Search

Although, gastric cancer is quite common in Korea, the treatment outcome is relatively favorable compared to that of Western countries. However, there is no Korean multidisciplinary guideline for gastric cancer and thus, a guideline adequate for domestic circumstances is required. Experts from related societies developed 22 recommendation statements for the diagnosis (n=9) and treatment (n=13) based on relevant key questions. Evidence levels based on systematic review of literatures were classified as five levels from A to E, and recommendation grades were classified as either strong or weak. The topics of this guideline cover diagnostic modalities (endoscopy, endoscopic ultrasound, radiologic diagnosis), treatment modalities (surgery, therapeutic endoscopy, chemotherapy, radiotherapy) and pathologic evaluation. External review of the guideline was conducted at the finalization phase.

Background/aims: DNA double strand breaks (DSB) is one of the critical types of DNA damage. If unrepaired, DSB is accumulated in the nucleus of cells, the cells become apoptotic or transform to tumor by way of genomic instability. Some of malignant cancers and its premalignant lesions were proven to have DSB in their nuclei. There was no report that Helicobacter pylori (H. pylori), the gastric carcinogen, induce DNA DSB in gastric epithelium in vivo. The aim of this study was to investigate whether H. pylori induce DSB in the gastric epithelial cells of chronic gastritis., Methods: Immunohistochemical stains were performed for the DSB markers, phospho-53BP1 and gH2AX, in the gastric epithelium derived from 44 peptic ulcer disease patients before and after H. pylori eradication. DNA fragmentation assay was performed in the cell line to investigate the DNA damage by H. pylori infection., Results: The mean expression score of gH2AX was significantly higher in the H. pylori infected gastric epithelium as compared to the H. pylori eradicated gastric epithelium (8.8±5.5 vs. 6.2±5.3 respectively; p=0.008). The expression score of phospho-53BP1 between before and after eradication of H. pylori was not statistically different, but tended to be higher in H. pylori infection. DNA fragmentation was developed significantly more in the cell lines after infection with H. pylori., Conclusions: DSB of DNA damage was typical feature of H. pylori infection in the gastric epithelium.

Background/aims: An association between past history of hepatitis B virus (HBV) infection and pancreatic cancer (PC) has recently been reported. We investigated whether HBV and hepatitis C virus (HCV) infections are associated with the development of PC in Korea., Methods: We retrospectively recruited patients with PC and sex- and, age-matched control patients with stomach cancer (SC) during the previous 5 years. Serum HBsAg and anti-HCV were examined, and data on smoking, alcohol intake, diabetes, and the history of chronic pancreatitis (CP) were collected., Results: A total of 506 PC and 1008 SC were enrolled, with respectively 58.1% and 97.3% of these cases being confirmed histologically. The mean age and sex ratio (male:female) were 63.5 years and 1.5:1 in the PC patients and 63.9 years and 1.5:1 in the SC patients respectively (P>0.05). The odds ratios (95% confidence interval, 95% CI) in univariate analysis were 0.90 (0.52-1.56; P=0.70) for HBsAg, 1.87 (0.87-4.01; P=0.11) for anti-HCV, 2.66 (2.04-3.48; P<0.001) for the presence of diabetes, 2.30 (1.83-2.90; P<0.001) for smoking, 1.14 (0.89-1.46; P=0.31) for alcohol intake, and 4.40 (1.66-11.66; P=0.003) for the history of CP. Independent risk factors for PC were presence of diabetes (OR, 2.67; 95% CI, 2.00-3.56; P<0.001), smoking (OR, 2.49; 95% CI, 1.93-3.21; P<0.001) and history of CP (OR, 4.60; 95% CI, 1.56-13.53; P=0.006)., Conclusions: There was no significant association between seropositivity for HBsAg or anti-HCV and PC. Further studies are warranted to clarify the association between HBV infection and PC in regions where HBV is endemic.

No abstract availble.

