Role of Th22 cells in Helicobacter pylori-related gastritis and peptic ulcer diseases.

Helicobacter pylori (H. pylori) has been shown to be one of the leading causes of peptic ulcer diseases (PUDs) and gastritis. T helper-22 (Th22) cells and its most important cytokine, interleukin-22 (IL-22) are importantly active in inflammation and inflammatory tissues. Since inflammation is one of the main attributes of infection caused by H. pylori and resulting complications (gastritis and gastrointestinal ulcer), this study was designed to evaluate the Th22 cells count and the IL-22 protein expression in people suffering from PUD and gastritis. The present study was conducted on 55 patients with gastritis, 47 patients with PUD and 48 uninfected subjects. After preparation of section and extraction of protein from antral biopsies, immunohistochemistry and western blot methods were used to evaluate the Th22 cells and IL-22 protein expression level, respectively. According to findings, the Th22 cells count and the IL-22 protein expression level in the infected subjects were siginficantly more than in the uninfected subjects. It should be noted that the Th22 cells count and the IL-22 protein expression level in the infected subjects with PUD were significantly greater than those in the infected subjects with gastritis. In addition, the Th22 cells count had positive correlation with the density of H. pylori, chronic inflammation score and acute inflammatory score in the infected subjects with PUD. The Th22 cells count had positive correlation with the Th17 cells count and inverse correlation with the Treg cells count in the infected subjects with PUD and gastritis. Our data demonstrated that abnormal hyper-activation of Th22 cells as well as its correlation with the Th17 cells during infection caused by H. pylori might damage tissues through immunopathological responses.

Expression of vasoactive proteins in gastric antral mucosa reflects vascular dysfunction in patients with cirrhosis and portal hypertension.

BACKGROUND & AIMS: Patients with cirrhosis display hypocontractility of splanchnic vessels because of dysregulation of vasoactive proteins, such as decreased effect of RhoA/ROCK and increased activity of ß-Arrestin-2 and eNOS. However, it is unknown whether the dysregulation of vasoactive proteins is displayed in other vessels. We investigated whether expression of vasoactive proteins can be evaluated in gastric mucosa vessels. METHODS: Biopsies from the gastric mucosa of 111 patients with cirrhosis were collected at three different centres and from 13 controls. Forty-nine patients had received TIPS. Portal pressure gradient was measured in 49 patients with TIPS and in 16 patients without TIPS. Biopsies from the antrum were conserved in formaldehyde for immunohistochemistry or shock-frozen for PCR and Western blot. RESULTS: The mucosal transcription of vascular markers (αSMA, CD31) was higher in cirrhotic patients than controls, which was confirmed by immunohistochemistry. On average, relative mucosal levels of RhoA and ROCK were lower, while ß-Arrestin-2 levels were higher in cirrhotic patients compared to controls. Transcriptional levels of eNOS increased with presence of ascites and grade of oesophageal varices. Patients with TIPS showed less pronounced markers of vascular dysfunction in gastric mucosa. CONCLUSION: This is the first evidence that the expression of vasoactive proteins in mucosa from the gastric antrum of patients with cirrhosis reflects their vascular dysfunction and possibly changes after therapeutic interventions.

The gastric mucosa 25 years after proximal gastric vagotomy.

OBJECTIVE: Vagotomy causes inhibition of basal and post-prandial acid secretion in humans, but the knowledge about the trophic effect of the vagal nerves is limited. Vagotomy is known to induce hypergastrinemia and we aimed to study the long-term effects of proximal gastric vagotomy (PGV) on the oxyntic mucosa and the enterochromaffin-like (ECL) cell density in particular. MATERIAL AND METHODS: Eleven patients operated with PGV because of duodenal ulcer and age- and sex-matched controls were examined 26 to 29 years postoperatively by gastroscopy with biopsies from the antrum and oxyntic mucosa. Neuroendocrine cell volume densities were calculated after immunohistochemical labeling of gastrin, the general neuroendocrine cell marker chromogranin A (CgA) and the ECL cell marker vesicular monoamine transporter 2 (VMAT2). Gastritis was graded and Helicobacter pylori (H. pylori) status was determined by polymerase chain reaction of gastric biopsies. Fasting serum gastrin and CgA were measured. RESULTS: Serum gastrin was higher in the PGV group compared to controls (median 21.0 [interquartile range (IQR) = 22.0] pmol/L vs 13.0 [IQR = 4.0] pmol/L, p = 0.04). However, there was neither a significant difference in serum CgA or in CgA (neuroendocrine) nor VMAT2 (ECL cell) immunoreactive cell volume density in the oxyntic mucosa. There was significantly more inflammation and atrophy in H. pylori-positive patients, but PGV did not influence the grade of gastritis. CONCLUSION: Despite higher serum gastrin concentrations, patients operated with PGV did not have higher ECL cell mass or serum CgA. Vagotomy may prevent the development of ECL cell hyperplasia caused by a moderate hypergastrinemia.

