Search

The organ allocation system should be fair and efficient to predict the prognosis of patients with end-stage organ failure. The liver allocation system in Korea was changed to the model for end-stage liver disease (MELD) score system from Child-Turcotte-Pugh score-based status system in 2016. Since then, there have been some changes in matching liver graft to recipients in deceased liver transplantation. The severity of sickness of the end-stage liver failure patients has been increased in the MELD era than before. Since 2013, liver transplantation for alcoholic liver disease has been gradually increasing in Korea. We should take proper evaluation into consideration when we decide early liver transplantation particularly for patients with severe alcoholic hepatitis, who have a high MELD score. Above all, overcoming organ shortage, it is necessary for us to try to increase the number of deceased donors to meet the need for liver transplantation for end-stage liver disease patients.

Background/aims: The translocation of bacteria and their lipopolysaccharides from the gut can promote fibrosis in cirrhotic patients. The aim of this study was to investigate the effects of rifaximin on hepatic fibrosis in a bile duct-ligated rat model., Methods: The bile duct ligation (BDL) was carried out for eight days (acute injury model: sham-operated rats [G1], BDL rats [G2], and BDL rats treated with rifaximin [G3]) or 22 days (chronic injury model: sham-operated rats [G4], BDL rats [G5], and BDL rats treated with rifaximin [G6]). Rifaximin (50 mg/kg/day) was administered daily via gavage after BDL. Liver function, serum tumor necrosis factor-alpha (TNF-α), and hepatic hydroxyproline levels were measured. Moreover, a histological analysis of fibrosis contents was performed using sirius red stain., Results: In the acute injury model, the liver function and TNF-α level were not improved after the rifaximin treatment. The hydroxyproline levels (µg/g liver tissue) in G1, G2, and G3 were 236.4±103.1, 444.8±114.4, and 312.5±131.6, respectively; and fibrosis contents (%) were 0.22±0.04, 1.64±0.53, and 1.66±0.44, respectively. The rifaximin treatment did not ameliorate acute BDL-induced fibrosis. In the chronic injury model, the hydroxyproline levels in G4, G5, and G6 were 311.5±72.9, 1,110.3±357.9, and 944.3±209.3, respectively; and fibrosis contents (%) were 0.19±0.03, 5.04±0.18, and 4.42±0.68, respectively (G5 vs. G6, p=0.059). The rifaximin treatment marginally ameliorated chronic BDL-induced fibrosis., Conclusions: Rifaximin did not reduce inflammation and fibrosis in bile duct-ligated rat model.

Background/aims: Hepatitis C genotypes 1 and 2 are widely distributed globally. In contrast, genotype 6 is found mainly in Southeast Asia, while genotype 6 is rare in Korea. This study aims to investigate the prevalence, risk factors and clinical characteristics of patients with genotype 6 chronic hepatitis C., Methods: We retrospectively identified 133 HCV-infected patients who underwent HCV genotype analysis between January 2012 and December 2012, and analyzed the prevalence, risk factors and clinical characteristics of patients diagnosed with genotype 6 chronic hepatitis C., Results: Among 133 patients, 53 patients (39.8%) were infected with genotype 1, 62 patients (46.6%) with genotype 2, 2 patients (1.5%) with genotype 3, 14 patients (10.5%) with genotype 6, and 2 patients (1.5%) with mixed genotypes (genotype 1 and 6). The risk factors associated with genotype 6 were acupuncture (n=4, 28.6%), intravenous drug use (n=3, 21.4%), tattoo (n=2, 14.3%), and transfusion (n=2, 14.3%). Of the 14 patients with genotype 6, 6 patients were treated with pegylated interferon and ribavirin. Five patients had reached the end of treatment. All patients reaching end of treatment for genotype 6 showed early virological response and sustained virological response., Conclusions: The prevalence of genotype 6 is 10.5% and mixed infections of genotype 1 and 6 are 1.5% in patients with chronic hepatitis C. A major potential risk factor is intravenous drug use and the treatment response rate to pegylated interferon plus ribavirin is high in patients with genotype 6 chronic hepatitis C. Large scale multicenter studies are needed.

