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A gastric leiomyosarcoma in a 68-yr-old female was followed for 18 months by serial roentgenography. On initial x-ray, the lesion was diagnosed as a benign submucosal tumor. However, it rapidly increased in size, with doubling time subsequently calculated as 5 months. After 18 months' periodic observation, a gastrectomy was performed for a suspected malignancy. Histologic examination of the resected tumor revealed a leiomyosarcoma originating in the muscular layer of the stomach. It appears that the poor prognosis of leiomyosareoma is related to its rapid growth; in addition, it is seldom detected at an early stage. Follow-up of the patient with a gastric submucosal tumor should be done first, 6 months after the initial examination, and thereafter, be done continuously according to the patient's condition. It is useful in differentiating a benign from a malignant myogenic tumor. [ABSTRACT FROM AUTHOR]

Editorial. Determines the possible role of Helicobacter pylori infection in Zollinger Ellison syndrome (ZES)-associated peptic ulcer. Comparison of acid secretion in H. pylori-positive patients and H. pylori-negative patients; Possible mechanisms for gastric acid secretion in H. pylori-positive patients; Information on intestinal metaplasia.

Background Helicobacter pylori infection produces progressive mucosal damage that may eventually result in gastric cancer. We studied the changes that occurred in the presence and severity of atrophic gastritis and the prevalence of H. pylori infection that occurred coincident with improvements in economic and hygienic conditions in Japan since World War II. Materials and Methods The prevalence of H. pylori infection and histologic grades of gastric damage were retrospectively evaluated using gastric biopsy specimens obtained over a 40-year period. Gastric atrophy and intestinal metaplasia were scored using the updated Sydney classification system. Results The prevalence of H. pylori and severity of atrophy were examined in 1381 patients including 289 patients examined in the 1970s (158 men; mean age, 44.9 years), 787 in the 1990s (430 men; 44.2 years), and 305 in the 2010s (163 men; 53.2 years). Overall, the prevalence of H. pylori infection decreased significantly from 74.7% (1970s) to 53% (1990s) and 35.1% (2010s) ( p < .01). The prevalence of atrophy in the antrum and corpus was significantly lower in the 2010s (33, 19%, respectively) compared to those evaluated in either the 1970s (98, 82%) ( p < .001) or 1990s (80, 67%) ( p < .001). The severity of atrophy and intestinal metaplasia also declined remarkably among those with H. pylori infection. Conclusions There has been a progressive and rapid decline in the prevalence of H. pylori infection as well a fall in the rate of progression of gastric atrophy among H. pylori-infected Japanese coincident with the westernization and improvements in economic and hygienic conditions in Japan since World War II. [ABSTRACT FROM AUTHOR]

Abstract Background and Aim: Helicobacter pylori infection in gastric mucosa is a form of chronic active gastritis that leads to expression of inducible nitric oxide synthase in host macrophages and polymorphonuclear leukocytes. Nitric oxide produced by these cells infiltrating the gastric mucosa could damage DNA. We correlated apoptosis in H. pylori -infected antral tissue from peptic ulcer patients with serum nitrate-plus-nitrite. Methods: Biopsy specimens were obtained endoscopically from antrum and fundus in 17 peptic ulcer patients before and after H. pylori eradication. Tissue samples were subjected to rapid urease testing and histopathological scoring (updated Sydney system), as well as immunohistochemical detection of single-stranded DNA indicating apoptotic cells. Fasting serum samples were analyzed for combined nitrate and nitrite content. Results: In all cases atrophy was absent to mild in antral mucosa and H. pylori was eradicated successfully. A strong positive correlation was present between apoptosis and both inflammation and activity scores in infected antral mucosa. A significant positive correlation also was noted between apoptosis and H. pylori density. Serum nitrite concentrations were decreased significantly by successful eradication of H. pylori , and showed a strong positive correlation with H. pylori density. Serum nitrite concentrations showed a significant positive correlation with numbers of single-stranded DNA-positive cells. Conclusions: High H. pylori density was associated with elevated serum nitrate-plus-nitrite (a marker of nitric oxide production in gastric mucosa). Increased apoptosis and abnormal gastric cell turnover are likely results. © 2003 Blackwell Publishing Asia Pty Ltd. [ABSTRACT FROM AUTHOR]

