gastrins and Polyps

Gastric carcinoids (GCs) or neuroendocrine tumours (NETs) are increasingly identified at endoscopy, and account for 0.6-2% of all gastric polyps identified. The SEER database in the US has demonstrated a rising incidence of gastric NETs amongst all NETs; from 2.2% between 1950 and 1969 to 6.0% between 2000 and 2007.. To review the literature and assist clinicians in managing patients with GCs.. A literature search was conducted through MEDLINE using search terms: gastric, carcinoid, neuroendocrine tumour, therapy, endoscopy, mucosal resection, submucosal dissection. Relevant articles were identified through manual review. The reference lists of these articles were reviewed to include further appropriate articles.. There are three types of GCs with important epidemiological, pathophysiological, histological and endoscopic differences that affect prognosis and management. Type 1 and 2 GCs develop in the context of hypergastrinaemia that originates from achlorhydria in atrophic gastritis and a gastrinoma, respectively. Type 3 GCs occur sporadically and independent of gastrin. The histological type, grade and Ki67 index are used to determine prognosis and direct clinical management. Type 1 GCs >1 cm in size and type 2 GCs should be assessed for invasion beyond the submucosa with EUS prior to endoscopic resection with EMR or ESD. Type 3 GCs should be managed as per recommendations for gastric adenocarcinoma. The treatment of advanced disease is multimodal.. Patients with gastric carcinoids should be discussed in a specialist neuroendocrine tumour multidisciplinary meeting to ensure all treatment options are explored in localised and advanced disease. Areas of controversy exist that need further research.

Topics: Dissection; Endoscopy; Gastrins; Gastritis, Atrophic; Humans; Neuroendocrine Tumors; Polyps; Prognosis; Stomach Neoplasms

Gastric carcinoid tumors comprise 7% of all gastrointestinal carcinoids and have significantly increased in incidence over the past few decades. Seventy to 80% of gastric carcinoids are type I, which usually are clinically asymptomatic and found incidentally at endoscopic evaluation for abdominal pain or anemia. In this review, advances in understanding the pathophysiology of type I gastric carcinoid are highlighted. In addition, various current diagnostic and treatment options are discussed. Although type I carcinoids generally hold a benign course, rigorous investigation is needed to ensure accurate diagnosis and optimal treatment. This includes appropriate diagnostic procedures and imaging and accurate staging of tumor. Tumor size, depth of invasion, presence of metastasis, and the tumor's gastrin dependency dictate treatment options. Appropriate treatments can consist of endoscopic resection, antrectomy, medical management, or frequent follow-up. This article provides a systematic method of evaluating and treating type I gastric carcinoid.

Topics: Carcinoid Tumor; Enterochromaffin Cells; Gastrectomy; Gastric Acidity Determination; Gastric Fundus; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Humans; Neoplasm Staging; Polyps; Prognosis; Pyloric Antrum; Radionuclide Imaging; Risk Factors; Stomach Neoplasms

Topics: Gastric Acid; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Polyps; Stomach Neoplasms

Several case reports have emphasized that esophageal carcinoid tumors are associated with a poor prognosis. To expand our knowledge about the pathology and biologic behavior of these rare tumors, we reviewed the clinicopathologic and immunohistochemical findings of four cases of primary esophageal carcinoid. The age of the patients ranged from 48 to 82 years (mean 63 years; median 61 years). The lower segment of the esophagus was involved in two cases and the mid segment was involved in one case. The sizes of the tumors ranged from 0.3 cm to 3.5 cm. Two tumors were confined to the lamina propria and two invaded into the muscular wall. Two tumors appeared polypoid, whereas the remaining two were incidental findings and associated with adenocarcinoma arising in a background of Barrett esophagus. The adenocarcinoma was superficially invasive in one case, whereas it penetrated the muscular wall in the other. All four carcinoid tumors were immunoreactive with chromogranin and synaptophysin. There was focal expression of serotonin in two cases, glucagon in one case, and pancreatic polypeptide in one case. Endocrine cell hyperplasia was noted in both the Barrett esophagus and the invasive adenocarcinoma. One patient died secondary to postoperative pneumonia. Three patients are alive and disease free at 1, 6, and 23 years status post therapy. None of the patients had metastatic disease. These findings show that esophageal carcinoids are associated with a favorable prognosis. They arise in two settings: (1) a single large polypoid tumor or (2) an incidental finding and in association with adenocarcinoma arising in the background of Barrett esophagus. The presence of endocrine cell hyperplasia in the Barrett mucosa and the adenocarcinoma supports the hypothesis that these lesions arise from a common stem cell.

Topics: Adenocarcinoma; Aged; Aged, 80 and over; Barrett Esophagus; Carcinoid Tumor; Chromogranins; Esophageal Neoplasms; Female; Gastrins; Glucagon; Humans; Immunohistochemistry; Keratins; Male; Middle Aged; Pancreatic Polypeptide; Polyps; Prognosis; Synaptophysin

Fundic gland polyps (FGPs) are tiny multiple sessile polyps of the acid-secreting gastric mucosa. They have been described both in a sporadic form, mainly in middle-aged females, and in a syndromic form, associated with familial adenomatous polyposis (FAP)-Gardner's syndrome and attenuated variants (AFAP). They share the same histology, characterised by superficial and deep cystic dilatations, shortened gastric pits, with an inconspicuous lamina propria. They have been for a long time described as innocuous lesions, but some recent reports have shown that FGPs may harbour dysplastic foci and ultimately (particularly syndromic polyps) gastric cancer. Factors influencing their genesis are unknown. A circulating factor in FAP patients has been postulated and a role of female hormones has been suggested for sporadic FGPs. Whereas patients with sporadic FGPs have normal basal acid output, normal fast serum levels of gastrin and pepsinogen I, the role of gastrin seems crucial for the development of cystic changes in flat body-fundus mucosa, and for the appearance of FGPs in patients with Zollinger-Ellison syndrome. A role of H. pylori induced gastritis has been excluded. Actually, patients with both sporadic and syndromic FGPs appear consistently free from H. pylori colonisation, again for an unknown factor(s). Some recent reports have claimed a role for omeprazole in the genesis of FGPs, a highly controversial issue. Ultimately, the nature of FGPs is still debated: some have interpreted them as hamartomatous lesions, others as a peculiar form of hyperplastic polyp.