Background/aims: Nonalcoholic fatty liver disease (NAFLD) may be one of the important causes of cryptogenic hepatocellular carcinoma (HCC). The aim of this study was to evaluate whether patients with cryptogenic HCC share clinical features similar to that of NAFLD., Methods: Cryptogenic HCC was defined as HCC that occurs in patients with the following conditions: HBsAg(-), anti-HCV(-), and alcohol ingestion of less than 20 g/day. All patients diagnosed with cryptogenic HCC from 2005 to 2012 (cryptogenic HCC group), and all patients diagnosed with HBV associated HCC between 2008 and 2012 (HBV-HCC group) were enrolled in the present study. Clinical features, BMI, lipid profiles, presence of diabetes mellitus, hypertension, and metabolic syndrome were compared between the two groups., Results: Cryptogenic HCC group was composed of 35 patients (19 males and 16 females) with a mean age of 70 ± 11 years. HBV-HCC group was composed of 406 patients (318 males and 88 females) with a mean age of 56 ± 7 years. Patients in the cryptogenic HCC group were older (p=0.001) and female dominant (p=0.042) than those in the HBV-HCC group. There were no differences in the laboratory test results including lipid profiles and Child-Turcotte-Pugh class between the two groups. Patients in the cryptogenic HCC group had higher prevalence of diabetes (37% vs. 17%, p=0.015), hypertension (49% vs.27%, p=0.051), metabolic syndrome (37% vs. 16%, p=0.001), and higher BMI (25.3 kg/m(2) vs. 24.1 kg/m(2), p=0.042) than those in the HBV- HCC group. The tumor stage was more advanced (stage III and IV) at diagnosis in the cryptogenic HCC group than in the HBV-HCC group (60% vs. 37%, p=0.007)., Conclusions: Cryptogenic HCC has clinical features similar to that of NAFLD and is diagnosed at a more advanced tumor stage.

Hepatocellular carcinoma (HCC) is a critical global health issue and the third most common cause of cancer-related deaths worldwide. The majority of patients who present HCC are already at an advanced stage and their tumors are unresectable. Sorafenib is a multi-kinase inhibitor of the vascular endothelial growth factor pathway and was recently introduced as a therapy for advanced HCC. Furthermore, studies have shown that oral sorafenib has beneficial effects on survival. However, many patients experience diverse side effects, and some of these are severe. Liver abscess development has not been previously documented to be associated with sorafenib administration in HCC. Here, we report the case of a HCC patient that developed a liver abscess while being treated with sorafenib.

Background/aims: Clevudine is a potent antiviral agent against HBV. However, long-term clevudine therapy may cause myopathy. This study was carried out to identify the efficacy of entecavir switching therapy in chronic hepatitis B patients experiencing clevudine-induced myopathy., Methods: One hundred forty six patients with chronic hepatitis B treated with 30 mg of clevudine per day for 73 weeks (range, 36-132 weeks) were enrolled. Among them, clevudine-induced myopathy occurred in 21 patients (14.4%) which was diagnosed if the patients had symptoms related to myopathy with concurrent CK and AST elevation. All the patients who were diagnosed as clevudine-induced myopathy stopped the therapy, and 17 patients (81%) were switched to entecavir 0.5 mg., Results: The patients with clevudine-induced myopathy were switched to entecavir 0.5 mg for median 68 weeks, and all of them showed disappearance of clinical myopathic symptoms and normalization of CK and AST level within median 2.2 months. Eight patients (47%) were HBeAg positive before entecavir treatment, and HBeAg seroconversion was achieved in 2 patients (25%). HBV DNA level was elevated in 3 patients (17.6%) at the time when the patients were diagnosed as myopathy, all of them achieved virological response with entecavir switching therapy. ALT level was elevated in 3 patients (17.6%) before entecavir treatment, all of them showed normalization of ALT level. During entecavir therapy, genotypic resistance to entecavir or virological breakthrough was not noted., Conclusions: In chronic hepatitis B patients experiencing clevudine-induced myopathy, switching to entecavir 0.5 mg per day showed a resolution of myopathy and adequate viral suppression.