Background/aims: DNA double strand break (DSB) is one of the critical types of DNA damage. When unrepaired DSB is accumulated in the nucleus of the cells having mutations in such genes as p53, it will lead to chromosomal instability and further more to mutation of tumor-activating genes resulting in tumorogenesis. Some of malignant cancers and its premalignant lesions were proven to have DSB in their nuclei. The aim of this study was to define the differences in expression of 53BP1 and gamma-H2AX, the markers of DSB, among normal, gastric adenoma, and gastric adenocarcinoma tissues., Methods: Tissue microarray was made with the tissues taken from 121 patients who underwent gastrectomy for gastric adenocarcinoma, and 51 patients who underwent endoscopic mucosal resection for gastric adenoma. Immunochemical stain was performed for the marker of DSB, 53BP1 and gamma-H2AX in the tissue microarray. The normal tissues were collected from histologically confirmed tissues with no cellular atypia obtained from the patients with gastric adenocarcinoma., Results: In gastric carcinoma cells, 53BP1 and gamma-H2AX were highly expressed as compared to normal epithelial cells and gastric adenoma (p<0.01). There were no differences in the expression of 53BP1 and gamma-H2AX between normal epithelium and gastric adenoma. The expression of 53BP1 in the adenoma with grade II and III atypism was more elevated than in those with grade I atypism. The expression of 53BP1 and gamma-H2AX were not significantly different according to the clinicopathologic parameters in the patients with gastric adenocarcinoma., Conclusions: The DSB in DNA seems to be associated with the development of gastric adenocarcinoma, but does not affect the premalignant adenoma cells.

Epithelioid hemangioendothelioma is a neoplasm of vascular origin with a low-to-intermediate malignant potential and is one of the rare sarcomas arising from the liver. Its etiology is unknown and its clinical outcome is unpredictable. There is no generally accepted therapeutic strategy because of its rarity and the variable natural course between hemangioma and angiosarcoma. We report a case of a 64-year old woman who underwent hepatic resection due to epithelioid hemangioendothelioma in the right lobe that progressed to extrahepatic metastases of the bone, pleura, and peritoneum 22 months later. However, after resection there was no primary hepatic recurrence.

Henoch-Schonlein purpura (H-S purpura) is a systemic small-vessel vasculitis involving skin, joint, gastrointestinal tract, and kidney. It is characterized by the classic tetrad of abdominal pain, arthralgia, typical rash, and renal involvement. All of these clinical findings can occur in any order and at any time over several days to weeks. Gastrointestinal manifestations such as abdominal pain, melena, or hematochezia occur in 45-85% and preceed skin lesions up to 40% in H-S purpura. However, endoscopically proven gastrointestinal lesion is rare because majority of involved sites are small intestine. We report a case of Henoch-Schonlein purpura with terminal ileal ulcer, healed after treatment with high dose steroid, proven by colonoscopy.

Background/aims: Deterioration of renal function in patients with cirrhosis and spontaneous bacterial peritonitis (SBP) is the most sensitive predictor of in-hospital mortality. It has been shown that high dose intravenous albumin in addition to antibiotics reduces the incidence of renal impairment and improve hospital survival in these patients. Besides, it is important to know which patients would benefit from albumin infusion. Therefore, we conducted a retrospective study to elucidate the incidence and risk factors of renal dysfunction in cirrhotic patients with SBP., Methods: All medical records of 76 consecutive episodes of SBP in 60 patients were analyzed. Renal dysfunction after SBP was defined as elevation of BUN >30 mg/dL or serum creatinine >1.5 mg/dL in patients without preexisting renal insufficiency, or elevation of more than 50% of the baseline level in patients with renal dysfunction at the diagnosis of infection., Results: Of the 76 episodes, renal dysfunction was present in 31 (40.8%). Age, concurrent use of diuretics, large volume paracentesis (LVP) with volume expander, initial BUN and creatinine level were significant risk factors on univariate analysis. Of these, age and LVP were independent risk factors on logistic regression model., Conclusions: Renal dysfunction occurs in 40.8% of hospitalized patients after SBP. Considering poor prognosis of patients with renal dysfunction in SBP, close monitoring of renal function is needed and high dose intravenous albumin with antibiotics should be used especially in the elderly and those with LVP.

Background/aims: Serum alpha-fetoprotein (AFP) is frequently used for the diagnosis of hepatocellular carcinoma (HCC). Most available data concerning AFP came from studies of patients with chronic hepatitis B or mixed etiologies. Studies concerning the diagnostic value of AFP for HCV-related liver cirrhosis (LC) are limited. We evaluated the factors influencing AFP elevation in the absence of HCC and analyzed the diagnostic value of serum AFP in HCC surveillance of HCV-related LC patients., Methods: We enrolled 55 patients of HCV-related LC with HCC and 62 patients without HCC as a case-control study were analyzed. The sensitivity and specificity were calculated and the clinical and biochemical factors influencing serum AFP levels., Results: The sensitivities and specificities of serum AFP for the detection of HCC in HCV-related LC were 72.7% and 59.7% for AFP>or=20 ng/mL, and 47.3% and 92.5% for AFP>or=100 ng/mL, respectively. Elevated serum AST was independently associated with elevated serum AFP level in HCV-related LC. In cases of ASTor=100 ng/mL for the diagnosis of HCC was 100%. However, in case of AST>2 ULN, the specificity was 85.0% for AFP>or=100 ng/mL and 95.0% for AFP>or=200 ng/mL., Conclusions: Serum AST levels influence serum AFP level in HCV-related LC. In cases of AST2 ULN.