Gastrin Staining in Inflamed Stomach Biopsies Labeled as "Antral" Rarely Detects Atrophic Gastritis.

OBJECTIVES: Autoimmune metaplastic atrophic gastritis (AMAG) is an underrecognized entity, especially in its early stage. This study assessed whether the use of gastrin immunohistochemistry would increase sensitivity for diagnosing early AMAG. METHODS: Three-hundred gastric biopsies were prospectively stained for gastrin by immunohistochemistry. Inclusion criteria included well-oriented gastric mucosa with mucus glands and minimal plasma cell infiltrate not suspected to represent pyloric metaplasia. Patient age, sex, designated location of biopsy, presence or absence of intestinal metaplasia, and clinical information were not criteria. Any case with absence of gastrin-positive endocrine cells reflexed to chromogranin immunohistochemistry. Maloriented biopsies or cases with current Helicobacter infection were excluded. RESULTS: The 298-patient study cohort comprised 222 females (mean age, 47 years; range, 16-80 years) and 76 males (mean age, 49 years; range, 7-80 years). Biopsies were designated as "antral/antral nodules" (61%), and the rest were labeled "gastric/random stomach" (39%). Nine cases (3%) exhibited absence of gastrin-positive endocrine cells; one of those showed endocrine cell hyperplasia by chromogranin staining. CONCLUSIONS: Pathologists should be aware of the histologic features of early AMAG and meticulously analyze tissue regardless of specimen labeling. Gastrin immunostain is a supplemental diagnostic tool when encountering inflamed antral-appearing specimens.

Nutrient-sensing components of the mouse stomach and the gastric ghrelin cell.

BACKGROUND: The ability of the gut to detect nutrients is critical to the regulation of gut hormone secretion, food intake, and postprandial blood glucose control. Ingested nutrients are detected by specific gut chemosensors. However, knowledge of these chemosensors has primarily been derived from the intestine, while available information on gastric chemosensors is limited. This study aimed to investigate the nutrient-sensing repertoire of the mouse stomach with particular emphasis on ghrelin cells. METHODS: Quantitative RT-PCR was used to determine mRNA levels of nutrient chemosensors (protein: G protein-coupled receptor 93 [GPR93], calcium-sensing receptor [CaSR], metabotropic glutamate receptor type 4 [mGluR4]; fatty acids: CD36, FFAR2&4; sweet/umami taste: T1R3), taste transduction components (TRPM5, GNAT2&3), and ghrelin and ghrelin-processing enzymes (PC1/3, ghrelin O-acyltransferase [GOAT]) in the gastric corpus and antrum of adult male C57BL/6 mice. Immunohistochemistry was performed to assess protein expression of chemosensors (GPR93, T1R3, CD36, and FFAR4) and their co-localization with ghrelin. KEY RESULTS: Most nutrient chemosensors had higher mRNA levels in the antrum compared to the corpus, except for CD36, GNAT2, ghrelin, and GOAT. Similar regional distribution was observed at the protein level. At least 60% of ghrelin-positive cells expressed T1R3 and FFAR4, and over 80% expressed GPR93 and CD36. CONCLUSIONS AND INFERENCES: The cellular mechanisms for the detection of nutrients are expressed in a region-specific manner in the mouse stomach and gastric ghrelin cells. These gastric nutrient chemosensors may play a role modulating gastrointestinal responses, such as the inhibition of ghrelin secretion following food intake.

Alterations of gastric homeoprotein expression in Helicobacter pylori infection, incisural antralisation, and intestinal metaplasia.

