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Background/aims: Globally, the population aged 80 years or older is growing faster due to the rising life expectancy. Korea has already entered into an advanced aged society, and a post-aged society is expected in 2025. This study evaluated the patterns of gastrointestinal disease in the population aged 80 years or older during the recent decade in Korea., Method: This study retrospectively reviewed the medical records of patients admitted to the gastrointestinal department of Suwon St. Vincent's hospital, Incheon St. Mary's hospital, and Uijeongbu St. Mary's Hospital - general hospitals of Seoul-Gyeonggi province in Korea. It was a repeated cross-sectional study in 2009 and 2019., Results: The number of admitted patients aged 80 years or older increased from 549 (9.0%) in 2009 to 1,073 (14.4%) in 2019 (p<0.01). As for the in-hospital mortality, there was no significant difference (p=0.25). On the other hand, the combined morbidities increased, and the duration of admission also increased (7.2±7.8 days vs. 8.1±8.2 days, p=0.03). The number of upper gastrointestinal hemorrhage and patients who are bleeding associated with drugs users increased (p<0.01). The proportion of lower gastrointestinal disease decreased (p<0.01) because of the decrease in procedure-related admissions (p<0.01). The number of those with pancreaticobiliary tract disease increased markedly (p<0.01), and the rate of cases that could not perform the procedure decreased (p=0.04)., Conclusion: The patterns of gastrointestinal disease in the population aged 80 years or older have changed in the recent decade in Korea. Hence, more preparation for this medical environment is needed.

Paraneoplastic hypercalcemia without bone metastasis occurs rarely in esophageal cancer. A 75-year-old man was admitted for general weakness and lethargy. Laboratory data showed high serum calcium level (corrected calcium 14.6 mg/dL), low parathyroid hormone level (3.3 pg/mL) and high parathyroid hormone-related peptide level (3.5 pmol/L). Esophagogastroscopy showed a malignant tumor in the esophagus. Histology showed moderately differentiated squamous cell carcinoma. Bone scan showed no evidence of bone metastasis. Since the patient's calcium levels remained high and mental state did not show improvement despite intravenous fluid therapy, diuretics and intravenous bisphosphonate, hemodialysis was started. After hemodialysis treatment, the serum calcium level subsequently normalized and his mental status improved. Herein, we report a rare case of paraneoplastic hypercalcemia in a patient with esophageal cancer.

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: Ligands for peroxisome proliferator-activated receptorgamma (PPARgamma), a member of the ligand-activated nuclear receptor superfamily, exhibit anti-tumoral effects and are associated with de novo synthesis of proteins involved in regulating the cell cycle and cell survival/death. Helicobacter pylori (H. pylori) is an etiologic agent for gastric adenocarcinoma, and raises the cell turnover of gastric epithelium. The aim of this study was to investigate the effect of PPARgamma ligand rosiglitazone on the cell proliferation and the expressions of p27 and Skp2 protein in H. pylori infected gastric epithelial cells., Methods: We examined the expression of PPARgamma by Western blot in H. pylori infected AGS human gastric epithelial cells. The effect of rosiglitazone on the survival of H. pylori infected AGS cells was assessed by cell viability assay. After the treatment of rosiglitazone in H. pylori infected AGS cells, the expressions of p27 and Skp2 were assessed by Western blot., Results: The expression of PPARgamma protein was increased in H. pylori infected AGS cells. Cell growth was inhibited and decreased in dose- and time- dependent manner in H. pylori infected AGS cells treated with rosiglitazone. A decrease in Skp2 expression and a reciprocal increase in p27 expression were found in dose- and time-dependent manner in H. pylori infected AGS cells treated with rosiglitazone., Conclusions: Rosiglitazone inhibited the growth of H. pylori infected AGS cells. Rosiglitazone attenuated Skp2 expression, thereby promoting p27 accumulation in H. pylori infected human gastric epithelial cells. Further studies will be needed to find the effects of accumulation on cell turnover in H. pylori infection and the role in the H. pylori-associated gastric carcinogenesis.

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.

Background/aims: The cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), the proteins that have the role in the gastric carcinogenesis, are stimulated by H. pylori infection in the gastric mucosa. The aim of this study was to evaluate the expression of COX-2 and iNOS proteins one year after the eradication of H. pylori., Methods: Gastric antral mucosa from fifty eight patients with chronic gastritis who were all infected with H. pylori was examined for the expression of COX-2 and iNOS proteins before and one year after the eradication of H. pylori by immunohistochemical stain., Results: COX-2 and iNOS proteins were expressed in the epithelial cells and interstitial inflammatory cells of gastric mucosa. Percent expressions of COX-2 and iNOS were significantly decreased one year after the eradication in the patients with cured infection, but not in those having persistent H. pylori. COX-2 and iNOS expressions were well correlated with H. pylori density, acute and chronic inflammation of gastric mucosa., Conclusions: The eradication of H. pylori can decrease the expression of COX-2 and iNOS in the gastric mucosa in long-term period. This seems to be due to the removal of H. pylori itself and related regression of gastric inflammation.