Topics: Adenomatous Polyposis Coli; Anti-Ulcer Agents; Female; Gardner Syndrome; Gastric Fundus; Gastric Mucosa; Gastrins; Helicobacter pylori; Humans; Male; Omeprazole; Pepsinogen A; Polyps; Stomach Neoplasms; Syndrome; Zollinger-Ellison Syndrome

Three cases of gastric carcinoid polypi associated to atrophic gastritis and high levels of seric gastrin, are presented. One of the cases was a multiple micropolyposis the literature regarding this association is reviewed and the therapy discussed. Tumors of greater than 2 cm have to be considered potentially malignant and be treated likewise. The treatment of the micropolyposis is not well established.

Topics: Achlorhydria; Adult; Autoimmune Diseases; Carcinoid Tumor; Female; Follow-Up Studies; Gastrins; Gastritis, Atrophic; Humans; Male; Middle Aged; Neoplasms, Multiple Primary; Polyps; Pyloric Antrum; Stomach Neoplasms

Rabeprazole at 10 or 20 mg twice daily (b.i.d.) has been reported to be highly effective in the treatment of proton pump inhibitor (PPI)-resistant reflux esophagitis (RE) that is refractory to the standard once-daily PPI regimen. We evaluated the efficacy and safety of rabeprazole maintenance therapy at 10 mg once daily (q.d.) or b.i.d. for longer than 8 weeks.. Patients with RE refractory to standard PPI regimens for at least 8 weeks were enrolled. They were treated with rabeprazole at 10 or 20 mg b.i.d. for 8 weeks during the open-label treatment period. After endoscopic examination, those with confirmed healing entered the subsequent double-blind maintenance therapy. During this period, the subjects were randomized to receive rabeprazole 10 mg q.d. (control) or 10 mg b.i.d. The primary endpoint was the endoscopic no-recurrence rate at Week 52.. In total, 517 subjects entered the treatment, and 359 subjects continued on maintenance therapy. The full analysis set for central assessment included 343 subjects. The no-recurrence rate at Week 52 was significantly higher in the b.i.d. group (73.9%; p < 0.001, χ. In the maintenance treatment of PPI-resistant RE, rabeprazole at 10 mg b.i.d. exerted a stronger recurrence-preventing effect than 10 mg q.d. over 52 weeks. No particular safety issues were noted during long-term administration. ClinicalTrials.gov number: NCT02135107.

Topics: Aged; Anti-Ulcer Agents; Double-Blind Method; Drug Administration Schedule; Drug Resistance; Endoscopy; Esophagitis, Peptic; Female; Gastrins; Gastroesophageal Reflux; Humans; Japan; Kaplan-Meier Estimate; Male; Middle Aged; Polyps; Proton Pump Inhibitors; Rabeprazole; Recurrence; Secondary Prevention; Treatment Outcome

Body-predominant atrophic gastritis is considered a risk factor for gastric cancer and carcinoid. Timing of follow-up for patients with this disorder has not been defined. This study was undertaken to determine the optimal time for the first endoscopic/histologic follow-up in patients with body-predominant atrophic gastritis.. Forty-two patients with body-predominant atrophic gastritis were randomly assigned to 1 of 2 follow-up intervals: group A (n = 22) at 24 months and group B (n = 20) at 48 months. At baseline and follow-up patients underwent gastroscopy at which biopsies were obtained from the antrum and body for histopathology and evaluation for enterochromaffin-like cells.. In group A patients, 2 antral hyperplastic polyps (9.1%) were present at baseline and 4 antral hyperplastic polyps (18.2%) were found at follow-up. In group B patients, baseline gastroscopy revealed 2 antral hyperplastic polyps (10%) and follow-up 2 antral hyperplastic polyps (10%) and 1 carcinoid tumor (5%) in the body. Atrophy and intestinal metaplasia scores in gastric body and antral mucosa in both groups did not change significantly between baseline and follow-up, except an increase in antral mucosa atrophy in group B patients (p = 0.02) was revealed.. The results of this study indicate that performing the first follow-up in patients with body-predominant atrophic gastritis need not be earlier than at 4 years after diagnosis. This interval is satisfactory for detection of potential neoplastic lesions.