PURPOSE: This study was to determine whether gastric expression of homeoproteins is altered in Helicobacter pylori infection, incisural antralisation, and intestinal metaplasia (IM). METHODS: Gastric biopsy specimens were taken from 98 patients with non-ulcer dyspepsia for the detection of H. pylori infection; histological examinations; immunohistochemical staining of CDX2, PDX1, PAX6, and NKX6.1. RESULTS: Of the patients, 38 were positive for H. pylori infection, 44 had antral-type mucosa at the incisura, and 22 had IM in the stomach. At the incisura, the expression of PDX1, NKX6.1, and PAX6 in cytoplasm compartment was down-regulated in antral-type mucosa compared with that in the transitional- or body-type mucosa (all P<0.01). The expression of PDX1, PAX6, and NKX6.1 in cytoplasm at the incisura was down-regulated in H. pylori-infected patients compared with that in those without H. pylori infection (all P<0.01). CDX2 expression in whole stomach was up-regulated, but PDX1 expression at the incisura was down-regulated in patients with IM compared with that in those without IM (all P<0.01). CONCLUSIONS: Gastric expression of PDX1, PAX 6, and NKX6.1 is down-regulated in H. pylori infection and incisural antralisation. CDX2 is up-regulated but PDX1 is down-regulated in the presence of IM.

Prohormone convertases 1/3 and 2 together orchestrate the site-specific cleavages of progastrin to release gastrin-34 and gastrin-17.

Cellular synthesis of peptide hormones requires PCs (prohormone convertases) for the endoproteolysis of prohormones. Antral G-cells synthesize the most gastrin and express PC1/3, 2 and 5/6 in the rat and human. But the cleavage sites in progastrin for each PC have not been determined. Therefore, in the present study, we measured the concentrations of progastrin, processing intermediates and alpha-amidated gastrins in antral extracts from PC1/3-null mice and compared the results with those in mice lacking PC2 and wild-type controls. The expression of PCs was examined by immunocytochemistry and in situ hybridization of mouse G-cells. Finally, the in vitro effect of recombinant PC5/6 on progastrin and progastrin fragments containing the relevant dibasic cleavage sites was also examined. The results showed that mouse G-cells express PC1/3, 2 and 5/6. The concentration of progastrin in PC1/3-null mice was elevated 3-fold. Chromatography showed that cleavage of the Arg(36)Arg(37) and Arg(73)Arg(74) sites were grossly decreased. Accordingly, the concentrations of progastrin products were markedly reduced, alpha-amidated gastrins (-34 and -17) being 25% of normal. Lack of PC1/3 was without effect on the third dibasic site (Lys(53)Lys(54)), which is the only processing site for PC2. Recombinant PC5/6 did not cleave any of the dibasic processing sites in progastrin and fragments containing the relevant dibasic processing sites. The complementary cleavages of PC1/3 and 2, however, suffice to explain most of the normal endoproteolysis of progastrin. Moreover, the results show that PCs react differently to the same dibasic sequences, suggesting that additional structural factors modulate the substrate specificity.

Helicobacter pylori infection and short-term intake of low-dose aspirin have different effects on alpha-1 antitrypsin/alpha-1 peptidase inhibitor (alpha1-PI) levels in antral mucosa and peripheral blood.

OBJECTIVE: Alpha-1 protease inhibitor (alpha1-PI) is the major circulating serine protease inhibitor. The purpose of the study was to investigate alpha1-PI expression in gastroduodenal mucosa and blood with respect to two major etiological risk factors for gastroduodenal diseases, Helicobacter pylori infection and intake of low-dose aspirin. MATERIAL AND METHODS: Twenty volunteers (H. pylori-positive and -negative: n=10) received 2 x 50 mg aspirin/day for 7 days. H. pylori-positive subjects underwent eradication therapy and repeated the protocol. Blood and tissue samples were obtained on days 0, 1, 3 and 7; alpha1-PI levels were determined by enzyme-linked immunosorbent assay (ELISA) and quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and analyzed for histopathological findings. RESULTS: Mucosal alpha1-PI expression was between 30 and 75 pg/10 microg total protein in H. pylori-negative subjects, and found to be similar in antral, corpus and duodenal mucosa. In H. pylori-infected subjects, alpha1-PI levels were significantly increased in the antrum (mean: 111 versus 37.4 pg/10 microg protein; p=0.019), whereas corresponding levels in the corpus, duodenum and sera were unchanged. Alpha-1-PI transcript levels were similarly induced in H. pylori-infected subjects (0.13+/-0.15 versus 0.027+/-0.043 a.u. (arbitrary units), p=0.018). Immunohistochemistry demonstrated that infiltrating immune cells and antral surface epithelium contributed to elevated alpha1-PI expression in H. pylori-infected subjects. The concomitant use of low-dose aspirin did not change mucosal alpha1-PI levels, but led to a 2-fold increase in alpha1-PI levels in sera independently of the H. pylori status (p<0.009). CONCLUSIONS: Antral alpha1-PI expression is specifically induced by H. pylori infection, suggesting a pathophysiological role of this protease inhibitor in the upper gastrointestinal tract, whereas low-dose aspirin led to an increase in systemic alpha1-PI levels.

