POSTER PRESENTATIONS HCC screening with ultrasound and AFP, AFP-L3 and DCP testing and were free of HCCs at the start of HCV therapy. A retrospective control cohort of untreated HCV patients fulfilling stringent inclusion and exclusion criteria was recruited out of 3715 hepatitis C patients being followed at our center between 2007 and 2013. Results: Overall, 158 treated (AVT) and 184 untreated control patients (Con) with liver cirrhosis were included in this analysis. 132 (85%) and 142 (78%) patients had compensated cirrhosis, ChildPugh classes B and C were present in 24 (15%) AVT and 40 (22%) Con patients. Both groups did not differ in terms of gender and genotype distribution, severity of liver disease (MELD- and ChildPugh-Scores), biochemical markers of liver function (with the exception of bilirubin levels, which were slightly higher in the AVT group), BMI, and prevalence of diabetes mellitus. Patients were followed for a median of 440 (range 91–908) and 592 (range 90– 1000) days. HCCs developed in 6 and 14 patients during follow-up, resulting in an HCC incidence of 2.9 (AVT) and 4.48 (Con) per 100 person years, respectively. HCC free survival was not significantly different in Kaplan-Meier estimates of both groups (log rank p = 0.39, Figure 1). In the AVT group there was no new case of HCC later than 450 days after treatment initiation. In multivariate analysis independent factors associated with HCC were higher MELD-Score and Alpha-Fetoprotein levels. Patient survival and transplant-free survival were similar in both groups.
2015 with a follow-up time of at least six months. Medical records were reviewed for patient/lesion characteristics, management and complications. Results: We included 194 patients, 2 male and 192 female. A comparison between the surveillance group (n = 86) and treatment group (n = 108) showed significantly higher BMI (31,6 vs 28,5 kg/m2, p = .029), smaller baseline diameter of the HCA (71 vs 88 millimeters, p < .001), more centrally located HCA (60 vs 25% p < .001) and multiple lesions (85 vs 64%, p < .001) in the patients who did not undergo treatment for HCA. No significant differences were found for gender, baseline-age, symptoms, complication-rate and HCA-subtype distribution. In the surveillance group 61 HCA (71%) showed regression to ≤5 cm after a median time of 85 weeks (95% > CI 59–111 weeks). Larger hepatocellular adenomas take longer to regress to ≤5 cm ( p = 0.001), no differences for time to regression were found between HCAsubtypes. No complications were documented during follow-up.
Conclusions: IFN-free therapy of chronic hepatitis C does not alter the short-term risk for HCC in patients with liver cirrhosis. A reduced HCC incidence may become evident after more than 1.5 years of follow-up. THU-082 Resection of larger hepatocellular adenomas: when is it justified? A.J. Klompenhouwer1, M.E. Bröker1, M.G. Thomeer2, M.P. Gaspersz1, R.A. de Man3, J.N. IJzermans1. 1Surgery; 2Radiology; 3Gastroenterology and Hepatology, ERASMUS MC, Rotterdam, The Netherlands E-mail:
[email protected] Background and Aims: Hepatocellular adenoma (HCA) is a benign liver tumor for which resection may be indicated if the lesion size is >5 cm six months after withdrawal of oral contraceptives. The aim of this study was to evaluate whether this interval is sufficient to expect regression to ≤5 cm in large HCA and to assess the differences between conservatively treated patients and patients who underwent surgical treatment for hepatocellular adenoma >5 cm. Methods: In this retrospective cohort study we included all subsequent patients with HCA > 5 cm diagnosed between 1999 and
Conclusions: This study suggests that a six-month cut-off point for consideration of resection in HCA > 5 cm may lead to overtreatment. We recommend to prolong the cut-off point in females with typical, non-β-catenin mutated HCA to at least twelve months irrespective of baseline diameter. For hepatocellular adenomas >7 cm it might be justifiable to wait up to 24 months assuming that the risk of complications does not increase.
Journal of Hepatology 2017 vol. 66 | S95–S332
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