Topics: Adult; Aged; Anemia, Pernicious; Biopsy; Carcinoid Tumor; Enterochromaffin-like Cells; Female; Follow-Up Studies; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Polyps; Prospective Studies; Pyloric Antrum; Random Allocation; Stomach Neoplasms; Time Factors

Helicobacter pylori infection is common in patients with hyperplastic gastric polyps.. To study the effect of eradication of H. pylori on the clinical course of patients with hyperplastic gastric polyps.. Single-blind, randomized, controlled trial.. University-based gastroenterology outpatient clinic.. 35 patients with H. pylori infection and hyperplastic gastric polyps at least 3 mm in diameter.. Patients were randomly assigned to a treatment group (n = 17), which received a proton-pump inhibitor (omeprazole or lansoprazole), amoxicillin, and either clarithromycin or ecabet sodium, or to a control group (n = 18), which received no treatment.. Patients underwent endoscopy before enrollment and 12 to 15 months after the end of treatment. Serum gastrin levels and titers of IgG to H. pylori were measured.. In the treatment group, the polyps had disappeared by 3 to 15 months (average, 7.1 +/- 1.2 months) after the end of treatment in 12 of all 17 patients (71%) and in 12 of the 15 patients (80%) in whom H. pylori was eradicated. However, 12 to 15 months after the start of the study, no change in polyps or H. pylori status was seen in any controls (P < 0.001). Histologic findings of inflammation and activity, serum gastrin levels, and titers of IgG to H. pylori showed significant regression in the treatment group compared with the control group (P < 0.01).. Most hyperplastic polyps disappeared after eradication of H. pylori. Thus, eradication should be attempted before endoscopic removal is done in patients with hyperplastic gastric polyps and H. pylori infection.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Abietanes; Adult; Aged; Amoxicillin; Anti-Bacterial Agents; Clarithromycin; Diterpenes; Drug Therapy, Combination; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Hyperplasia; Immunoglobulin G; Lansoprazole; Male; Middle Aged; Omeprazole; Penicillins; Polyps; Proton Pump Inhibitors; Single-Blind Method; Statistics, Nonparametric; Stomach Neoplasms

Gastric polyps represent an abnormal proliferation of the gastric mucosa. Chronic atrophic autoimmune gastritis (CAAG) targets parietal cells and results in hypo-achlorhydria and hypergastrinemia, which exerts a proliferative effect on the gastric mucosa.. We investigate the incidence of gastric polyps in CAAG patients.. This is a single-center retrospective study examining patients with confirmed CAAG from January 1990 until June 2022. Demographic, clinical, biochemical, and serological data were collected for each included patient. The histopathological characteristics of the detected polyps were recorded.. A total of 176 CAAG patients were included. Eighty-nine (50.5%) had 163 incidental polyps. Seventy-six patients (85%) had 130 non-endocrine lesions, among which 118 (90.7%) were inflammatory, 6 (4.6%) adenomatous, and 4 (3%) fundic; 33 patients (37%) had gastric neuroendocrine neoplasms (gNENs), and 21 (23.6%) both; one had MALToma and one gastric adenocarcinoma. Higher circulating levels of gastrin and chromogranin A were observed among patients with polyps (median 668 vs 893 pg/ml p = 0.0237, 146 vs 207 ng/ml p = 0.0027, respectively).. CAAG implies a high incidence of gNENs and exocrine lesions. Gastrin plays a possible trophic role on the mucosa. Further evidence is needed to validate its predictive role for increased polyp risk in CAAG.

Topics: Autoimmune Diseases; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Polyps; Precancerous Conditions; Retrospective Studies; Stomach Neoplasms

The aim of this study was to clarify the correlation between gastrin receptor (GR) expression in the gastric oxyntic mucosa and fundic gland polyps (FGPs) and the histological and immunohistochemical findings of the mucosa as well as the history of proton pump inhibitor (PPI) administration. The unique membranous linear positivity of GR in parietal cells was reproducibly observed by immunohistochemistry, which was also validated by immunofluorescence. Further histological and immunohistochemical examination of 34 oxyntic mucosae and 43 FGPs revealed the following: 1) parietal cells (PCs) with membranous linear GR expression (mGR) were observed to be limited to the isthmus-neck region in the normal state; 2) appearance of PCs with mGR in the deep oxyntic gland regions was significantly related to the PPI medication history; 3) PCs with mGR were more frequently observed in the deep oxyntic gland regions when the oxyntic mucosa showed derangement of mucosal component cell compartmentalization revealed by MUC5AC and MUC6 immunohistochemistry, which was also significantly related to the PPI use; and 4) PCs with intense membranous linear positivity of GR were observed to be diffusely distributed in all of the cases of FGPs. In conclusion, the distribution of unique GR membranous linear expression in PCs of the oxyntic mucosa under PPI medication and FGPs could reflect the pathologic mucosal state characterized by derangement of the compartmentalization of mucosal component cells, which could be another basis for evaluating physiologic and/or pathophysiologic conditions of the gastric mucosa.

Topics: Adenomatous Polyps; Gastric Mucosa; Gastrins; Humans; Parietal Cells, Gastric; Polyps; Proton Pump Inhibitors; Receptor, Cholecystokinin B; Stomach Neoplasms

We herein report a case of gastric hyperplastic polyps after argon plasma coagulation (APC) for gastric antral vascular ectasia (GAVE) in the antrum of a 65-year-old man with liver cirrhosis and hypergastrinemia induced by long-term proton pump inhibitor (PPI) use. Two years after APC therapy, endoscopy demonstrated multiple gastric polyps in the antrum and angle. A gastric polyp biopsy indicated foveolar epithelium hyperplasia, which was diagnosed as gastric hyperplastic polyps. One year after switching to an H2 blocker antagonist, endoscopy revealed that the polyps and GAVE had disappeared, with normal gastrin levels suggesting that PPI-induced hypergastrinemia had caused gastric hyperplastic polyps after APC therapy, and the polyps had disappeared after discontinuing PPIs.

