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In the ABC method, which is a method for risk stratification of gastric cancer using serum anti-Helicobacter pylori antibody and pepsinogen (PG) test, subjects with normal PG and seronegative for H. pylori are named as "Group A" and are regarded as having a low risk of gastric cancer. These "Group A" subjects include unintentionally eradicated cases at relatively high risk, and this study aimed to identify these subjects.Of the 109 subjects, 76 were classified as uninfected Group A subjects with negative histologic H. pylori infection and no histologic and endoscopic atrophy, and 33 subjects were classified serologically as Group A after successful eradication, which are serologically equal to the unintendedly eradicated cases in Group A. The usefulness of measuring PG levels to detect post-eradication cases was validated by using a receiver operating characteristic (ROC) curve analysis.The area under the ROC curve for PGI level was 0.736 ± 0.06 (p0.01; cutoff value, 37.0 ng/mL; sensitivity, 77.6%; specificity, 72.7%), and that for the PGI/II ratio was 0.660 ± 0.06 (p0.01; cutoff value, 5.1; sensitivity, 84.2%; specificity, 43.4%).PGI levels of ≤37 ng/mL and PGI/II ratios of ≤5.1 effectively identified unintendedly eradicated cases in Group A.

Backgrounds/Aims: In the ABC method, which is a method for risk stratification of gastric cancer using serum anti-Helicobacter pylori antibody and pepsinogen (PG) test, subjects with normal PG and seronegative for H. pylori are named as “Group A” and are regarded as having a low risk of gastric cancer. These “Group A” subjects include unintentionally eradicated cases at relatively high risk, and this study aimed to identify these subjects. Methods: Of the 109 subjects, 76 were classified as uninfected Group A subjects with negative histologic H. pylori infection and no histologic and endoscopic atrophy, and 33 subjects were classified serologically as Group A after successful eradication, which are serologically equal to the unintendedly eradicated cases in Group A. The usefulness of measuring PG levels to detect post-eradication cases was validated by using a receiver operating characteristic (ROC) curve analysis. Results: The area under the ROC curve for PGI level was 0.736 ± 0.06 (p < 0.01; cutoff value, 37.0 ng/mL; sensitivity, 77.6%; specificity, 72.7%), and that for the PGI/II ratio was 0.660 ± 0.06 (p < 0.01; cutoff value, 5.1; sensitivity, 84.2%; specificity, 43.4%). Conclusion: PGI levels of ≤37 ng/mL and PGI/II ratios of ≤5.1 effectively identified unintendedly eradicated cases in Group A.

The “ABC method” is a serum gastric cancer screening method, and the subjects were divided based onH. pyloriserology and atrophic gastritis as detected by serum pepsinogen (PG): Group A [H. pylori(−) PG (−)], Group B [H. pylori(+) PG (−)], Group C [H. pylori(+) PG (+)], and Group D [H. pylori(−) PG (+)]. The risk of gastric cancer is highest in Group D, followed by Groups C, B, and A. Groups B, C, and D are advised to undergo endoscopy, and the recommended surveillance is every three years, every two years, and annually, respectively. In this report, the reported results with respect to further risk stratification by anti-H. pyloriantibody titer in each subgroup are reviewed: (1) high-negative antibody titer subjects in Group A, representing posteradicated individuals with high risk for intestinal-type cancer; (2) high-positive antibody titer subjects in Group B, representing active inflammation with high risk for diffuse-type cancer; and (3) low-positive antibody titer subjects in Group C, representing advanced atrophy with increased risk for intestinal-type cancer. In these subjects, careful follow-up with intervals of surveillance of every three years in (1), every two years in (2), and annually in (3) should be considered.