Background: We investigated the effects of rabeprazole compared with those of omeprazole on enterochromaffin-like cells and parietal cells in rats.Methods: Rabeprazole or omeprazole was administered for 7 days by intraperitoneal injection (100 mg/kg or 20mg/kg once a day) and the serum gastrin concentration, the antral density of G cells and D cells, fundic histamine content, fundic H+, K+-ATPase mRNA level, and parietal cell morphology were determined.Results: Both rabeprazole and omeprazole inhibited gastric acid secretion and increased the intragastric pH to over 6.5, as well as causing a marked increase in the serum gastrin concentration. The serum gastrin level was lower with rabeprazole treatment than with omeprazole treatment at both doses. Also, the antral G-cell density was higher with omeprazole than with rabeprazole, while the increase in both the histamine content and the H+, K-ATPase mRNA level in the fundic mucosa was higher with omeprazole treatment at both doses, with the difference being significant at 100 mg/kg. Ultrastructural examination indicated that the stimulation of parietal cells by omeprazole was stronger than that by rabeprazole.Conclusions: Rabeprazole treatment does not drive enterochromaffin-like cells and parietal cells as strongly as omeprazole treatment despite its potent acid suppressive effect, suggesting that it represents a new generation of proton pump inhibitors. [ABSTRACT FROM AUTHOR]

Abstract Background and Aims: The aim of this study was to clinicopathologically distinguish the pathogenesis of gastric mucosa-associated lymphoid tissue (MALT) lymphoma and diffuse large B-cell lymphoma without a MALT lymphoma component (DLL). Methods: We investigated clinicopathological features of these gastric lymphomas including age, sex ratio, tumor location and depth, macroscopic appearance, and infection with Helicobacter pylori of these gastric lymphomas and hepatitis viruses in 24 patients with gastric low-grade MALT lymphoma, 10 patients with high-grade MALT lymphoma, and 19 patients with DLL. The frequency of H. pylori infection in lymphoma patients was compared with that in age- and sex-matched control subjects. Results: There was a predominance of females with MALT lymphoma (male to female ratio, 8/16 for low-grade MALT lymphomas and 1/9 for high-grade MALT lymphomas), and there was a predominance of males with DLL (male to female ratio, 13/6); the ratios differed significantly (P < 0.05). Ninety-two percent of low-grade MALT lymphomas and 80% of high-grade MALT lymphomas were confined to the mucosal and submucosal layers, but lymphoma cells invaded the muscular layer or more deeply in 74% of DLL. Helicobacter pylori infection occurred significantly more often in patients with low-grade MALT lymphoma than in age- and sex-matched controls (96 vs 67%, P < 0.01). Conversely, the frequency of H. pylori infection in DLL patients did not differ from that in controls. Conclusions: These data suggest that H. pylori infection may be associated with the development of gastric MALT lymphoma, but not DLL, and that MALT lymphoma and DLL may have a different pathogenesis. [ABSTRACT FROM AUTHOR]