Topics: Aged; Argon Plasma Coagulation; Gastric Antral Vascular Ectasia; Gastrins; Humans; Liver Cirrhosis; Male; Polyps; Stomach Neoplasms

We report a case of developing multiple adenocarcinoma foci in multiple hyperplastic polyps in a patient with Helicobacter pylori infection and hypergastrinemia during long-term proton pump inhibitor (PPI) therapy. A 57-year-old man, who was undergoing hemodialysis for chronic renal failure, underwent an upper gastrointestinal endoscopy to elucidate the cause of anemia. Atrophic gastritis with H. pylori infection and multiple adenocarcinoma foci in multiple hyperplastic polyps were found in the endoscopic and histological examinations. Enterochromaffin-like micronests and parietal cell protrusion in the background of the polyps suggested the existence of hypergastrinemia. The serum gastrin level was markedly high-10,206 pg/ml (normal range 37-172 pg/ml). The cause of this marked hypergastrinemia was not autoimmune gastritis and gastrinoma. After discontinuing PPI therapy and successful eradication of H. pylori, the serum gastrin level decreased to normal range. These findings indicate that hypergastrinemia may be caused by long-term PPI therapy in patients with H. pylori infection. This case suggests that hypergastrinemia may mediate gastric carcinogenesis in patients with H. pylori infection.

Topics: Adenocarcinoma; Cocarcinogenesis; Drug Administration Schedule; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Hyperplasia; Male; Middle Aged; Polyps; Proton Pump Inhibitors; Stomach Neoplasms

A number of different therapies, including endoscopic resection, have been suggested for the treatment of Type 1 gastric neuroendocrine tumors (NETs). The current study aimed to determine the long-term efficacy of endoscopic resection for Type 1 gastric NETs.. Twenty-two patients (from 1999 to 2012) with Type 1 gastric NETs were included in the study. All patients were treated with endoscopic resection and received regular followed-up appointments at a tertiary referral center.. All patients were initially diagnosed with hypergastrinemia, atrophic gastritis and intestinal metaplasia. Polyps' diameters were >1 cm in 4 patients, and between 0.5 and 1 cm in 18 patients. All detectable lesions were successfully resected. One patient required surgery due to gastric perforation during endoscopic mucosal resection. Recurrence was detected in four patients (18%) and endoscopic resection was performed again. Local or distant metastasis was not observed in any patient during follow-up. Median follow-up time was 7 years, with a maximum of 14 years. Seventeen patients (78%) completed a 5-year follow-up period, and overall disease-free survival rate was 100%.. Long-term follow-ups with 22 patients suggest that endoscopic resection of Type 1 gastric NETs is a safe and effective treatment option with a relatively low recurrence rate.

Topics: Adult; Aged; Chromogranin A; Disease-Free Survival; Female; Follow-Up Studies; Gastric Mucosa; Gastrins; Gastroscopy; Humans; Male; Middle Aged; Neoplasm Recurrence, Local; Neuroendocrine Tumors; Polyps; Prospective Studies; Reoperation; Stomach Neoplasms

Recent studies have suggested that Helicobacter pylori (H. pylori) constitutes a risk for the development of colonic neoplasia. Hypergastrinemia can be induced by H. pylori infection, and gastrin can act as putative promoter of colorectal carcinogenesis. Aim of our study was to assess whether H. pylori infection and/or increased serum gastrin levels are associated with the occurrence of colonic neoplasms. For this, we reviewed prospectively collected data of 377 patients with a minimum age of 50 years who underwent colonoscopy. H. pylori and CagA status were determined by serology. Serum gastrin levels were measured in fasting state by commercially available assay. In H. pylori infected patients (n = 138; 36.6%), the overall prevalence of colonic neoplasms was more frequent compared to H. pylori negative patients (n = 239; 63.4%) (OR = 2.73, 95% CI: 1.76-4.24). H. pylori infection occurred more frequently in patients with hyperplastic polyps (OR = 2.66, 95% CI: 1.23-5.74) and adenomas presenting with low grade intraepithelial neoplasia (IEN) (OR = 1.85, 95% CI: 1.14-2.99). Attributable risk for adenomas with high grade IEN and colorectal adenocarcinoma (n = 14) was not assessed due to the low number of cases. The expression of CagA was also associated with an increased risk for colonic neoplasms (OR = 2.25, 95% CI: 1.29-3.94). Hypergastrinemia did not increase the risk for any colonic neoplasms and there was no difference in basal serum gastrin levels between H. pylori positive and negative patients. In conclusion, H. pylori infection, including CagA expression is associated with an increased risk for the development of colonic neoplasm.

Topics: Aged; Antibodies, Bacterial; Antigens, Bacterial; Bacterial Proteins; Colon; Colonic Neoplasms; Colonoscopy; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Inflammation; Male; Polyps; Prospective Studies; Risk Factors

Autoimmune gastritis (AIG) may predispose to gastric carcinoid tumors or adenocarcinomas and may also cause unexplained iron and/or vitamin B(12) deficiency. The aims of this study were to explore clinical manifestations, endoscopic findings and laboratory features of patients with AIG.. 109 patients with AIG were enrolled into the study. In addition to demographic and clinical data, gastric lesions, serum gastrin, vitamin B(12), antiparietal cell antibody (APA), current Helicobacter pylori status, and anti-H. pylori IgG were also investigated.. The mean age of the patients was 53.06 ± 12.7 years (range 24-81; 72 (66.1%) women). The most common main presenting symptom was abdominal symptoms in 51 patients, consultation for iron and/or vitamin B(12) deficiency in 36, and non-specific symptoms including intermittent diarrhea in 15 patients. Endoscopic lesions were detected in 17 patients, hyperplastic polyps in 8, gastric carcinoid tumor in 4, fundic gland polyps in 3, and adenomatous polyps in 2 patients. H. pylori was negative in all patients in biopsy specimens; however, anti-H. pylori IgG was positive in 30 (27.5%) patients. 91 patients (83.4%) were positive for APA.. In patients with AIG, the main symptoms prompted for clinical investigation were: abdominal symptoms, iron/B(12) deficiency and non-specific symptoms. 20% of patients with AIG had various gastric lesions including type I gastric carcinoids. None of the patients were positive for H. pylori by means of invasive tests; however, anti-H. pylori IgG was found in 27.5% of patients. Patients referring with non-specific abdominal symptoms such as bloating, diarrhea and iron/B(12) deficiency should be investigated for the presence of AIG.

