 thousand person-years spent with HCC. When reducing the probability of treatment to 10%, economic burden increased to $189.6 million or $1,254 per person-year and 3.5 thousand person- years spent with HCC. When increasing probability of treatment to 95%, economic burden increased to $151 million, or $887 per person- year and 1.2 thousand person-years spent with HCC. Deterministic Analysis Univariate Sensitivity Analysis Treatment Probability 85% 10% 95% Total Costs of CHB $149,735,221 $189,612,355 $150,965,312 Costs per Person-Year $884.31 $1,254.05 $887.33 Person-Years with HCC 1,412 3,498 1,247 Total Person-Years Accumulated 169,324 151,200 170,134 Conclusion: These data suggest that the burden of CHB in the United States is driven by the incidence and costs of HCC and LT. Sensitivity analysis demonstrates that lower costs of treatment with a 10% treatment probability are offset by the increased incidence of HCC and associated costs, increasing costs per-person year by 42% even with decrease in total person-years accumulated by11% due to high mortality rate of HCC. Viral hepatitis C: Post SVR and long term follow up FRI419 Exaggerated risk of vitamin B12 deficiency after HCVeradication with direct-acting antivirals Diego Casas Deza 1,2 , Vanesa Bernal Monterde 1,2 , Eva Fernandez Bonilla 1 , Silvia Espina 3 , Marta Fernández Esgueva 4 , Ana Martinez-Sapiña 4 , Javier Fuentes 1,2 , Jose M Arbones Mainar 2,5 . 1 Hospital Universitario Miguel Servet, Gastroenterology and hepatology, Zaragoza, Spain; 2 IIS Aragon. Unidad de Investigación Cli ́ nica HUMS; 3 Hospital Santa Barbara, Soria, Spain; 4 Hospital Universitario Miguel Servet, Microbiology, Zaragoza, Spain; 5 Hospital Universitario Miguel Servet, Unidad de investigación traslacional, CIBEROBN, Instituto Aragonés de Ciencias de la Salud (IACS), Zaragoza., Zaragoza, Spain Email: 630552@unizar.es Background and Aims: Elevated vitamin B12 levels have been considered as a predictive marker of acute and chronic liver disease of different etiologies. However, no reports have investigated the variation of vitamin B12 after the treatment of the underlying hepatic disease. Objetive: To evaluate the changes in vitamin B12 levels and the prevalence of its deficiency (vitamin B12 <180 pg/ml) after the eradication of HCV with direct-acting antivirals (DAA). Method: Longitudinal prospective study including all treatment naive patients with DAA therapy for HCV eradication during the year 2018 in the GastroenterologyDepartment at the University Hospital Miguel Servet (Zaragoza. Spain). Basal vitamin B12 and homocysteine levels were analyzed and then, at the end of treatment, SVR 12, and SVR 48. This study was approved byour Institutional Review Board and all participants signed informed consent forms. Results: 167 patients with HCV were included: 93 (58.12%) F1, 21 (13.12%) F2, 24 (15%) F3 and 22 (13.75%) F4. 52.7% werewomen. The median age was 53 years (range 20–87). Vitamin B12 levels (median [interquartile range]) decreased significantly during follow-up (323 pg/ml [246; 388] at baseline vs. 282 pg/ml [213; 344] in SVR48, p = 0.004). In turn, homocysteine tended t to increase (9.95 μmol/l [8.35; 11.7] baseline vs. 10.6 [9.13; 12.8] SVR48, p = 0.085). The prevalence of vitamin B12 deficit increased significantly (3.1% baseline, 13.33% in SVR and 12% in SVR 48, (p = 0.009), while folic acid levels did not show significant changes during the follow-up (8.15 ng/ mL [6.06; 11.4] vs. 7.50 [5.34; 10.4], p = 0.117). Table 1: Vitamin B12, folic acid and homocysteine along the follow up. Variable Basal SVR 48 P* Median [interquartilic range] Vitamin B12 (pg/ml) 323 [246;388] 282 [213;344] 0.004 Homocysteine (μmol/l) 9.95 [8.35;11.7] 10.6 [9.13;12.8] 0.085 Folic acid (ng/mL) 8.15 [6.06;11.4] 7.50 [5.34;10.4] 0.117 B12 deficit (%) 3.1 12 0.009 *p-value for the media comparation (t-Student) or proportions (Chi 2 ). Conclusion: DAA-treated patients have a progressive decrease in vitamin B12 levels after HCV eradication, with an increase in the prevalence of B12 deficiency one year after treatment. The POSTER PRESENTATIONS S605 Journal of Hepatology 2020 vol. 73 | S401–S652