Hepatoid carcinoma is a primary extrahepatic neoplasm exhibiting features of hepatocellular carcinoma (HCC) in terms of morphology, immunohistochemistry, and behavior. In many cases, tumor cytoplasm is positive for alpha- fetoprotein (alpha-FP) with elevated serum alpha-FP level. Because not all hepatoid carcinomas are associated with alpha- FP overproduction, diagnosis should be made essentially by histological features of the tumor. We present a case of hepatoid carcinoma of the pancreas in a 21-year-old male patient. Abdominal computed tomography and magnetic resonance imaging revealed an inhomogeneously enhanced pancreatic head mass. Serum alpha-FP level was markedly elevated. He underwent pylorus-preserving Whipple's operation. The tumor showed hepatoid and neuroendocrine components simultaneously. The histopathological diagnosis was hepatoid carcinoma associated with neuroendocrine tumor of the pancreas. Seven months after the surgery, the patient is healthy without evidence of recurrence. To date, only 7 cases of hepatoid carcinoma of the pancreas have been reported in the literature, and this is the first case report in Korea.

Cholestasis in a patient with Hodgkin's disease is uncommon, and the causes of cholestasis are mainly direct tumor involvement of the liver, hepatotoxic effects of drugs, viral hepatitis, sepsis and opportunistic infections. Vanishing bile duct syndrome (VBDS) represents a very rare cause for cholestasis in this disease. We report here on a case of a 45-year-old man who developed VBDS during the complete remission stage of Hodgkin's lymphoma. There was no history of hepatitis or intravenous drug abuse, and the patient had negative results for hepatitis A virus, hepatitis B virus, hepatitis C virus, cytomegalovirus, and human immunodeficiency virus. The serological studies for antinuclear antibodies, anti-mitochondrial antibodies and anti-smooth muscle antibodies were also negative. Liver biopsy disclosed the absence of interlobular bile ducts in 9 of 10 portal tracts without any active lymphocyte infiltration and there were no Reed-Sternberg cell in the liver. The patient's cholestasis was in remission and the serum bililrubin level was normalized after two months without treatment, but tumor recurrence was noted at multiple sites of the abdominal lymph nodes on follow-up abdomino-pelvic computed tomogram.

Background/aims: E-cadherin is involved in intercellular binding and cellular polarity formation. beta-catenin plays a fundamental role in regulation of the E-cadherin cell adhesion complex. The abnormalities of the components of the complex may disrupt this adhesive function. We investigated the expression patterns of E-cadherin and beta-catenin to determine the clinical significance of these proteins in hepatocellular carcinoma., Materials/methods: Thirty-six hepaticellular carcinoma tissues and adjacent non-tumor specimens were analyzed. Subcellular distribution of E-cadherin and beta-catenin was examined by immunohistochemistry staining. We evaluated the patterns of the expression, and investigated the relationship with the cause of HCC; level of AFP; TNM stage; tumor size; growth types; metastasis; differentiation grade of HCC; and presence of portal vein thrombosis., Results: Immunohistochemistry showed that all non-tumor tissues had membranous type staining of E-cadherin. All non-tumor tissues showed cytoplasmic type staining of beta-catenin, but no beta-catenin accumulation in nuclei was found. 58% (21/36) of HCC showed positive expression of E-cadherin in cytoplasmic membrane. The cytoplasmic expression of beta-catenin in HCC was 83% (30/36); nuclear expression in 14% (5/36); and no staining in 3% (1/36). Nuclear beta-catenin expression was observed in none (0/4) of the well-differentiated HCC; 17%(3/9) of moderate-differentiated HCC; and 17%(2/6) of poorly-differentiated HCC. There were no relationships between E-cadherin and beta-catenin expression with other clinicopathologic factors., Conclusions: Loss of cytoplasmic staining of E-cadherin and nuclear accumulation of beta-catenin were observed in HCC. Nuclear accumulation of beta-catenin was not found in well differentiated HCC but was found in poorly differentiated HCC.