Topics: Adenomatous Polyps; Adult; Age Factors; Aged; Aged, 80 and over; Antibodies, Bacterial; Autoimmune Diseases; Carcinoid Tumor; Diarrhea; Female; Gastrins; Gastritis; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Iron; Iron Deficiencies; Male; Middle Aged; Parietal Cells, Gastric; Polyps; Sex Factors; Stomach Neoplasms; Vitamin B 12 Deficiency; Young Adult

Autoimmune metaplastic atrophic gastritis (AMAG) is an early manifestation of pernicious anemia that precedes the hematologic changes by years to decades. It is associated with metaplastic changes and neoplasms, including pyloric gland adenomas (PGAs). We investigated the frequency of PGAs and other lesions in all nonconsultation gastric biopsies and resections (1988 to 2008) diagnosed as AMAG. We further selected cases confirmed as AMAG by immunohistochemical identification of the gastric body (negative gastrin) and linear and nodular enterochromaffin-like cell hyperplasia (chromogranin). From this subset, all polyps and neoplasms were reviewed. We identified a total of 41,245 patients with gastric biopsies or resections from 46.7% males and 53.3% females comprising patients self-identified as 67.0% white, 23.6% African-American, 1.4% Asian, 0.8% non-White Hispanic, and 7.2% other or unknown. AMAG was diagnosed in 461 patients (1.1%), and had the following percentages based on race: 1.1% White, 1.3% African-American, 1.4% Asian, and 2.7% non-White Hispanic. The female:male ratio was 2:1 with an overall median age at presentation of 67.0 years. Of the 461 patients with AMAG, 143 had endoscopically identifiable lesions. These lesions (n=240) consisted of 179 polyps (138 hyperplastic polyps, 20 oxyntic mucosa pseudopolyps, 18 intestinal-type gastric adenomas, and 3 PGAs), 46 well-differentiated neuroendocrine neoplasms (carcinoid), 1 gastrointestinal stromal tumor, 3 lymphomas, and 11 adenocarcinomas. In summary, AMAG occurred with similar frequency across all racial groups. Although PGAs are associated with AMAG, they remain rare in the setting of AMAG.

Topics: Adenoma; Aged; Autoimmune Diseases; Baltimore; Biopsy; Chromogranins; Female; Gastrectomy; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Immunohistochemistry; Male; Metaplasia; Middle Aged; Polyps; Precancerous Conditions; Stomach; Stomach Neoplasms

Proton pump inhibitors (PPIs) have become the mainstay of therapy in acid-related upper gastrointestinal disorders including gastroesophageal reflux disease and peptic ulcer disease. Alltough these medications are generally accepted as safe, the long-term clinical consequences of the inducing hypochlorhydria are not completely clear. Gastric acid production is mainly controlled by the hormone gastrin through a negative feedback in which hypochlorhydria induces an increase in serum gastrin. PPIs have been shown to increase serum gastrin levels. Gastric endocrine cell hyperplasia can occur in 10 to 30% of patients without carcinoid tumors. Recent studies indicate no association between PPI use and the risk of colorectal and gastric cancers. Proton pump inhibitor-associated gastric polyps are totally benign tumors that should not be followed. There is an association between PPIs-induced acid suppression and an increased risk of enteric infection. PPIs do not inhibit intestinal absorption of lipids, iron, phosphorus, magnesium or zinc from food but can affect vitamin B12 status in older patients. Despite the undoubted benefits of PPIs, the practitioner always needs to consider risks and benefits before initiating them.

Topics: Bacterial Infections; Colonic Neoplasms; Gastric Acid; Gastrins; Humans; Polyps; Proton Pump Inhibitors; Vitamin B 12 Deficiency

Use of proton-pump inhibitors (PPIs) causes hypergastrinemia, and it is well known that gastrin has a trophic effect on the oxyntic mucosa. Some PPI users develop fundic gland polyps. The purpose of this study was to determine whether patients developing fundic gland polyps have a more pronounced gastric hypoacidity, hypergastrinemia or increased serum chromogranin A (CgA), which is an enterochromaffin-like (ECL) cell marker.. Five PPI users who developed multiple fundic gland polyps during PPI use were included in the study. PPI users without fundic gland polyps (n = 6) as well as healthy individuals (n = 6) were used as controls. In PPI users, we measured 24-h gastric pH, serum gastrin and CgA during one day, with standardized meals, whereas only gastrin and CgA were measured in the healthy individuals. Helicobacter pylori status was determined.. Gastric pH, serum gastrin and CgA did not differ significantly between PPI users with and those without fundic gland polyps. All patients with fundic gland polyps were H. pylori negative, whereas 4 out of 6 PPI users without fundic gland polyps were H. pylori positive. Fasting CgA levels were elevated in all PPI users, and CgA more than doubled during the day in all groups.. Fundic gland polyps induced by PPIs are not related to the level of hypergastrinemia. Serum CgA is markedly affected by meals and should be measured in samples from fasting patients.