Objectives Several clinical factors; overweight, male gender and increasing age, have been implicated as the etiology of hiatal hernia. Esophageal shortening due to acid perfusion in the lower esophagus has been suggested as the etiological mechanism. However, little is known about the correlation between gastric acidity and sliding hiatus hernia formation. This study examined whether increased gastric acid secretion is associated with an endoscopic diagnosis of hiatal hernia. Methods A total of 286 consecutive asymptomatic patients (64 were diagnosed as having a hiatal hernia) who underwent upper gastrointestinal endoscopy were studied. Clinical findings including fasting gastric juice pH as an indicator of acid secretion, age, sex, body mass index, and Helicobacter pylori infection status determined by both Helicobacter pylori serology and pepsinogen status, were evaluated to identify predictors in subjects with hiatal hernia. Results Male gender, obesity with a body mass index >25, and fasting gastric juice pH were significantly different between subjects with and without hiatal hernia. The cut-off point of fasting gastric juice pH determined by receiver operating curve analysis was 2.1. Multivariate regression analyses using these variables, and age, which is known to be associated with hiatal hernia, revealed that increased gastric acid secretion with fasting gastric juice pH 25 (OR = 3.49, 95% CI: 1.77–6.91) and age >65 years (OR = 1.86, 95% CI: 1.00–3.45), were also significantly associated with hiatal hernia. Conclusions This study suggests that increased gastric acid secretion independently induces the development of hiatal hernia in humans. These results are in accordance with the previously reported hypothesis that high gastric acid itself induces hiatal hernia development.

Few reports have analyzed the clinical importance of sporadic fundic gland polyps (FGPs). The aim of this study was to investigate the relationship between sporadic FGPs and condition of the gastric mucosa stratified by serum pepsinogen levels and Helicobacter pylori antibody level.Three hundred and seventy-five subjects undergoing gastrointestinal endoscopy were enrolled. Subjects on proton pump inhibitors were excluded. Pathologically proven FGPs, and other endoscopic findings (reflux esophagitis, gastric and duodenal ulcer) were examined and serum pepsinogen levels, H. pylori antibody concentration and gastric juice pH were measured simultaneously. Subjects with normal serum pepsinogen and negative H. pylori antibodies were defined as having "low risk" stomachs, suggesting low risk of gastric carcinogenesis.Of the 375 subjects, 44 showed FGPs. The prevalence of "low risk" stomach in subjects with and without FGPs was 98% and 48%, respectively. Multivariable logistic regression analysis indicated three variables as independent factors positively associated with "low risk" stomachs: FGPs (odds ratio [OR] 38.6), reflux esophagitis (OR 4.8), and age60 years (OR 1.89). Gastric juice pH, which is associated with mucosal atrophy grade and low pH indicates less mucosal atrophy, was significantly lower in subjects with (1.64 ± 0.64) than without FGPs in "low risk" (1.94 ± 1.12) and "high risk" stomachs (3.99 ± 2.31).Sporadic FGPs tend to be related to the least atrophic mucosa among non-gastric atrophy subjects without H. pylori infection, and can be used as predictors of a low risk of gastric carcinogenesis.

A cystic artery aneurysm is a rare cause of hemobilia. Herein, we report two cases of acute cholecystitis with a ruptured cystic artery pseudoaneurysm. Two patients (a 69-year-old man and an 83-year-old man) were admitted to our hospital because of acute cholecystitis with gallstone impaction in the neck. Percutaneous transhepatic gallbladder drainage (PTGBD) was performed for both patients. After a few days of PTGBD, gallbladder hemorrhage was observed. Abdominal angiography showed cystic artery aneurysm. A transcatheter arterial embolization was therefore performed, followed by an open cholecystectomy.

An otherwise-healthy 82-year-old woman presented to the emergency department with abdominal pain gradually migrating to the right and vomiting. Her body temperature was 37.2°C, abdominal examination showed tenderness in the right lower abdomen, and her WBC was 8,400/μL no plasma levels of enzymes were elevated. She was thin (body mass index 20.4 kg/m2 ) with scoliosis. Non-enhanced Computed Tomography (CT) revealed a massively swollen gallbladder with high dense (Figure 1) and contrast enhanced CT demonstrated poorly-enhanced edematous wall thickening (Figure 2), with twisted pedicle detached from the liver, suggesting gallbladder torsion. Emergent cholecystectomy was performed, revealing a 270° counterclockwise torsion of the gallbladder. Gallbladder torsion is more prevalent in thin elderly females with spinal deformation [1]. Characteristic contrast enhanced CT findings are poorly-enhanced and thickened gallbladder wall, pericholecystic fluid, and twisted pedicle (whirl sign) [2]. Contrast enhanced CT can help establish the preoperative diagnosis of gallbladder torsion in cases involving elderly females complaining abdominal pain.

