Aim: Interferon (IFN) therapy is a powerful treatment for HCV-related hepatitis and is known to decrease the incidence of progression of hepatocellular carcinoma (HCC). However, thrombocytopenia is a common side effect of IFN treatment, often leads to discontinuance without insufficient therapeutic effect. In this study, we investigated the efficacy and safety of laparoscopic splenectomy ( ) in reversing thrombocytopenia in patients with hepatitis C cirrhosis and portal hypertension. Patients and Methods: Out of 41 patients who underwent LS in our department during Aug 2003 and December 2007, 13 patients associated with portal hypertension. Among these patients, three patients had HCC, and they were simultaneously underwent partial hepatectomy after splenectomy. Platelet count, operative time, blood loss, complications and length of stay were calculated. Results: Thirteen patients underwent laparoscopic splenectomy; their mean age was 59 years (range 20 to 68 years). Six patients were Child's class A and seven patients were class B. Mean operative time was 178 minutes (range 97 to 255 minutes). Blood loss was little, and none required transfusion with packed red cells. A hand-assisted laparoscopic technique was used in four cases (30.8%). Average length of stay was 12.7 days. There have been no major complications during follow-up. Platelet counts improved from a preoperative mean of 62000/ul (44000 to 108000) to 273000/ul (126000 to 469000) postoperatively. Six patients are ongoing IFN treatment without remarkable thrombocytopenia. Conclusion: Laparoscopic splenectomy is safe and in patients with portal hypertension and thrombocytopenia. It may allows these patients by reversing thrombocytopenia. Background: Hepatic encephalopathy (HE) is a significant cause of mortality in advanced cirrhosis patients. L-acyl-carnitine has been suggested as an alternative treatment for patients with HE patients. To assess the clinical efficacy of acetyl-L-carnitine in the treatment of hepatic encephalopathy in cirrhotic patient, especially in diminishing the recurrence and reduction serum ammonia level. Methods: We performed a randomized placebo-controlled, cross-over study. We administered acetyl-L-carnitine to group 1 during 3 months first then placebo during later 3 months, and administering acetyl-L-carnitine to group 2 alternatively. Results: Between January 2008 and February 2008, thirty two selected cirrhotic patients were enrolled in this study. Following randomization, the patients were divided into two groups (group 1=14, group 2=18). During administering acetyl-L-carnitine period, serum ammonia level was decreased significantly in both groups significantly (p=0.005, vs. p=0.001 respectively). However, during administering placebo period, serum ammonia level changes were not significant. In group 1, the first recurrence cases of hepatic encephalopathy were more than group 2(group 1=5, group 2=2), and the first recurrences were occurred during first 3 months in all groups. Conclusion: Our study demonstrates that acetyl-L-carnitine administration reduced serum ammonia level, but not definitely diminishing the recurrence of hepatic encephalopathy. Sodium (Na + ) and water retention are the most common abnormalities in cirrhotic patients and the magnitude varies from patients to patients. Aim: To assess the relationship between the MELD score and urinary excretion of Na+ in non-azotemic cirrhotic patients. Methods: Fifty four cirrhotic patients with ascites and normal serum creatinine (<1.5 mg/ml) were admitted and placed on a low sodium diet (4g/day), while all diuretics were withdrawn for 3 days. The electrolytes (Na + , K + , Na + / K + ) were measured in a random urine and both the volume and Na + concentration of urine collected for 8 h after administration of furosemide 80 mg i.v. were determined. Results: Table. Conclusions: The MELD score was significantly correlated with the degree of impairment of urinary Na+ excretion. The ratio of Na + /K + in a random urine specimen and furosemide-induced Na+ excretion reflect the degree of impaired natriuresis in non-azotemic cirrhotic patients with ascites. Background: Portal hypertensive gastropathy (PHG) is common finding in patients with liver cirrhosis and portal hypertension. Despite portal hypertension remains the crucial trigger for the development of PHG, the relationship between portal hypertension and PHG has not been widely investigated. Methods: Fifty-three cirrhotic patients (48 males, mean age 51 