Topics: Aryl Hydrocarbon Hydroxylases; Chromogranin A; Cytochrome P-450 CYP2C19; Gastric Acidity Determination; Gastric Fundus; Gastrins; Helicobacter pylori; Humans; Middle Aged; Polymorphism, Genetic; Polyps; Proton Pump Inhibitors; Stomach Diseases

The disorders of gallbladder motility may play an important role in the formation of gallstones. Many neural and hormonal factors and their interactions regulate gallbladder motility and bile flow into the duodenum. Further study in these factors may help to reveal the etiology of gallbladder diseases. This study was undertaken to assess the relationship of the levels of motilin, vasoactive intestinal peptide (VIP) and gastrin in blood and gallbladder tissues with the formation of cholelithiasis.. The levels of motilin, gastrin and VIP in blood and gallbladder tissues of 36 patients with gallbladder stones, 14 patients with gallbladder polyps, 10 healthy volunteers and 10 patients with common bile duct stones were measured by radioimmunoassay.. The level of motilin in plasma and gallbladder tissues of the gallbladder stone group was higher than that of the control and gallbladder polyp groups (P<0.05). The levels of plasma VIP and serum gastrin were much higher than those of the other three groups (P<0.01). The level of VIP in gallbladder tissues was higher than that of the control and gallbladder polyp groups (P<0.01).. The abnormal excretion of hormonal factors is closely related to gallstone formation. The high level of VIP in gallbladder tissues may be an important cause of gallbladder hypomotility. The abnormal level of serum gastrin may be related to the gastrointestinal symptoms of patients with gallstones.

Topics: Common Bile Duct; Female; Gallbladder; Gallstones; Gastrins; Gastrointestinal Hormones; Humans; Male; Middle Aged; Motilin; Polyps; Vasoactive Intestinal Peptide

Topics: Gastric Antral Vascular Ectasia; Gastric Mucosa; Gastrins; Gastroscopy; Humans; Hyperplasia; Laser Coagulation; Polyps; Postoperative Complications; Stomach Neoplasms; Stomach Ulcer

Type I gastric carcinoid tumors result from hypergastrinemia in 1%-7% of patients with pernicious anemia. We diagnosed pernicious anemia in a 48-year-old female patient with complaint of fatigue for three months. She had no gastrointestinal symptoms. Endoscopic examination ot the upper gastrointestinal tract revealed atrophic gastritis and a polypoid lesion in the corpus of 3-4 mm in size. Endoscopic polypectomy was performed. Histopathological examination of the specimen revealed positive chromogranin A and synaptophysin stainings compatible with the diagnosis of a carcinoid tumor. Serum gastrin level was increased, urinary 5-hydroxyindoleacetic acid was within the normal range. There was no other symptom, sign, or laboratory finding of a carcinoid syndrome in the patient. No metastasis was found with indium-111 octreotide scan, computed tomographies of abdomen and thorax. Type I gastric carcinoid tumors are only rarely solitary and patients with tumors < 1 cm in size may benefit from endoscopic polypectomy.

Topics: Anemia, Pernicious; Carcinoid Tumor; Endoscopy; Female; Gastrins; Humans; Middle Aged; Polyps; Stomach Neoplasms

Topics: Adult; Carcinoid Tumor; Duodenal Diseases; Endoscopy, Gastrointestinal; Female; Gastrectomy; Gastrins; Hematemesis; Humans; Neoplasm Recurrence, Local; Polyps; Prolapse; Stomach Neoplasms

The most common types of benign gastric polyps are fundic gland polyps, hyperplastic polyps, and adenomas. The aim of this study was to determine on which morphological and functional background benign gastric polyps develop. The study includes 85 consecutive patients with gastric polyps and sex- and age-matched controls without polyps selected at random from a general population sample. The type of polyp was hyperplastic in 52 (61%), fundic gland in 18 (21%), adenoma in 10 (12%), carcinoid in 2 (2%), hamartoma in 2 (2%), and inflammatory fibroid in 1 (1%) of the cases. Routine biopsies from the gastric corpus and antrum were examined for presence of gastritis and H. pylori. Blood samples were analyzed for H. pylori antibodies, H+,K+-ATPase antibodies, gastrin, and pepsinogen I. Patients with hyperplastic polyps had increased P-gastrin concentrations and S-H+,K+-ATPase antibody titers and decreased S-pepsinogen I concentrations with a high prevalence of atrophic corpus gastritis or pangastritis. A similar pattern was observed among patients with adenomas, whereas patients with fundic gland polyps had normal serology and a lower prevalence of gastritis and H. pylori infection than controls. In conclusion, hyperplastic polyps and adenomas are generally associated with atrophic gastritis. Patients with fundic gland polyps seem to have a sounder mucosa than controls. Whereas the risk of malignant gastric neoplasia is increased in patients with hyperplastic polyps or adenomas, this does not seem to be the case in patients with fundic gland polyps.