Expression of somatostatin receptor subtype 3 in the gastric mucosa of dyspeptic patients in relation to Helicobacter pylori infection and a family history of gastric cancer.

BACKGROUND AND AIM: The cytotoxic activity of Helicobacter pylori contributes significantly to the pathogenesis of gastric carcinoma. A preliminary study suggested that somatostatin receptor subtype 3 (SSTR3) might play a role in cell apoptosis and the growth of gastric cancer. The aim of the present study was to determine the influence of H. pylori infection and a family history of gastric cancer on the expression of SSTR3 in the gastric mucosa of non-cancer patients with dyspepsia. METHODS: The expression of the SSTR3 gene in the gastric mucosa of the stomach antrum and corpus of 53 patients was determined by the use of quantitative reverse transcription-polymerase chain reaction. RESULTS: The SSTR3 mRNA level was lower in the H. pylori-infected patients, as compared to the non-infected patients, independently of a family history of gastric cancer and stomach topography. The greatest decrease of approximately 40% and 35% (P < 0.05) was observed for the antrum of the H. pylori-positive patients without and with a family history of gastric cancer, respectively. In the corpus, these differences were much smaller, regardless of a family history of gastric cancer. Interestingly, for H. pylori-negative patients, the density (at the mRNA level) of the SSTR3 receptor in the antrum was higher than in the corpus mucosa. CONCLUSIONS: A decrease in the density of SSTR3 (especially in the antrum) in individuals with H. pylori infection and particularly with a family history of gastric cancer may point to an environmental and inherited predisposition in the development of distal gastric cancer.

Chemiluminescence assay of mucosal reactive oxygen species in gastric cancer, ulcer and antral mucosa.

BACKGROUND/AIMS: Reactive oxygen species (ROS) have been implicated in inflammatory and cancerous illness, including that of the gastrointestinal tract. The oxidative damage incurred during human gastric ulcer or cancer mucosa may be related to acumination of ROS. In this study, we aimed to demonstrate oxidative stress of gastric ulcer and cancer mucosa compared to gastric antral mucosa. PATIENTS: Thirty-four patients with gastric ulcer and gastric cancer were enrolled in this study. Gastric mucosa specimens, taken from upper GI endoscopic biopsy, from the lesion (ulcer or cancer) and antrum were sent for the activity of O2- or H2O2 determined by chemiluminescence assay. Protein concentrations in the tissue homogenates were determined by Bio-Red protein assay. The production of O2- or H2O2 per unit of protein was calculated by dividing the tissue CL level by the protein content of a tissue. RESULTS: The oxidative stress metabolites O2- and H2O2 of mucosa were evaluated by chemiluminescence assay in gastric lesions (27 ulcers and 7 cancers) and gastric antrum. Gastric lesion showed significantly increased O2- than antral mucosa (18.77 +/- 45.18 (counts/sec x microg), 95% CI 3.01, 34.53 vs. 3.58 +/- 6.89 (counts/sec x microg), 95% CI 1.18, 5.98, p < 0.05). There was also significantly greater expression of H2O2 in gastric lesion than gastric antral mucosa (76.06 +/- 148.36 (counts/sec x microg), 95% CI 24.30, 127.83 vs. 912.41 +/- 20.22 (counts/sec x microg), 95% CI 5.35, 19.46, p = 0.008). Differences of mucosal O2- and H2O2 between gastric ulcer and cancer were not significant. There was significant correlation of O2- and H2O2 generation in gastric lesion mucosa. CONCLUSIONS: Oxidative stress is now thought to make a significant contribution to inflammatory disease and malignancy. The reason that overproduction of free radicals is a feature of such a broad spectrum of diseases derived from the fact that oxidative metabolism is a necessary part of every cell's metabolism. In this study, we demonstrated increased ROS production in gastric ulceration and cancer compared with gastric antral mucosa.