Purpose: The purpose of this study was to investigate the mechanism of the regulation of histamine synthesis in enterochromaffin-like cells, chemically and structurally, by treatment with omeprazole and pirenzepine.Methods: The ultrastructures of enterochromaffin-like cells and parietal cells were examined in rats treated with oral omeprazole (20 mg/kg) or intraperitoneal pirenzepine (1 mg/kg) administration. Serum gastrin concentrations, mRNA levels of H+-K+-ATPase and histidine decarboxylase, and the fundic concentrations of somatostatin and histamine were determined.Results: Pirenzepine treatment suppressed omeprazole-induced increases in serum gastrin levels and mRNA levels of H+-K+-ATPase and histidine decarboxylase. Pirenzepine also decreased omeprazole-induced increases of histamine concentration in fundic mucosa. Pirenzepine elevated somatostatin mRNA level, previously decreased by omeprazole treatment, in fundic mucosa. In the cytoplasm of enterochromaffin-like cells, omeprazole markedly reduced the numbers of vesicles and granules, but significantly increased their diameters, whereas pirenzepine treatment changed neither of these features. The densities and diameters of both vesicles and granules produced by treatment with omeprazole and pirenzepine were between those produced by treatment with omeprazole alone and pirenzepine alone.Conclusions: Omeprazole-induced hypergastrinemia and pirenzepine-induced somatostatin synthesis play important roles not only in histamine synthesis but also in ultrastructural changes in enterochromaffin-like cells. [ABSTRACT FROM AUTHOR]

AbstractBackground and Aims: Although antroduodenal motility has usually been studied by using manometric or scintigraphic methods, ultrasonography is an established, non-invasive method to evaluate duodenogastric motility. We used ultrasonography to evaluate gastric motility in patients with functional dyspepsia. Methods: Sixty-four patients with functional dyspepsia and 36 asymptomatic healthy subjects were given liquid and solid test meals. We investigated the gastric emptying rate, motility index, and duodenogastric reflux for the liquid meal and gastric emptying time, half-emptying time, and motility index for the solid meal. Results: After the liquid meal, the gastric emptying rate and motility index were significantly lower and the duodenogastric reflux was significantly higher in functional dyspepsia patients than in healthy subjects. After the solid meal, gastric emptying time, half-emptying time and the motility index were significantly lower in the patients than in the healthy subjects. Delayed gastric emptying of both meals occurred in only 20.3% of patients. Delayed emptying of the liquid or solid meal occurred in 62.5% of patients. In both groups, gastric emptying time of the solid meal was positively correlated with the motility index at 15 min post-ingestion. Conclusion: In functional dyspepsia patients, delayed gastric emptying of a solid meal was related to antral hypomotility during the early postprandial phase. Ultrasonographic assessment of gastric motility in both liquid and solid meals may provide a better understanding of the pathogenesis of functional dyspepsia. [ABSTRACT FROM AUTHOR]

AbstractBackground: Whether gastric acid secretion decreases with age is still controversial. With the discovery of Helicobacter pylori, the association of this bacterium with gastric acid secretion has also been discussed. The aim of this study was to investigate the relationship between gastric acid secretion, age and H. pylori infection. Methods: The presence of H. pylori infection, the grade of fundic atrophic gastritis (FAG), and gastric acid secretion were investigated in 280 subjects without localized lesions in the upper gastrointestinal tract. Helicobacter pylori infection was confirmed by Giemsa and immunohistochemical staining, and FAG of biopsy specimens was graded on a scale of 0–4. Results: Both basal and maximal acid output decreased with age in H. pylori-positive subjects, while they did not change with age in H. pylori-negative subjects. Gastric acid secretion decreased with the progression of FAG. An age-correlated decrease in gastric acid secretion in H. pylori-positive subjects depended on an increasing prevalence of FAG with age. Conclusions: In the population studied, advancing age had no influence on gastric acid secretion in H. pylori-negative subjects. Gastric acid secretion decreases with age in H. pylori-positive subjects because of the increasing prevalence of FAG with age. © 2000 Blackwell Science Asia Pty Ltd. [ABSTRACT FROM AUTHOR]