Topics: Adenomatous Polyps; Adult; Aged; Aged, 80 and over; Antibodies; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Humans; Male; Middle Aged; Pepsinogen A; Polyps; Prospective Studies; Sodium-Potassium-Exchanging ATPase; Stomach Neoplasms

Evidence indicates that eradication of Helicobacter pylori leads to the disappearance of hyperplastic polyps in the stomach. However, there are some exceptions. We have compared endoscopic and serologic findings of responder and non-responder cases with hyperplastic polyps to try to identify the cause(s), other than H. pylori infection, of the formation or growth of gastric hyperplastic polyps.. We retrospectively studied 33 patients whose hyperplastic polyps disappeared after eradication of H. pylori and 10 patients whose hyperplastic polyps did not disappear after eradication. The patients were examined both endoscopically and serologically before, 1-3 months after and 12-15 months after the eradication.. The responder and non-responder groups were similar with respect to age, sex, coexisting diseases, and histologic findings. The number and maximum size of polyps tended to be larger before treatment in the non-responder group than in the responder group. The serum gastrin level was higher in the non-responder group than in the responder group before, 1-3 months after and 12-15 months after the eradication (p=0.0096, p>0.2, p=0.0014). On histologic examination, similar reductions in the degree of inflammatory cell infiltration in the gastric mucosa of the antrum and body were seen in both the responder and non-responder groups. In the non-responders, the size and numbers of the polyps regressed in 5 of the 10 patients. The score of glandular atrophy in the antrum and the serum gastrin levels in the non-regressed cases was higher than those in the regressed cases at 1-3 and 12-15 months after eradication.. Persistent high gastrin levels were found in the non-responder cases with gastric hyperplastic polyps.

Topics: Adult; Aged; Anti-Bacterial Agents; Chi-Square Distribution; Drug Therapy, Combination; Endoscopy, Gastrointestinal; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Hyperplasia; Immunoglobulin G; Male; Middle Aged; Penicillins; Pepsinogen A; Polyps; Proton Pump Inhibitors; Retrospective Studies; Statistics, Nonparametric; Stomach Neoplasms

Previous reports have suggested a possible association between hyperplastic polyposis and colorectal neoplasms. Increased gastrin may be the link between these two conditions insofar as gastrin has been reported to be a growth-promoting tumoural agent. This report describes gastric polyposis, hypergastrinaemia and colorectal neoplasms in four elderly patients.. Four male patients with no family history of cancer, who were found to have multiple gastric hyperplastic polyps, hypergastrinaemia and colorectal cancers or an adenomatous polyp, were evaluated. Assessment included clinical evaluation, biochemical and haematological profiles, fasting gastrin levels, Helicobacter pylori serology, cobalamin, parietal cell antibodies, gastroscopy with biopsies of polyps and gastric mucosa, urease tests, and colonoscopy with biopsies of colorectal neoplasms. Immunohistochemistry of specimens from gastric polyps and colonic carcinomas was performed for chromogranin A, synaptophysin, Leu 7, neuron-specific enolase and gastrin.. The mean age at diagnosis of gastric polyps was 71.2 years and at removal of colorectal neoplasm was 70.0 years. In two patients, the gastric lesion was diagnosed before the colonic lesion and conversely in the two remaining patients. Gastrin was very high (1604 pg/ml; normal level, < 115 pg/ml) in one patient with pernicious anaemia, and the mean level for the other three was 324 pg/ml. H. pylori were found in two patients. Immunohistochemistry failed to identify neuroendocrine cells in the hyperplastic gastric polyps and three of the colonic carcinomas.. Occurrence of sporadic colorectal neoplastic lesion in patients with diffuse hyperplastic gastric polyposis and hypergastrinaemia may represent a new syndrome. Gastrin is not secreted by the gastric polyps or colonic carcinomas and may be related to gastric mucosal changes and H. pylori colonization. In patients with hyperplastic gastric polyposis and hypergastrinaemia, colorectal neoplasms should be ruled out.

Topics: Aged; Colorectal Neoplasms; Gastrins; Humans; Hyperplasia; Male; Polyps; Stomach Neoplasms; Syndrome

Topics: Gastric Fundus; Gastrins; Humans; Polyps; Stomach Neoplasms; Zollinger-Ellison Syndrome

Topics: Cysts; Gastric Fundus; Gastric Mucosa; Gastrins; Gastroesophageal Reflux; Humans; Omeprazole; Parietal Cells, Gastric; Polyps; Stomach Diseases

To document our experience with gastric carcinoids over the past decade and to identify lesion frequency and the existence of a relationship to low acid states.. Retrospective case series.. Tertiary care referral center.. A consecutive sample of 16 patients with gastric carcinoids was evaluated over the last decade. Only two cases were recorded in the prior decade. Ages ranged from 30 to 93 years (mean, 65.9 years). There were eight men and eight women. Three patients were unavailable for follow-up.. Therapy included total gastrectomy (n = 4), subtotal gastrectomy (n = 3), endoscopic polypectomy (n = 3), and endoscopic surveillance (n = 6).. Pathobiological tumor characteristics and survival.. All carcinoids were of gastric fundic origin. None of the patients exhibited the carcinoid syndrome. Chronic atrophic gastritis was the most frequently observed comorbid pathologic condition (63%). Half of the patients had multiple polypi. Mean follow-up was 4.7 years (n = 13). There were 10 survivors. The only related death occurred in a patient with a solitary tumor.. Diagnosis of the complex and ill-defined entity of gastric carcinoid is increasing. This may be due to an increased awareness and increased upper gastrointestinal endoscopy rate rather than an increase in real incidence. Criteria for prediction of malignant progression are not available. Multiple gastric carcinoids associated with hypergastrinemia predominantly display nonaggressive behavior. Conservative gastric surgery may be appropriate therapy for such patients.

