Demographic and clinical data regarding liver disease were collected from patients’ medical charts, pathology and radiology records and a self administered questionnaire. BMD was assessed using dual-energy x-ray absorptiometry at the hip (TH) and lumbar spine (LS). Bone turnover markers Torin 1 and hormonal assays were performed as per clinical pathology services. Data were analysed using SPSS version12. Results: 94 patients were studied with a median age of 56 years (range, 23–76) and 60 (64%)

were male. The mean (±SD) MELD (Model for End Stage Liver Disease) score was 9.5 (3.6). Hepatocellular liver diseases were presence in 82 (88%) patients. Chronic hepatitis C and B was the pirmary aetiology in 32% and 13% patients respectivlely, and alcohol in a further 26%. 70% (47/67) patients had low BMD: 32 had osteopaenia at either LS or TH and 15 had osteoporosis. 41 (61%) were male. Mean vitamin D level for those not on supplements was 78 nmol/L. There was no relationship between BMD (t or z score) at the LS or TH and patient’s MELD score.

Patients with hepatocellular and cholestatic liver diseases had similar BMD t and z-scores. 39% (37/94) had hypogonadism (primary or hypogonadotropic hypogonadism). Mean P1NP (a marker of collagen production) was 71 μmol/L (normal to high). Mean CTX (a marker of bone breakdown) was 42 nmol/L (normal to high). When secondary SCH772984 mw causes of high bone turnover (hypogonadism (including menopause), thyrotoxicosis, hyperparathyroidism) were excluded, there was no significant change to the bone turn over markers. These results suggest high bone turnover as a cause for osteoporosis in this group, contrary to the prevailing belief that hepatic osteodystrophy is primarily due to anabolic failure (in which case bone turnover see more markers are typically low). Conclusion: A significant proportion of patients with cirrhosis have low bone mass which is related to underlying liver disease

etiology or severity. Vitamin D deficiency was not a common finding. Results suggest the presence of increased bone turnover as the dominant mechanism for low bone mass in patients with cirrhosis, contrary to the prevailing belief that hepatic osteodystrophy is primarily due to anabolic failure. This finding provides a rationale for the use of antiresorptive medications in the management of low bone mass in patients with cirrhosis. 1. Al Vargas et al. (2012). “Prevalence and characteristics of bone disease in cirrhotic patients under evaluation for liver transplantation.” Transplant Proc 44(6): 1496–1498. ES GONSALKORALA,1,2 RS SKOIEN,1 J MASSON2 1Department of Gastroenterology and Hepatology, Royal Brisbane and Women’s Hospital, Brisbane, Australia, 2Department of Gastroenterology, The Townsville Hospital, Townsville, Australia Background: The addition of a protease inhibitor (boceprevir) to standard of care dual therapy (pegylated interferon and ribavirin) represents a new era in the treatment of genotype 1 chronic hepatitis C (CHC).