Background/aims: A combination of peginterferon and ribavirin is the standard therapy for chronic hepatitis C (CHC). However, the respective study has not been carried out in a large scale in Korea. The purpose of this study was to collect the studies that have been reported in Korea in order to analyze the therapeutic effect of combination therapy and compare to find racial difference., Methods: Twenty-eight papers related to the therapeutic effect of combination therapy in CHC patients were analyzed based on pooled analysis., Results: Based on the analysis for genotype 1 in Korea, early virologic response (EVR), end of treatment response (ETR), and sustained virologic response (SVR) were 79.6% (125/157), 80.1% (166/207), and 62.7% (341/543). The EVR, ETR, and SVR for genotype 2 and 3 were 89.4% (119/133), 92.2% (203/220), and 84.1% (434/516). Data from other Asians showed that EVR and SVR for genotype 1 were 88.9% (290/326) and 64.4% (491/762) respectively and 88.8% (135/152), and 79.4% (151/190) for genotype 2 and 3 respectively. In Western, EVR and SVR for genotype 1 were 51.3% (1,981/3,860) and 42.4% (1,798/4,231) respectively, and for genotype 2 and 3 were 87.7% (350/399) and 77.8% (533/685) respectively. Based on the comparative analysis, no statistical difference in SVR between Koreans and other Asians (p=0.955) was observed; However, the SVR of Koreans was higher with significance than that of Westerns (p<0.001) On the other hand, there was no difference what so ever, in SVR for genotype 2 amongst the different races., Conclusions: The SVR of combination therapy for the Korean chronic hepatitis C patients was similar to other Asians but higher than Westerns.

Background/aims: In the Helicobacter pylori (H. Pylori)-negative normal stomach, collecting venules are visible over all the gastric body as numerous minute points evaluated with standard endoscopy. This finding was termed regular arrangement of collecting venules (RAC), and its absence suggests H. pylori gastritis. The aim of this study was to evaluate the correlation between the RAC and rapid urease test., Methods: Two hundred sixty three consecutive adults undergoing upper digestive endoscopy and rapid urease test were included. The lesser curvature of the lower corpus was evaluated for the RAC pattern using a standard endoscope and different hemoglobin index. Two biopsies from the lesser curvature of the antrum and the greater curvature of the body were collected for rapid urease test., Results: H. pylori were detected in 51.3% (135/263) patients. Of the 57 patients with H. pylori-negative normal stomachs 53 patients (93%) had RAC. As a determinant of the normal stomach without H. pylori infection, the presence of RAC had 41.4% sensitivity, 97.0% specificity, 93.0% positive predictive value and 63.6% negative predictive value., Conclusions: RAC-positive finding by standard endoscopy showed high positive predictive value and specificity of H. pylori-negative normal stomach. RAC-positive finding by standard endoscopy could be an useful finding to predict H. pylori negativity.

Complications of acute pancreatitis usually occur in pancreas and its contiguous organs. The prevalence of colonic invasion is rare, however, the consequence is fatal, with mortality above 50%. The initial symptoms and onset times are variable and major affected sites are transverse colon and splenic flexure. The spread of inflammatory exudates into the colon is the main mechanism of colonic invasion. If the colonic stenosis develops, it is necessary to manage it surgically. We report a case who arrived at the hospital with watery diarrhea and abdominal distension in the recovery period of acute alcoholic pancreatitis and was diagnosed as a colonic obstruction in the splenic flexure. The patient underwent loop ileostomy instead of the resection of the lesion because of severe adhesion around the splenic flexure. The patient died due to sepsis 5 days after the operation.

Background/aims: Pancreatic acini of streptozotocin (STZ)-induced diabetic rats release amylase less than normal acini on cholecystokinin (CCK) stimulation. Pancreatic enzyme secretion has been closely related to the intracellular calcium concentration ([Ca2(+)](i)) of the acinar cell. In the present study, sequential changes of the intracellular calcium signal which probably underlie the altered enzyme secretion in response to CCK-8 were investigated using pancreatic acini from diabetic rats., Methods: Diabetic rats were prepared by single intravenous injection of STZ (70 mg/kg). Stimulating experiments with CCK-8 were performed 7 days later. Pancreatic acini were isolated by collagenase digestion. Amylase release and [Ca2(+)](i) were measured by colorimethod and calcium imaging, respectively. The geometry of intracellular calcium signal was analyzed., Results: Normal acini exhibited concentration-dependent [Ca2(+)](i) increase and regular oscillatory calcium signal on CCK-8 stimulation. Amylase release was also concentration-dependent. However, diabetic acini showed significantly less [Ca2(+)](i) increase, prolonged time to peak [Ca2(+)](i), decreased calcium spikes number, and decreased amylase release compared with normal acini. The decreased [Ca2(+)](i) in diabetic acini was restored significantly by insulin treatment., Conclusions: Relatively decreased amylase release in diabetic pancreatic acini in response to CCK, appears to be associated with altered calcium signal due to insulin deficiency.

