Phlebosclerotic colitis is a rare form of ischemic colitis characterized by the thickening of the wall of the affected colon due to fibrous degeneration of submucosal layer of colon and fibrotic obstruction of the colono-mesenteric vein, resulting in the disturbance of venous return from the colon. The pathogenic mechanism of this entity remains unknown but chronic liver disease with portal hypertension is maybe thought to be one of the speculated mechanisms. Here we first report the case of surgically confirmed phlebosclerotic colitis, that was in the early stage but showed the aggressive nature, in a 61-yr-old cirrhotic patients with portal hypertension in Korea.

Background/Aims: Acute hepatitis A (HAV) is markedly increasing recently on. Some patients with acute hepatitis A show severe clinical course. The seroprevalence rate of IgG anti-HAV has been changing with the regions and the times. Vaccination and seroconversion rate of HAV are not well known. In this study, we aimed to study the difference of seroprevalence rate of IgG anti-HAV according to various clinical factors and to know the vaccination rate and seroconversion rate below 10 years old in the central region of South Korea including Cheonan city. Methods: Seven hundred seventy two subjects were included in the study from January to September 2009. We analyzed seroprevalence rate of IgG anti-HAV according to sex, age, region, and other viral markers. We interviewed the history of vaccination(1st, 2nd) and analyzed seroconversion rate according to vaccination time below 10 years old. Results: The total seroprevalence rate of IgG anti-HAV was 65.3%. The seroprevalence rate of IgG anti-HAV rate in 2nd, 3rd, and 4th decade was very low (1.9%, 18.8%, 44.8%). The vaccination rate of children was about 50%. The seroconversion rate after 1st, and 2nd vaccination were 85%, 96%. Conclusions: Catch-up vaccination for teenagers and young adults is needed. Immunizing children with HAV vaccine as a routine schedule should be considered. (Korean J Gastroenterol 2011;57:166-172)

Survivin was down-regulated in the growth inhibition of hepatoma cells induced by a selective COX-2 inhibitor, NS-398, in a concentration- and time-dependent manner. These results suggest the therapeutic inhibition of COX-2 via suppression of survivin in HCC.

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