Evaluation of differences between breeds for substance P, vasoactive intestinal polypeptide, and neurofilament 200 in the abomasal wall of cattle.

OBJECTIVE: To compare the content of substance P, vasoactive intestinal polypeptide, and neurofilament 200 in biopsy specimens taken from the abomasal wall of healthy cows of 2 breeds. SAMPLE POPULATION: Biopsy specimens taken from different sites of the abomasal wall from 20 German Holstein cows and 20 German Fleckvieh cows. PROCEDURES: Biopsy specimens were examined immunohistochemically, and the content of substance P, vasoactive intestinal polypeptide, and neurofilament 200 was determined by measuring the immunoreactive areas. RESULTS: Significant differences between the breeds were detected. Substance P-immuno-reactive area in the corpus abomasi was significantly smaller in the German Holsteins (geometric mean +/- geometric SD, 679 +/- 1.83 microm2) than in the German Fleckvieh cows (1,020 +/- 1.65 microm2). Concerning vasoactive intestinal polypeptide, differences between breeds were not significant. Overall nerve density in the antral abomasal wall was significantly greater in German Holsteins than in German Fleckvieh cows (immunoreactive areas for neurofilament 200 in German Holsteins was 4,842 +/- 1.29 microm2 and in German Fleckvieh cows was 3,333 +/- 1.63 microm2). Conclusions and Clinical Relevance-The significantly lower content of substance P in the corpus abomasi could explain why German Holstein cows are predisposed to abomasal displacement, compared with German Fleckvieh cows, in which this disease is a rare finding.

Relationship between irritable bowel syndrome and plasma and tissue ghrelin levels.

BACKGROUND/AIMS: This study aimed to evaluate the relationship between irritable bowel syndrome (IBS) and plasma and tissue ghrelin levels. MATERIALS AND METHODS: Patients who had undergone gastroscopy procedure for any reason previously were enrolled in the study. Among these, patients with IBS symptoms were evaluated according to the Roma III criteria. The healthy control group comprised patients with no IBS symptom and had undergone gastroscopy procedure for another reason. The plasma ghrelin level and tissue ghrelin level obtained by immunohistochemical examination of biopsy specimens taken from the gastric antrum and corpus were evaluated in all participants. RESULTS: The mean age of 90 participants was 43.64}12.64 years. The median value of the plasma ghrelin level was 3.29 (1.2-12.7) in the diarrhea group (IBS-D), 1.49 (0.82-7.08) in the constipation group (IBS-C), and 1.5 (0.2-3.7) in the control group. The plasma ghrelin levels between the groups were found to be significantly higher in IBS-D than in IBS-C and the control groups (p=0.001 and p=0.001, respectively). On comparing antral mucosal gland biopsy outcomes among the groups, staining intensity score was found to be significantly high in IBS-C as compared with the control group, whereas no significant difference was observed between IBS-D and the control groups (p=0.020 and p=0.429, respectively). CONCLUSION: The plasma ghrelin level in IBS-D and the staining intensity in the antral mucosal gland in IBS-C were found to be significantly higher. In addition, there was no difference between the groups in terms of ghrelin staining intensity in the gastric corpus.

Effects of Helicobacter pylori eradication on methylation status of E-cadherin gene in noncancerous stomach.

PURPOSE: Promoter hypermethylation of E-cadherin plays an important role on gastric cancer development. Whereas E-cadherin methylation was frequently detected in the stomach of Helicobacter pylori-infected individuals, we tested whether eradication of H. pylori alters the methylation status of the noncancerous gastric epithelium. EXPERIMENTAL DESIGN: Endoscopic biopsies were taken from the antrum and corpus of H. pylori-infected subjects without gastric cancer. Presence of methylated E-cadherin sequences in the gastric specimens was detected by methylation-specific PCR. Bisulfite DNA sequencing was done to determine the topographical distribution and changes in methylation profiles with H. pylori eradication. RESULTS: Among the 28 H. pylori-infected subjects (median age, 44.5 years), 15 (53.6%) had E-cadherin methylation detected in stomach at baseline. Discordant methylation patterns between the antrum and corpus were noted in six patients. One year after successful H. pylori eradication, there was a significant reduction in the methylation density of the promoter region and exon 1 of the E-cadherin gene as detected by bisulfite DNA sequencing (P < 0.001). CONCLUSION: Promoter methylation in E-cadherin was frequently detected in the stomach of H. pylori-infected individuals. Eradication of H. pylori might possibly reduce the methylation density in E-cadherin gene and the chance of subsequent neoplastic transformation.

