Mean platelet volume (MPV) has been actively investigated in liver disease such as steatosis, cirrhosis and hepatitis. Recently, MPV/platelet count (PC) ratio has been proposed as a predictor of long-term mortality after myocardial infarction. As PC is known to be decreased in various liver diseases such as cirrhosis, hepatosplenomegaly and malignancy, we planned to evaluate MPV/PC ratio in patients with hepatocellular carcinoma (HCC) in this study. Mean of MPV levels showed significant difference, which were 8.69 fl (range 6.7-12.2 fl) in patients group and 8.02 fl in control group (range 6.7-11.0 fl). In receiver operating characteristic (ROC) curve analysis, the MPV/PC ratio (fl/(10(9)/l)) presented 74.5% of sensitivity and 96.5% of specificity at the criterion > 0.0491 (area under the curve (AUC) = 0.884), while MPV alone showed 57.4% of sensitivity and 81.4% of specificity at the criterion > 8.4 fl. Further studies should evaluate underlying pathogenic mechanisms of MPV/PC ratio difference and various possibilities of this ratio as an indicator of presence of a tumor in HCC.

Interleukin-1B and IL-1 receptor antagonist gene polymorphisms are associated with an increased risk of gastric cancer (GC) in Caucasian populations. However, recent studies could not find any association between IL-1B-511T polymorphism and the risk of GC in Asians. We tested for an association between IL-1 loci polymorphisms with increased gastric mucosal levels of IL-1␤ and an increased risk of developing GC in a Korean population. Polymorphisms of IL-1A-889, IL-1B-31, IL-1B-511 and IL-1RN were genotyped in 434 controls and 234 patients with GC. Mucosal IL-1␤ cytokine was measured using an ELISA. The frequencies of IL-1A, IL-1B-511, IL-1B-31 and IL-1RN were not statistically different between controls and all patients with GC. After subclassification of GC, only patients with intestinal-type GC showed a higher frequency of IL-1B-31T homozygotes (OR ‫؍‬ 2.2; 95% CI ‫؍‬ 1.1-4.3) compared with controls. Risk was also significantly increased in these patients for IL-1B-31T homozygotes compared with patients with diffuse-type GC (OR ‫؍‬ 3.4; 95% CI ‫؍‬ 1.5-7.7). As in Caucasian populations, linkage disequilibrium between IL-1B-31 and IL-1B-511 was nearly complete, but the pattern of haplotype related to the risk of GC (IL-1B-31T/IL-1B-511C) was opposite (IL-1B-511T/IL-1B-31C). Mucosal IL-1␤ levels in H. pylori-infected GC patients were higher in patients homozygous for IL-1B-31T compared with IL-1B-31C/T and IL-1B-31C/C. Thus, the combined effects of H. pylori infection and IL-1B-31T/IL-1B-511C polymorphisms with enhanced mucosal IL-1␤ production contributed to the development of intestinal-type GC in this Korean population.

Symptomatic hepatic injury develops usually within the first few months of PTU administration with rare frequency, but its clinical course is relatively benign once the drug is withdrawn. However, it may be difficult to predict its development, so all patients should be monitored for rise in LFTs at regular intervals, especially during the early period.

Cyclophilin B (CypB) performs diverse roles in living cells, but its role in hepatocellular carcinoma (HCC) is largely unclear. To reveal its role in HCC, we investigated the induction of CypB under hypoxia and its functions in tumor cells in vitro and in vivo. Here, we demonstrated that hypoxia-inducible factor 1a (HIF-1a) induces CypB under hypoxia. Interestingly, CypB protected tumor cells, even p53-defective HCC cells, against hypoxiaand cisplatin-induced apoptosis. Furthermore, it regulated the effects of HIF-1a, including those in angiogenesis and glucose metabolism, via a positive feedback loop with HIF-1a. The tumorigenic and chemoresistant effects of CypB were confirmed in vivo using a xenograft model. Finally, we showed that CypB is overexpressed in 78% and 91% of the human HCC and colon cancer tissues, respectively, and its overexpression in these cancers reduced patient survival. Conclusions: These results indicate that CypB induced by hypoxia stimulates the survival of HCC via a positive feedback loop with HIF-1a, indicating that CypB is a novel candidate target for developing chemotherapeutic agents against HCC and colon cancer.