years) who were performed hepatic vein catheterization between November 2006 and August 2008 were prospectively included in this study. The degree of PHG was assessed according to the Third Baveno International Consensus Workshop, and classified three degrees as no, mild and severe. The hepatic venous pressure gradient (HVPG=WHVP-FHVP) measurements were performed by triplicate in each case, and results were given as arithmetic means of the three determinations. Result: HVPG values did not differ between the patients without PHG (13.28±4.72 mmHg) and those with PHG (14.91±3.84, p=0.187), nor between those with mild (15.31±3.69 mmHg) or severe PHG (14.27±4.12mmHg, p=0.323). The degree of PHG and HVPG did not differ regarding the etiology of the cirrhosis(p=1.0, p=0.085) nor regarding the Child Pugh classification(p=0.085, p=0.738). No correlations were found between the degree of PHG and Child Pugh score, age, with or without ascites, albumin, bilirubin, creatinine, MELD score and the degree of gastroesophageal varices. Conclusions: Our data show that the presence and the severity of PHG does not correlate with the degree of HVPG, and that correlate with esophageal varices in patients with liver cirrhosis. Introduction: Phlebosclerotic colitis is a rare form of ischemic colitis characterized by the thickening of the colonic wall due to fibrous degeneration of the submucosal layer and fibrotic sclerosis of the venous wall. There are a few reports those this entity might be related to portal hypertension with disturbed venous return from the colon and mesentery. Case description: A 61-year old man with alcoholic liver cirrhosis presented with right lower abdominal pain/tenderness and bloody diarrhea. A colonoscopy revealed multiple circumferential ulcerations in the transverse colon and the scope could not get through the ascending colon due to luminal stenosis, showing histologic finding of ulcerative inflammation with inflammed granulation tissue. Abdominal computed tomography demonstrated liver cirrhosis with splenomegaly, multiple portosystemic venous collaterals, diffuse vascular engorgement and the wall thickening of right proximal to mid ascending colon with increased density in the surrounding fatty tissue. A follow-up colonoscopy performed one month later showed still remained multiple ulcerations in the transverse colon and could not further advance to ascending colon. Superior mesenteric angiography revealed no main branch occlusion but pooling at the venous phase on ascending colon. A right hemicolectomy was performed because of the colonic obstruction. Gross findings on operation showed thickening of the cecum and ascending colon. Microscopic examination showed fibrous thickening in the submucosa, abundant neurovascular bundles in the mesentery and several intravascular hyaline thrombi of the mesenteric vessels. Here we report the first case of early stage of phlebosclerotic colitis in a cirrhotic patient in Korea. Spontaneous bacterial peritonitis (SBP) is one of the severe complications in advanced cirrhotic patients with a high mortality rate. Although a more rapid diagnosis should lead to the better survival, it takes several days to detect the causal bacteria from ascitic fluid cultures. Furthermore, despite the use of sensitive methods, ascitic fluid cultures were negative in more than 50% of patients with suggestive clinical manifestations of SBP. Therefore, diagnosis of SBP is based on the polymorphonuclear leucocytes (PMN) cell count in the ascitic fluid. The Hybrizep kit (Fuso Pharmaceutical Industries, Osaka, Japan) detects the DNA of bacteria that have been phagocytized in neutrophils and macrophages, using in-situ hybridization method within one day. Here we present a case of the patient for whom the Hybrizep kit was used to detect the causal pathogen of SBP. A 76-year-old man had been admitted for the treatment of ascites and esophageal varices. One week after the admission, he complained abdominal pain and fever. Because the PMN cell count in ascites fulfilled the criteria of SBP (1141/mm 3 ), we started an empirical antibiotic therapy without waiting for a result of the culture, and his symptoms improved within a few days. On the following day of the onset, in situ hybridization showed the positive signals by the EK probe, which detected the genomeic DNA of E.coli species. However, the ascitic fluid culture was negative. This case suggested that the Hybrizep kit was useful for the rapid diagnosis of SBP with high sensitivity. 