Results: Complete data were available in 301 patients with cirrhosis (cryptogenic n = 94, non-cryptogenic n = 207). Patients with cryptogenic cirrhosis were older (mean selleck chemical age 66.4 vs. 60.7, p < 0.0001), had more females (43.6% vs. 26.6%, p = 0.003), less severe disease severity (Child Pugh C 8.5% vs 15.9%, p = 0.042) and a higher prevalence of the metabolic syndrome (83% vs. 51.2%, p < 0.0001)

compared with non-cryptogenic cirrhosis. During the 5-year study period, adults with cryptogenic cirrhosis had a longer total hospital admission stay compared to non-cryptogenic cirrhosis (median 10.5 vs 8 days, p = 0.08). Further analysis demonstrated a longer hospital admission duration for cryptogenic cirrhosis due to non-liver related morbidity (median 19.0 days vs. 13.0 days, p = 0.04), rather than liver related morbidity (median 14.0 days vs 11.0 days, p = 0.06). A higher proportion of stroke (6% vs 2%, p = 0.02) and cardiovascular disease (6% vs 3%, p = 0.05) were responsible for the increased hospitalization for non-liver related morbidity in

cryptogenic compared to non-cryptogenic cirrhotic patients. Kaplan-Meier survival analysis showed no significant difference in survival between both types of cirrhosis during the period of study (Log rank statistic 0.56). Conclusion: Cryptogenic Sotrastaurin cirrhosis is associated with an increased morbidity, but not mortality, compared to non-cryptogenic cirrhosis. This difference is due to a greater burden of non-liver related complications in the selleck chemicals former. Key Word(s): Na Presenting Author: KALAIYARASI KALIYAPERUMAL Additional Authors: Na Corresponding Author: KALAIYARASI KALIYAPERUMAL Affiliations: Tan Tock Seng Hospital Objective: We present a 57 year old gentleman, who has liver cirrhosis from likely chronic systemic iron overload, haemolysis and iron deposition due to a rare form of non transfusion dependant thalassaemia. His medical problems include hypergonadotrophic hypogonadism, osteoporosis and subclinical hypothyroidism. He had never undergone any blood or blood product transfusions in the past. He is a teetotaller. On physical examination he had

short stature, bronze skin, scleral icterus and multiple stigmata of chronic liver disease with hepatosplenomegaly. He had biochemical evidence of hemolysis and iron overload in addition to raised aspartate aminotransferase and unconjugated hyperbilirubinemia. Investigations done to rule out other causes of liver cirrhosis was negative in particular HFE gene mutation analysis (C282Y and H63D mutations were not detected). An ultrasound of the liver showed coarsened liver echo texture and nodular surface outline. Fibroscan stiffness reading was 27.4 kPa. Oesophagogastroduodenoscopy (OGD) showed the presence of portal hypertensive gastropathy. DNA sequence analysis revealed a rare IVSInt1 mutation in his Beta globin gene, forming an extremely rare and unusual compound heterozygote for a Beta globin and an unknown HPFH thalassaemia mutation.