Background: The clinical significance of Helicobacter pylori antibody titer has been controversial, and the association between the extent of gastric atrophy or acid secretion and H. pylori antibody concentration has not been elucidated. Materials and Methods: Serum pepsinogen, H. pylori antibody concentration, and fasting gastric pH (as an indicator of acid secretion) were measured in 231 patients undergoing upper gastrointestinal endoscopy. “Atrophic” pepsinogen was defined as pepsinogen-I

Background/Aims: In the normal acid-secreting stomach, luminally generated nitric oxide, which contributes to carcinogenesis in the proximal stomach, is associated with the concentration of nitrate plus nitrite (nitrate/nitrite) in gastric juice. We investigated whether the serum nitrate/nitrite concentration is associated with that of gastric juice and whether it can be used as a serum marker. Methods: Serum and gastric juice nitrate/nitrite concentration, Helicobacter pylori antibody, and gastric pH were measured in 176 patients undergoing upper endoscopy. Results: Multiple regression analysis revealed that serum nitrate/nitrite concentration was the best independent predictor of gastric juice nitrate/nitrite concentration. On single regression analysis, serum and gastric juice nitrate/nitrite concentration were significantly correlated, according to the following equation: gastric juice nitrate/nitrite concentration (µmol/l) = 3.93 – 0.54 × serum nitrate/nitrite concentration (µmol/l; correlation coefficient = 0.429, p < 0.001). In analyses confined to subjects with gastric pH less than 2.0, and in those with serum markers suggesting normal acid secretion (pepsinogen-I >30 ng/ml and negative H. pylori antibody), the serum nitrate/nitrite concentration was an independent predictor of the gastric juice nitrate/nitrite concentration (p < 0.001). Conclusion: Measuring the serum nitrate/nitrite concentration has potential in estimating the gastric juice nitrate/nitrite concentration. The serum nitrate/nitrite concentration could be useful as a marker for mutagenesis in the proximal stomach.

Previous studies have suggested that hypochlorhydria has the potential to produce adverse effects such as the development of infections of the intestinal or respiratory tract and impaired drug absorption. This indicates the importance of obtaining a noninvasive method by which this condition may be diagnosed. The purpose of this study was to determine whether fasting gastric pH could be predicted noninvasively using serum biological markers.One hundred thirty-two patients undergoing diagnostic upper gastrointestinal endoscopy were recruited. Serum levels of pepsinogen-I, pepsinogen-II and Helicobacter pylori antibody were analyzed and the pH of fasting gastric juice determined. Multiple linear regression analysis was used to determine the best predictors of fasting gastric pH.Pepsinogen-I and the presence of Helicobacter pylori were independent predictors of fasting gastric pH, and a high coefficient of determination was obtained (R2 = 0.503, root mean square error = 1.45). The equation for this model was as follows: fasting gastric pH = 2.97-0.026 (pepsinogen-I)+2.76 (presence of Helicobacter pylori: 0=absent, 1=present).The model equation offers a noninvasive method by which to identify patients at high-risk of developing complications induced by hypochlorhydria.

In this report, we describe two cases of small-cell lung cancer (SCLC) presenting with fulminant hepatic failure as the initial manifestation. Neither of the patients had a previous history of liver disease, evidence of viral infection, or exposure to hepatotoxins. Both presented with hepatomegaly and an increase in the serum LDH level. Although they had a history of smoking and respiratory symptoms such as dyspnea on exertion, their most striking initial symptoms were those of hepatic failure, which made it difficult to suspect the underlying primary lung cancer. In one case, contrast-enhanced CT of the abdomen revealed hypovascular nodules that were not visible on plain CT. After a rapidly deteriorating course, both patients died, 8 and 13 days after admission, respectively. Autopsy revealed diffuse infiltration of the hepatic sinusoids and extensive replacement of the liver parenchyma by metastatic small-cell carcinoma. We conclude that metastatic SCLC should be considered in the differential diagnosis in patients of advanced age with a smoking history presenting with rapidly progressive liver failure associated with hepatomegaly and elevation of the serum LDH.

Individuals negative for Helicbacter pylori antibody and with a normal pepsinogen test (group A) are regarded as being at low risk in serum gastric cancer screening known as the ABC method, and endoscopy is not recommended; however, this group may include 2-10% of gastric cancer cases.A total of 345 individuals who underwent upper gastrointestinal endoscopy and were classified by ABC as group A (H. pylori antibody titer10 U/ml, and pepsinogen-I70 ng/ml or I/II ratio3) were enrolled, and predictors of gastric neoplasia were investigated.Ten gastric neoplasia cases (gastric cancer and adenoma) were found to be included. Multiple logistic regression analyses identified H. pylori antibody titer ≥3 U/ml (odds ratio=14.4, 95% confidence interval=2.7-76.9; p0.01) and pepsinogen-I/II ratio ≤4.3 ng/ml (odds ratio=10.0, 95% confidence interval=2.1-47.9; p0.01), but not age as independent predictive factors of neoplasia.Endoscopy should be considered in individuals with H. pylori antibody titer of ≥3 U/ml and a pepsinogen-I/II ratio of ≤4.3 in those classed as group A by ABC method.