AbstractBackground: The purpose of this study was to establish a method to determine lower oesophageal sphincter (LOS) pressure using an endoscopic manometric sleeve assembly. Methods: We used a 250-cm, three-lumen, 2.2-mm external diameter silicon catheter with a 3-cm sleeve sensor that was passed easily through the biopsy channel (2.8 mm diameter) of the gastroscope. Each lumen was perfused with distilled water using a low-compliance, pneumohydraulic capillary infusion system. Forty-seven healthy subjects and 35 patients with oesophageal disorders underwent study during routine diagnostic endoscopy. In 27 of the subjects, standard transnasal manometry with a three-lumen, 4.5-mm diameter polyvinyl catheter with a 5-cm sleeve sensor was also performed. Results: Lower oesophageal sphincter pressure (LOS) was evaluated in all subjects (median pressure 16 mmHg, range 0–55 mmHg) for 6 min during routine endoscopic examination. The LOS pressure readings between standard and endoscopic manometry correlated well. The LOS pressure was significantly lower in healthy subjects with hiatal hernia than in those without hernia and was also significantly lower in patients with reflux oesophagitis than in healthy subjects. Conclusions: Endoscopic manometric sleeve assembly was used during routine endoscopic examination and was useful for easily determining LOS pressure. It could be used for evaluation of oesophageal motility disorders, thus avoiding the use of a more invasive and time-consuming method. [ABSTRACT FROM AUTHOR]

Association of breast tumor susceptibility gene products BRCA1 and BRCA2 with the RAD51 recombination protein suggested that cancer could arise through defects in recombination. The identification of NBS1, responsible for Nijmegen breakage syndrome, from the MRE11/RAD50 recombination protein complex also supports this hypothesis. However, our mutation analysis revealed that known members of the RAD52 epistasis group are rarely mutated in human primary cancer. Here we describe the isolation of a novel member of the SNF2 superfamily, characterized with sequence motifs similar to those in DNA and RNA helicases. The gene, designated RAD54B, is significantly homologous to the RAD54 recombination gene. The expression of RAD54B was high in testis and spleen, which are active in meiotic and mitotic recombination. These findings suggest that RAD54B may play an active role in recombination processes in concert with other members of the RAD52 epistasis group. RAD54B maps to human chromosome 8q21.3-q22 in a region associated with cancer-related chromosomal abnormalities. Homozygous mutations at highly conserved positions of RAD54B were observed in human primary lymphoma and colon cancer. These findings suggest that some cancers arise through alterations of the RAD54B function. [ABSTRACT FROM AUTHOR]

Background. This study examines endoscopic findings in the diagnosis of Helicobacter pylori (H. pylori) in the Japanese population. Materials and Methods. The endoscopic findings (including gastric fold findings and degree of atrophy by the Kimura-Takemoto classification system), histologic severity of inflammation, and glandular atrophy were assessed according to the Sydney system in 642 patients (419 men; 223 women; mean age 43.5 years, range 13–86). H. pylori infection was evaluated by Giemsa staining and serum IgG antibodies. Results. 391 of 642 patients (60.9%) were diagnosed as having endoscopic gastritis. Of the 391 patients with endoscopic gastritis, 318 (82.6%) had histologic gastritis and 310 (79.3%) had H. pylori infection. Of the 251 patients with endoscopically normal stomachs, 43 (17.1%) had histologic gastritis and 32 (12.7%) had H. pylori infection. Atrophic gastritis was the most prevalent finding (56.3%) among those with endoscopic gastritis. The prevalence of H. pylori infection in patients with atrophic gastritis (92.7%) and rugal hyperplastic gastritis (92.3%) was significantly higher than in those with other types of gastritis or with a normal stomach (12.7%). A markedly high prevalence of H. pylori infection was found in subjects with tortuosity, hyperrugosity, and/or hyporugosity of the gastric folds. Conclusions. The accurate endoscopic assessment of gastritis according to the Sydney system along with gastric fold findings and the endoscopically identified extent of gastric atrophy are valuable indicators for determining H. pylori infection and histologic gastritis in the Japanese population. [ABSTRACT FROM AUTHOR]

Established risk factors for gastric cancer include a diet high in nitrate or nitrite and low in vitamin C and the presence of achlorhydria or hypochlorhydria. The aim of this study was to investigate the relationship between intragastric nitrite concentration and atrophic change of the stomach or gastric carcinogenesis in Japanese Helicobacter pylori-infected patients. Gastric juice pH, nitrite, and total vitamin C concentrations in gastric juice, serum pepsinogen I and II concentrations, and specific Helicobacter pylori antibody were analyzed. Intragastric total vitamin C concentration was decreased by Helicobacter pylori infection of the gastric mucosa and with progression of the atrophic grade. There was a significant positive correlation between atrophic grade and intragastric nitrite concentration. In conclusion, the levels of nitrite in gastric juice play a causal role in the development of cancer in Helicobacter pylori-associated atrophic gastric mucosa.