Background/aims: Oxidative stress may contribute to gastric epithelial damage and mutagenesis caused by Helicobacter pylori (H. pylori). H. pylori induces recruitment and activation of inflammatory cells, which produces reactive oxygen species. H. pylori extract directly induces the synthesis of reactive oxygen species in gastric epithelial cells and causes DNA damage. The aim of this study was to investigate the association between the levels of glutathione (GSH) and H. pylori density, histological findings, endoscopic findings, clinical variables, and virulence factors., Methods: Gastric biopsy specimens were obtained from 73 consecutive patients. The 5,5'-dithiobis-(2-nitrobenzoic acid) reaction was used to determine GSH levels., Results: The infection rate of H. pylori was 68.5%. The GSH level was not related to age, sex, alcohol intake, and endoscopic findings. The GSH level was lower in patients infected with H. pylori. GSH levels were not correlated significantly with the grades of neutrophil, intestinal metaplasia, and atrophy. However, the GSH levels were significantly correlated with H. pylori density (r=-0.296, p=0.01) and monocyte grade (r=-0.257, p=0.02). The GSH levels were not related to CagA, VacA, and UreA., Conclusions: This study suggests that H. pylori causes oxidative stresses which deplete GSH in gastric mucosa of patients infected with H. pylori.

Background/aims: The genetic polymorphism of transforming growth factor-beta1 (TGF-beta1) at codons 10 and 25 which influences the production of TGF-beta1 is related to fibrogenesis in the lung and liver. We evaluated the genetic polymorphism at codons 10 and 25 in controls and in patients with liver cirrhosis (LC) and hepatocellular carcinoma (HCC)., Methods: Blood samples were collected from controls (n=35), patients with LC (n=64), and HCC (n=49). Genomic DNA was isolated and polymerase chain reaction (PCR) was done for a segment including codons 10 and 25. The results of direct sequencing for PCR products were compared between the controls and the patients., Results: There was no genetic polymorphism at codon 25 and three types of genetic polymorphism at codon 10. The leucine homozygous genotype (CTG/CTG) at codon 10 was more common in patients with LC than the controls (p=0.01) and especially in patients with LC caused by HBV (p=0.004). The polymorphism at codons 10 in patients with HCC was similar to the controls. However, leucine homozygous genotype was more common in patients with HCC of uninodular morphology than those of massive morphology (p=0.007)., Conclusions: The genetic polymorphism of TGF-beta1 at codon 10 might be associated with LC and morphology of HCC. The potential usefulness of TGF-beta1 genotyping needs further studies in large scale.

Background/aims: It was reported that the prevalence of Helicobacter pylori (H. pylori) infection decreased after gastrectomy, but persistent H. pylori infection may cause residual gastritis or stump cancer. We studied the prevalence of H. pylori infection in patients who had undergone subtotal gastrectomy for the treatment of gastric cancer and the factors that influence H. pylori positivity in the remnant stomach., Methods: Ninety-eight patients who had undergone radical subtotal gastrectomy (RSG group) for the treatment of gastric cancer and eighty-four patients diagnosed as having gastric cancer (GC group) were enrolled. H. pylori status was diagnosed by rapid urease test, histological examination, and 13C-urea breath test. We evaluated whether there were differences in various clinical characteristics according to the H. pylori status in the remnant stomach., Results: The prevalences of H. pylori infection in RSG group and GC group were 55% and 69%, respectively. In RSG group, the prevalence of H. pylori was 76.9% in patients aged 49 or less, and it decreased with age. The prevalence of H. pylori within 3 years of gastrectomy was 59.5% and it decreased to 28.6% after 3 years of gastrectomy., Conclusions: The positive rate of H. pylori in RSG group is lower than that in GC group and decreases with age and time interval after operation.