Careful close-up observation of the gastric mucosal pattern with standard endoscopy can predict H. pylori infection status.

Background/AimsHepatitis B virus (HBV) is the major cause of chronic liver disease in Korea, but viral prevalence has decreased because of hepatitis B vaccination programs. In this study, we investigated longitudinal changes in HBV in fection in the general Korean population.MethodsHBV surface antigen (hepatitis B surface antigen, HBsAg) seropositivity was assessed from the Korea National Health and Nutrition Examination Survey (I to V). In total, 50,140 subjects were tested for serum HBsAg positivity over a period of 12 years (1998 to 2010).ResultsThe prevalence of HBsAg seropositivity decreased over the study period. The rates of HBsAg carriers were 4.61% in 1998, 4.60% in 2001, 3.69% in 2005, 3.01% in 2008, and 2.98% in 2010 (p < 0.0001). The reduction in HBV infection rates was more prominent in younger age groups. Among teenagers (10 to 19 years), the percentage of HBsAg carriers decreased from 2.2% in 1998 to 0.12% in 2010 (p < 0.0001). Among those aged 10 to 39 years, the percentage of HBV infection decreased from 4.72% in 1998 to 2.29% in 2010 (p < 0.0001). However, no decreasing trend in HBsAg positivity was observed among those aged 50 or older (p > 0.05). Neither gender nor socioeconomic status were associated with the decreased prevalence of HBsAg carriers.ConclusionsHBV infection has decreased in the Korean population since the advent of vaccination programs. However, the decrease is limited to the younger population, and viral persistence remains in the middle-aged and older population.

A positive family history is an increased risk factor for gastric cancer within family members, and one of the possible causes of this is the intrafamilial clustering of Helicobacter pylori infection. Our study examined the prevalence of H. pylori infection, serum antibodies to CagA and VacA and atrophic gastritis and/or intestinal metaplasia in the offspring or siblings of gastric cancer patients. A total of 726 subjects included 300 relatives of 300 separate gastric cancer patients and 426 controls. All subjects underwent upper gastrointestinal endoscopic examination with a rapid urease test. Blood samples were obtained to test for the presence of serum antibodies to the CagA and VacA proteins of H. pylori. The prevalence of H. pylori infection was higher in relatives of cancer patients (75.3%) than in controls (60.1%), and the adjusted odds ratio was 2.1 (95% CI 1.5-2.9). When either siblings or 2 or more family members were gastric cancer patients, the prevalence of H. pylori infection was much higher compared to the prevalence in controls. Gastric cancer is the second most common cause of cancerrelated death in the world. 1 In Korea, gastric cancer is the most frequently diagnosed malignancy, although the associated mortality rate has been decreasing slowly for the past 10 years. 2 About 60% of Korean adults are infected with Helicobacter pylori. 3,4 Such infection is a causative factor in gastric carcinogenesis, and H. pylori infection is associated with a 2-fold increased risk of developing gastric adenocarcinoma. 5,6 A positive family history is also associated with an increased risk of gastric cancer. 7-10 The possible causes of familial aggregation of gastric cancer are common genetic backgrounds and common environmental risk factors including H. pylori infection, excessive intake of salt and N-nitroso compounds and a deficiency of dietary antioxidants among patients with gastric cancer and their family members. Among these risk factors, intrafamilial clustering of H. pylori infection is regarded as a leading cause of gastric carcinogenesis. This association is significantly greater for H. pylori strains that possess the cytotoxin-associated gene cagA, [11][12][13] a key gene of the so-called "pathogenicity island". 14 The first aim of our study was to examine the prevalence of H. pylori infection in offspring and siblings of patients with gastric cancer to evaluate its role in intrafamilial aggregation of gastric cancer. The second aim was to investigate the relationship between CagA or vacuolating cytotoxin (VacA) seropositivity as virulence markers of H. pylori strains and H. pylori infection in relatives of cancer patients. Finally, we examined the frequency of gastric precancerous lesion, atrophic gastritis and/or intestinal metaplasia in the H. pyloriinfected relatives of cancer patients. MATERIAL AND METHODS Recruitment of relatives of cancer patients and controlsFrom November 2000 to March 2002, we recruited subjects who wished to receive routine upper gastrointestinal endoscopy and evaluation ...

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