Somatostatin, a peptide distributed widely throughout the gut, inhibits a variety of gastrointestinal functions. We previously reported that fasting for 48 h increased gastric somatostatin peptide and mRNA content. Thus, somatostatin could contribute to the inhibition of gastric G cells during fasting. To investigate the effect of fasting on intestinal somatostatin, we determined tissue somatostatin concentration by radioimmunoassay, somatostatin mRNA expression by Northern analysis and reverse transcription polymerase chain reaction (RT-PCR), and mRNA expression for somatostatin receptor subtypes (sst) 1-5 by RT-PCR in ileum and colon of rats either freely fed or food-deprived for 48 h. In the colon, fasting increased somatostatin concentration, somatostatin mRNA expression, and mRNA expression for two receptor subtypes (sst2 and sst3). In the ileum, no change of somatostatin peptide concentration and receptor subtype mRNA expression was demonstrated; only somatostatin mRNA expression was augmented by fasting. These results suggest that in rat colon, fasting for 48 h increases somatostatin synthesis and receptor subtype expression. These changes may be important in maintaining homeostasis during starvation.

Background: Helicobacter pylori infection causes chronic gastritis and results in increased serum concentrations of pepsinogens I and II as well as gastrin, while the ratio of pepsinogen I to II (I : II) is decreased. Inducible nitric oxide synthase (iNOS) is induced in H. pylori-associated gastritis and may modulate inflammation. However serum nitrate and nitrite (NOx) concentrations in patients with H. pylori-induced chronic gastritis have not been reported. We examined differences in serum NOx between H. pylori-negative and positive volunteers relative to differences in pepsinogens and gastrin., Materials and Methods: Sera from 80 healthy asymptomatic volunteers younger than 36 years were analyzed for anti-H. pylori antibody, NOx, gastrin and pepsinogens., Results: In H. pylori antibody-positive subjects serum NOx concentrations were higher than in negative subjects (p < .005). In H. pylori-negative subjects, NOx correlated with pepsinogen II (r = .405, p < .05). In subjects with low pepsinogen I or II, NOx was higher in H. pylori-positive than negative subjects (p < .001). In subjects with high pepsinogen I : II (6 or higher), serum NOx was higher in H. pylori-positive than in negative subjects., Conclusions: H. pylori-induced gastritis increases serum NOx concentrations more prominently than those of pepsinogen. In H. pylori-negative subjects, serum correlates with serum pepsinogen II.

This study investigated whether the serum nitrite concentration reflects Helicobacter pylori-induced inflammation and atrophic changes of gastric mucosa. Ninety-seven patients underwent biopsy of both antrum and fundus. Samples were analyzed by the rapid urease test and histopathological examination according to the updated Sydney system. Fasting serum samples from each subject were analyzed for specific IgG Helicobacter pylori antibodies, pepsinogen I and II concentrations, and NO2-/NO3- content. Eleven patients had H. pylori eradicated with proton pump-based triple therapy. There was a strong positive correlation between the Helicobacter pylori density in the gastric mucosa and the serum nitrite concentration, but a negative correlation existed between the atrophic grade of the gastric mucosa and both serum nitrite concentration and Helicobacter pylori density in the gastric mucosa. Serum nitrite concentrations decreased significantly after successful eradication of Helicobacter pylori. Therefore, serum nitrite concentration may be a useful marker for oxidative DNA damage and apoptosis associated with Helicobacter pylori infection.