Background/aims: Sentinel lymph node (SLN) mapping of the stomach cancer using available techniques is limited by unpredictable lymphatic drainage patterns and skip metastasis. The aim of this study was to test the feasibility of gastric SLN mapping using fluorescent magnetic nanoparticles (FMNP) of uniform nano-size., Methods: Biocompatible silica-overcoated magnetic nanoparticles containing rhodamine B isothiocyanate (RITC) within a silica shell of controllable thickness with 60 nm thickness were used as model nanomaterials. Gastric lymphatic mapping was performed by injecting 100 microL of either FMNP or isosulafan blue subserosally. Gastric injections (n=7) were made into the body, approximately 5 cm from the lesser curvature of rabbits. Sentinel lymph nodes were visualized using fluorescent nanoparticle detection system., Results: In 7 rabbits, it was demonstrated that FMNP quickly and accurately detected sentinel lymph nodes. Injection into the stomach resulted in identification of a retrogastric lymph node. Histological analysis in all cases confirmed the presence of nodal tissue., Conclusions: FMNP can be a potential alternative to existing tracers in the detection of SLN in this animal experiment.

Background/aims: This study was designed to investigate the role of gastric acid in the extent of H. pylori-induced gastritis., Methods: Twenty eight mice were inoculated with live H. pylori. They were allocated into four groups. Mice in group I received no treatment, group II mice were treated with sham injection, group III received 125 microg/kg body weight of pentagastrin, while group IV received 250 microg/kg body weight of pentagastrin subcutaneously three times a week. After 7 months, the mucosal pH, H. pylori density, neutrophils and monocytes infiltration, and the degree of atrophy were assessed in the stomach., Results: In the gastric body, the densities of H. pylori were not different among groups. The degree of neutrophil infiltration was significantly lower in group IV compared to other groups (p<0.05). The degree of monocyte infiltration was also significantly lower in group IV than group III (p<0.05). In the gastric antrum, there was no significant difference of the H. pylori density, neutrophil and monocyte infiltration, and degree of atrophy among the groups. The mice with the gastric mucosal pH lower than mean of 3.2 had significant lower level of H. pylori density (1.4 vs. 2.4, p=0.04), and infiltration of neutrophils (0.9 vs. 2.3, p=0.018), and monocytes (1.2 vs. 1.8; p=0.011) than the those with mucosal pH above 3.2 in the body of stomach., Conclusions: Gastric acid plays a role in suppressing the proximal propagation of H. pylori-induced gastritis to the body of stomach.

Background/aims: Peroxisome proliferator-activated receptor gamma (PPAR gamma), a nuclear transcription factor, plays a critical role in the regulation of gene expression associated with inflammation and cancer. PPAR gamma is expressed in human gastric cancer as well as in colon cancer. Activation of PPAR gamma by ligand produces pro-apoptotic effect and ameliorate growing of cancer cells. Helicobacter pylori (H. pylori) is a main etiologic agent for gastric inflammation, and raises cell turnover in gastric epithelium. Longstanding infection with this organism is related with the development of non-cardiac gastric cancer. The aim of this study was to investigate the effect of H. pylori on the expression of PPAR gamma protein and mRNA in chronic gastritis., Methods: Gastric biopsy samples were taken from H. pylori infected (n=18) and non-infected (n=21) patients during endoscopic examination. PPAR gamma expressions were assessed by real time polymerase chain reaction and immunohistochemistry., Results: PPAR gamma was localized to the nuclei of the foveolar epithelial cells in both infected and non-infected mucosa. PPAR gamma protein expression was higher in H. pylori infected patients than in non-infected patients (3.8+/-0.4 vs. 2.6+/-1.0, H. pylori infected and non-infected, respectively; p<0.05). However, PPAR gamma mRNA levels were not significantly different between the two groups (24+/-18 vs. 29+/-25, H. pylori infected and noninfected, respectively)., Conclusions: PPAR gamma expression is increased in the gastric mucosa of H. pylori infected chronic gastritis, which suggests a certain role of PPAR gamma in the mucosal inflammatory reaction to H. pylori infection.

Inflammatory pseudotumor is a benign disease, which is histologically composed of the inflammatory cells such as mature lymphocytes, plasma cells, and histiocytes. It usually occurs in the respiratory system, liver, central nervous system, and gastrointestinal tracts. However, inflammatory pseudotumor rarely occurs in the spleen. Pathologic diagnosis is essential for the definitive diagnosis because of the difficulty in distinguishing pseudotumor from lymphoproliferative disorders of the spleen. We report a case of inflammatory pseudotumor of the spleen. A 35-year-old woman complained of the intermittent epigastric pain for several months. Physical examination and laboratory findings were normal. Ultrasonography and abdominal computerized tomography showed a low attenuation splenic mass suggesting lymphoma. However, the pathologic findings of the resected spleen were consistent with those of the inflammatory pseudotumor. The spleen weighed 230 g containing a 6 x 5 x 5 cm-sized, well-circumscribed gray mass. The microscopic findings indicated the inflammatory cell infiltrations.