An immunohistochemical study of endocrine cells in the stomach of hypertensive rats.

Essential hypertension is a complex disease with both genetic and environmental determinants. The effect of spontaneous hypertension on the distribution and occurrence of somatostatin-, gastrin- and serotonin-immunoreactive cells in the fundus and pylorus of the rat stomach was examined by immunohistochemistry. The animals were killed by decapitation at 4 and 16 weeks of age (5 control rats and 5 hypertensive rats). Endocrine cells generally increase in number in hypertensive rats as compared to control rats. However, the detailed responses of endocrine cells to hypertension depend on the cell type, region of gastric mucosa and age of animals. The present results suggest that hypertension has an influence on the intrinsic regulatory system by endocrine cells control in the rat stomach.

Neuropeptide W is present in antral G cells of rat, mouse, and human stomach.

Neuropeptide W (NPW) is a 30-amino-acid peptide initially isolated from the porcine hypothalamus as an endogenous ligand for the G protein-coupled receptors GPR7 and GPR8. An intracerebroventricular administration of NPW increased serum prolactin and corticosterone concentrations, decreased dark-phase feeding, raised energy expenditure, and lowered body weight. Peripherally, GPR7 receptors are abundantly expressed throughout the gastrointestinal tract; the presence of NPW in the gastrointestinal endocrine system, however, remains unstudied. Using monoclonal and polyclonal antibodies raised against rat NPW, we studied the localization of NPW in the rat, mouse, and human stomach by light and electron microscopy. NPW-immunoreactive cells were identified within the gastric antral glands in all three species. Double immunohistochemistry and electron-microscopic immunohistochemistry studies in rats demonstrated that NPW is present in antral gastrin (G) cells. NPW immunoreactivity localized to round, intermediate-to-high-density granules in G cells. NPW-immunoreactive cells accounted for 90% chromagranin A- and 85% gastrin-immunoreactive endocrine cells in the rat gastric antral glands. Using reversed-phase HPLC coupled with enzyme immunoassays specific for NPW, we detected NPW30 and its C-terminally truncated form, NPW23, in the gastric mucosa. Plasma NPW concentration of the gastric antrum was significantly higher than that of the systemic vein, suggesting that circulating NPW is derived from the stomach. Plasma NPW concentration of the gastric antrum decreased significantly after 15-h fast and increased after refeeding. This is the first report to clarify the presence of NPW peptide in the stomachs of rats, mice, and humans. In conclusion, NPW is produced in gastric antral G cells; our findings will provide clues to additional mechanisms of the regulation of gastric function by this novel brain/gut peptide.

Assay of gastrin and somatostatin in gastric antrum tissues of children with chronic gastritis and duodenal ulcer.

AIM: To study the expressions of gastrin (GAS) and somatostatin (SS) in gastric antrum tissues of children with chronic gastritis and duodenal ulcer and their role in pathogenic mechanism. METHODS: Specimens of gastric antrum mucosa from 83 children were retrospectively analyzed. Expressions of GAS and SS in gastric antrum tissues were assayed by the immunohistochemical En Vision method. RESULTS: The expressions of GAS in chronic gastritis Hp+ group (group A), chronic gastritis Hp-group (group B), the duodenal ulcer Hp+group (group C), duodenal ulcer Hp-group (group D), and normal control group (group E) were 28.50+4.55, 19.60+2.49, 22.69+2.71, 25.33+4.76, and 18.80+2.36, respectively. The value in groups A-D was higher than that in group E. The difference was not statistically significant. The expressions of SS in groups A-E were 15.47+1.44, 17.29+2.04, 15.30+1.38, 13.11+0.93 and 12.14+1.68, respectively. The value in groups A-D was higher than that in group E. The difference was also not statistically significant. CONCLUSION: The expressions of GAS and SS are increased in children with chronic gastritis and duodenal ulcer.

Comparison of pathological features of gastric carcinoma in Turkey and Germany.