A 64-year-old woman visited our outpatient clinic because of bloody stools and abdominal fullness. Digital rectal examination revealed a 6 x 4-cm oval mass. Abdominal CT scans demonstrated a concentric, multilayered structure in the rectum. Colonoscopy showed segments of the bowel were dark-purplish, and intussusception. Deeper insertion of the colonoscope through the lumen revealed a type 1 lesion. Under a diagnosis of sigmoid colon cancer with intrarectal intussusception, emergency surgery was performed. The resected specimen showed a type 1 advanced cancer and two early cancers at the base of the intussuscepted colon, all of which appear to have contributed to the intussusception.

Adrenomedullin (AM), a potent vasodilator peptide initially isolated from a human pheochromocytoma, functions as an antimicrobial peptide in host defense. In this study, we investigated changes in AM levels in intestinal epithelial cells and the mechanism of its secretion and cellular polarity after exposure to lipopolysaccharides (LPS). When a rat small intestinal cell line (IEC-18 cells) was exposed to LPS, enzyme-linked immunosorbent assay revealed a dose-dependent increase in AM together with an increase in AM mRNA expression, as determined by real-time polymerase chain reaction. Up-regulation of AM by LPS was dose-dependently inhibited by LY294002, PD98059, SP600125 and calphostin-C, suggesting the involvement of the phosphatidylinositol 3 kinase, extracellular signal-regulated kinase, c-Jun NH2-terminal kinase and protein kinase C pathways, respectively, in this process. When polarized IEC-18 cells in a Transwell chamber were stimulated with LPS, AM secretion was directed primarily toward the side of LPS administration (either the apical or basolateral side). In situ hybridization revealed that AM mRNA was expressed in epithelial cells and in the connective tissue in the lamina propria of the jejunum after intraperitoneal or oral administration of LPS. Higher levels of AM mRNA expression were observed in rats treated with LPS via the intraperitoneal route, compared with those treated via the oral route. These findings suggest that intestinal AM plays an important role in mucosal defense in the case of intestinal luminal infection, as well as in the modulation of hemodynamics in endotoxemia.

A 51-year-old male patient with esophageal cancer and cervical, thoracic and celiac artery lymph node metastases was treated by combination chemotherapy of TS-1 and cisplatin. TS-1 (80 mg/m2/day) was administered for 14 days followed by 14 days rest as 1 course. Cisplatin (70 mg/m2/day) was administered in 24-hour continuous intravenous infusion at day 8 after the start of TS-1. Before treatment, the tumor marker, CEA showed 27,060 ng/ml. After 5 courses of chemotherapy, endoscopy revealed that the primary tumor had disappeared and no cancer cells were detected by endoscopic biopsy. Chest and abdominal CT scan also showed almost total disappearance of the lymph nodes metastases. CEA decreased to 710 ng/ml. No high-grade toxicities (WHO grade 3 or 4) were seen during the chemotherapy. He is now very well. This TS-1/cisplatin chemotherapy regimen might be a useful treatment for metastatic esophageal cancer.

A 74-year-old male was admitted to our hospital in August 2006 because of an exacerbation of the symptom of diabetes mellitus. Abdominal CT showed locally advanced cancer of the head of the pancreas with encasement of the superior mesenteric artery, suggesting that the lesion was unresectable. The patient was scheduled for treatment with gemcitabine at the standard dose of 1000 mg/m2 once a week for 3 consecutive weeks followed by a one week rest, but on day 7 of cycle 1, grade 3 of hematological toxicity was diagnosed, and the schedule was changed to biweekly administration at a dose of 1000 mg/m2. The biweekly low-dose gemcitabine regimen slightly reduced tumor size, and the regimen was continued for 12 months. This case suggests that this new biweekly regimen of gemcitabine can be used as a safe and effective first-line chemotherapy for patients with advanced pancreatic cancer who are unable to tolerate the standard regimen of gemcitabine.