POSTERS Results: Patients with AH had a greater proportion of CD14 + CD16 + monocytes compared with HVs (0.31 v 0.11; p = 0.002) and fewer CD14 lo CD16 + cells (0.01 v 0.03; p = 0.002). In HVs, CD14 + CD16 + monocytes expressed more interleukin (IL)-10 mRNA (3.1 fold difference; p = 0.02) and less TNFa (0.6 fold; p = 0.002) than CD14 + CD16 − monocytes. CD14 lo CD16 + monocytes expressed particularly high levels of TNFa, and CD14 + CD16 + monocytes were less effective than CD14 + CD16 − cells at driving memory T-cell proliferation (14.6% v 28.4%; p = 0.001). Conclusions: Consistent with previous reports in CLD, patients with AH have a greater proportion of CD14 + CD16 + monocytes. Detailed phenotypic analysis of these cells in HVs questions whether CD14 + CD16 + cells are pro-inflammatory as they express more of the anti-inflammatory cytokine IL-10, and are less able to drive memory T-cell proliferation, than CD14 + CD16 − cells. Further studies are being conducted to assess the role of these 3 monocyte subsets in AH. 524 IN VITRO STEROID SENSITIVITY ACCURATELY PREDICTS 6 MONTH MORTALITY IN PATIENTS WITH SEVERE ALCOHOLIC HEPATITIS A. Dhanda 1,2 , A. di Mambro 3 , F. Gordon 2 , J. Portal 2 , A. McCune 2 , P. Collins 2 . 1 School of Clinical Sciences, University of Bristol, 2 Department of Liver Medicine, University Hospitals Bristol NHS Foundation Trust, Bristol, 3 Department of Gastroenterology, Weston General Hospital, Weston-super-Mare, UK E-mail: ashwin.dhanda@bristol.ac.uk Background and Aims: Severe alcoholic hepatitis (SAH) has a high mortality especially in those who fail to respond to steroid treatment. Early identification of steroid resistant patients may allow rapid implementation of other therapies, which may improve patient outcome. An early change in bilirubin has prognostic value but requires 7 days of steroid treatment first. Our group have previously reported that a simple 48h in vitro method for assessing steroid sensitivity (dexamethasone inhibition of lymphocyte proliferation; DILPA) correlates with 6 month mortality in patients with SAH (di Mambro et al, Hepatol 2011). We aimed to determine the accuracy of the DILPA in predicting outcome and to compare it to existing models of prognosis in SAH. Methods: Peripheral blood was drawn from consecutive patients with a clinical diagnosis of severe alcoholic hepatitis (Maddrey discriminant function [MDF]>32). Peripheral blood mononuclear cells were cultured for 48h in media supplemented with 10% FCS and the mitogen PHA in the presence or absence of dexamethasone. Tritiated thymidine was added for the final 6h of culture before proliferation was measured on a beta counter. Maximum suppression of lymphocyte proliferation by dexamethasone was calculated (Imax). An Imax of <60% indicates in vitro steroid resistance as previously determined. Results: 43 patients were recruited (21% female, median age 45). Patients who survived 6 months had a significantly higher Imax than those who didn’t (79.2% v 41.7%; p = 0.0003). There were no significant differences between baseline MDF or early change in bilirubin between patients that survived versus died at 6 months. An Imax of >60% had a 88% sensitivity and 78% specificity in predicting outcome. A Lille score >0.45 or a Glasgow score ≥9 had poorer sensitivity and specificity for predicting 6 month outcome (Lille: 53%, 57%; Glasgow: 67%, 61%). Neither score was significantly different between patients who survived versus died at 6 months. Conclusions: The DILPA provides a simple, fast and accurate in vitro method of predicting clinical outcome in patients with SAH. This could be applied in clinical practice to identify patients who will not respond to steroid therapy within 2 days of starting treatment. 525 BMI BUT NOT AETIOLOGY OR STAGE OF LIVER DISEASE AFFECTS THE DIAGNOSTIC SENSITIVITY OF CARBOHYDRATE DEFICIENT TRANSFERRIN K. Fagan 1,2 , K. Irvine 2 , B. McWhinney 3 , L. Fletcher 1 , L. Horsfall 1,2 , L. Johnson 3 , A. Clouston 2 , J. Jonsson 2 , P. O’Rourke 4 , J. Martin 5,6 , C. Pretorius 3 , J. Ungerer 3 , E. Powell 1,2 . 1 Gastroenterology and Hepatology, Princess Alexandra Hospital, 2 Centre for Liver Disease Research, School of Medicine, The University of Queensland, 3 Pathology Queensland, Royal Brisbane and Women’s Hospital, 4 Cancer and Population Studies Group, Queensland Institute of Medical Research, 5 Division of Medicine, Princess Alexandra Hospital, 6 School of Medicine, University of Queensland, Brisbane, QLD, Australia E-mail: kjf570@hotmail.com Background and Aims: A reliable biomarker is required in hepatology clinics for detection and follow-up of heavy alcohol consumption. Carbohydrate-deficient transferrin (CDT) increases with sustained heavy alcohol consumption and is the most specific biomarker of ethanol consumption [1]. Recent introduction of a standardised method for measuring CDT has improved its clinical application. This study was designed to determine whether alcohol- independent factors influence CDT levels in patients with chronic liver disease (CLD). Methods: The relationship between serum %CDT and self-reported history of alcohol consumption was examined in 254 patients referred for evaluation of liver disease. CDT analysis was performed on serum collected at time of liver biopsy. The volume distribution of ethanol was estimated from lean body weight using the Janmahasatian equation [2]. Results: CDT levels were not affected by aetiology or severity of CLD. 13 of 254 subjects had a %CDT >1.7, predictive of heavy alcohol intake, 6 of whom did not acknowledge heavy drinking. 12 of these 13 subjects were suspected heavy drinkers on review of their medical records and clinical results. Conversely, not all acknowledged heavy drinkers had %CDT >1.7. Heavy drinkers with a BMI in the overweight or obese range had significantly lower %CDT than lean heavy drinkers (Figure 1). This persisted even when lean body weight was used as an approximation of the ethanol volume of distribution. Figure 1. BMI affects %CDT. Alcohol consumption vs %CDT in lean and overweight drinkers. (Horizontal line represents the male heavy drinking threshold (>420 g/week), vertical line represents 1.7% CDT, # is female.) (Alcohol groups: 1 = females >0–140 g/week, males >0– 210g/week; 2 = females >140–<350 g/week, males >210–<420 g/week; 3 = females ≥350 g/week, males ≥420 g/week). Conclusion: An elevated BMI reduces the diagnostic utility of CDT at higher alcohol intake in subjects with CLD using the standardized method. In a hepatology outpatient setting, this assay is likely to be useful to confirm suspicion of heavy drinking in subjects who are not overweight, but cannot reliably identify moderate drinkers or heavy drinkers who are overweight. Reference(s) [1] Helander A et al. Clin Chem Lab Med (2010) 48: 1585–1592.2. [2] Janmahasatian S et al. Clin Pharmacokinet (2005) 44: 1051–1065. Journal of Hepatology 2013 vol. 58 | S63–S227 S215