Environmental factors play an important role in gastric carcinogenesis and in the morphological features of gastric carcinomas. The aim of our study was to examine whether gastric carcinoma cases from Turkey and Germany differ in their topographical localization and in their histopathological and immunophenotypic profiles. We studied 80 gastric carcinoma cases from Turkey and 80 cases from Germany. The tumors were classified according to the Lauren, Goseki, and Carneiro classifications. We also determined the immunophenotype of the tumors on the basis of their mucin (MUC1, MUC2, MUC5AC, and MUC6) and adhesion molecule (E-cadherin, alpha-catenin, beta-catenin) expression patterns. In the German series a proximal localization prevailed (p<0.02). In the Goseki classification, Grade I tumors were more frequent in the Turkish series, while Grade IV carcinomas (all of which stained positively for MUC5AC) were more common in the German series (p<0.24). The differences in adhesion molecule expression in the two groups were not significant. In conclusion, gastric carcinomas from Turkey and Germany differ in their topographical localization and the frequency of gland-forming versus signet-ring cell carcinomas. These differences may indicate that the factors thought to contribute to the development of gastric carcinoma, such as dietary habits and Helicobacter pylori infection, have different impact in the two countries.

Diagnostic utility of endoscopic ultrasound-guided fine-needle aspiration biopsy for glomus tumor of the stomach.

A 52-year-old man was referred for further investigation of a gastric submucosal tumor on the greater curvature of the antrum. Endoscopic ultrasonography demonstrated a hypoechoic solid mass, which was primarily connected to the muscular layer of the stomach. We performed endoscopic ultrasound-guided fine-needle aspiration biopsy. The pathological examination showed proliferation of oval-shaped cells with nest formation, which stained strongly positive for muscle actin, and negative for c-kit, CD34, CD56, desmin, S-100, chromogranin, and neuron-specific enolase. Therefore, we performed laparoscopy and endoscopy cooperative surgery based on the preoperative diagnosis of glomus tumor of the stomach. The final histological diagnosis confirmed the preoperative diagnosis. Although preoperative diagnosis of glomus tumor of the stomach is difficult with conventional images and endoscopic biopsy, endoscopic ultrasound-guided fine-needle aspiration biopsy is an essential tool to gain histological evidence of glomus tumor of the stomach for early diagnosis.

Detection of gastrin mRNA in fresh human colonic carcinomas by reverse transcription-polymerase chain reaction.

To investigate the hypothesis that gastrin might be synthesized by tumour tissues in cancer of the colon, samples from six human colon tumours, one hepatic metastasis, four normal colonic mucosal samples and two antral and one fundic gastric mucosal samples from nine patients were analysed to determine whether gastrin mRNA was present. RNA was extracted from surgical specimens by ultracentrifugation on a CsCl cushion, purified using the guanidinium thiocyanate method, reverse-transcribed and amplified by polymerase chain reaction. Gastrin mRNA was detected in each colonic carcinoma sample (including the hepatic metastasis), while no such signal was observed in normal colon biopsies. Positive and negative controls (gastric antrum and fundus respectively) gave the expected results. In each of the positive samples, the chemiluminescent revelation of amplified products after Southern blotting corresponded to gastrin mRNA without the intron. These findings demonstrate the ability of primary and metastatic human colonic tumours to produce gastrin mRNA. Since malignant cell lines have been reported to produce gastrin peptide, and since gastrin receptors were present in some cases, our results support the idea that gastrin may be involved in an autocrine mechanism.

Collagenous gastritis: a report of six cases.

Collagenous gastritis is an exceptional entity with eight cases documented to date characterized by the presence of a thick subepithelial collagen band associated with an inflammatory infiltrate of the gastric mucosa. The aim of our study was to describe the clinical and histologic characteristics of six new cases of collagenous gastritis. All cases showed a subepithelial collagen band that averaged 30 microm but often measured up to 120 microm. This finding was almost always accompanied by mixed chronic inflammation in the lamina propria and by surface epithelial damage of varying severity. Our study seems to delineate two subsets in patients with collagenous gastritis: 1) collagenous gastritis occurring in children and young adults presenting with severe anemia, a nodular pattern on endoscopy, and a disease limited to the gastric mucosa without evidence of colonic involvement, and 2) collagenous gastritis associated with collagenous colitis occurring in adult patients presenting with chronic watery diarrhea. These findings highlight the fact that subepithelial collagen deposition may be a generalized disease affecting the entire gastrointestinal tract.