Topics: Adult; Aged; Aged, 80 and over; Carcinoid Tumor; Comorbidity; Connecticut; Female; Follow-Up Studies; Gastrectomy; Gastric Acid; Gastric Fundus; Gastrins; Gastritis, Atrophic; Gastroscopy; Humans; Incidence; Male; Middle Aged; Polyps; Retrospective Studies; Stomach Neoplasms; Survival Rate

To determine serum concentration of gastrin and pepsinogens (PGs) as markers for the gastric mucosal status and to elucidate the prevalence of serum Helicobacter pylori (H pylori) IgG antibodies and parietal cell autoantibodies (PCAs) in patients with gastric polyps.. The subjects in this study were composed of 36 patients with fundic glandular polyps (FGP), 25 patients with foveolar hyperplastic polyps (FHP), and 27 asymptomatic healthy volunteers (controls). Serum concentrations of gastrin and PGs were determined by radioinmmunoassay. H. pylori IgG antibodies were measured through an enzyme-linked immunosorbent assay. PCAs were detected by an indirect immunofluorescence technique using cryostat sections of rat gastric mucosa.. There were no significant differences between FGP patients and controls in serum concentrations of gastrin, PG I and PG II. FHP patients showed significantly higher serum gastrin, lower PG I, higher PG II levels and, as a consequence, far lower PG I/PG II ratio compared with controls. The prevalence of H pylori infection was much higher in FHP patients (84.0%), whereas lower in FGP patients (19.44%) than that in controls (40.7%) was positive in 24.0% of FHP patients, 2.78% of FGP patients and 4% of controls.. These results suggest that FHP often develops in a gastric mucosa associated with H pylori infection, while FGP does not appear to be related to H pylori infection.

Topics: Antibodies, Bacterial; Autoantibodies; Biomarkers; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Male; Middle Aged; Parietal Cells, Gastric; Pepsinogens; Polyps; Stomach Neoplasms

The occurrence of H. pylori infection and the levels of fasting serum gastrin (SEGA) were examined in 97 patients with different morphological types of endoscopically diagnosed gastric polyps. According to the histology of the polyps the series was divided into three groups: inflammatory polyps (43 cases), polyps with foveolar hyperplasia (25 cases), and hyperplastic polyps including adenomas (29 cases). The prevalence of H. pylori infection was significantly lower in patients with hyperplastic polyps (45%) and foveolar hyperplasia (48%) than in the group with inflammatory polyps (81%). SEGA levels were higher in patients with hyperplastic polyps (mean +/- sd: 335 +/- 298 pmol/l) and foveolar hyperplasia (183 +/- 216) than in patients with inflammatory polyps (89 +/- 127). Signs of so-called "autoimmune" gastric, i.e. corpus atrophy and presence of parietal cell antibodies, were commonly found in patients with hyperplastic polyps and foveolar hyperplasia, but rarely in patients with inflammatory polyps. These results suggest that the polyps with hyperplastic changes (hyperplastic polyps and foveolar hyperplasia) are in some of the cases closely related to autoimmune gastritis. The presence of corpus atrophy, hypoacidity and various types of metaplasia, which characterizes autoimmune gastritis, could explain the low prevalence of H. pylori and the high SEGA levels found in these patients.

Topics: Adenoma; Aged; Female; Gastrins; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Hyperplasia; Male; Middle Aged; Polyps; Stomach Neoplasms

A 63-year-old woman was diagnosed as autoimmune gastritis by the presence of serum antibody against alpha-subunit of gastric H+,K(+)-ATPase. The patient did not have pernicious anemia, but showed achlorhydria, marked hypergastrinemia, enterochromaffin-like cell hyperplasia and an extremely high histidine decarboxylase activity in the gastric fundic mucosa. Intragastric acidification by infusion of hydrochloric acid via a nasogastric tube induced a transient reduction of serum gastrin level and fundic mucosal histidine decarboxylase activity. A marked increase in fundic mucosal histidine decarboxylase activity as well as hypergastrinemia appears to be the pathophysiologic response to achlorhydria caused by autoimmunity against gastric H+,K(+)-ATPase.

Topics: Achlorhydria; Autoimmune Diseases; Enterochromaffin Cells; Female; Gastric Fundus; Gastric Mucosa; Gastrins; Gastritis; Graves Disease; H(+)-K(+)-Exchanging ATPase; Histidine Decarboxylase; Humans; Hyperplasia; Middle Aged; Parietal Cells, Gastric; Polyps; Stomach Neoplasms

A solitary pedunculated gastric polyp in the gastric fundus was removed from an asymptomatic 36-year-old woman with normal gastric acid secretion and a normal serum gastrin level. This lesion exhibited distinctive histological features including prominent proliferation of pseudopyloric glands, fundic glands, foveolar epithelium and a fibromuscular stroma. Moreover, its surface was entirely covered by a layer of normal gastric epithelium. Biopsies of the background mucosa taken from the gastric fundus revealed only mild superficial gastritis. A gastric gland heterotopia was diagnosed because of its unique morphology.

Topics: Adult; Choristoma; Female; Gastric Acid; Gastric Fundus; Gastric Mucosa; Gastrins; Humans; Polyps; Stomach Neoplasms

We determined the maximum secretion of gastric acid and the fasting serum levels of pepsinogen I and gastrin in Japanese patients with gastric hyperplastic polyps or polypoid-type early gastric carcinoma, comparing those findings with observations in control subjects. Both the maximum acid secretion and fasting levels of serum pepsinogen I were significantly lower in the patients with gastric hyperplastic polyps or polypoid-type early gastric carcinoma than in the controls. Fasting serum gastrin levels were significantly higher in the patients with gastric hyperplastic polyps than in the other two groups of subjects. These data demonstrated that the combination of hypochlorhydria, a low level of pepsinogen I, and hypergastrinemia (type-A gastritis) was common in the patients with gastric hyperplastic polyps, whereas hypochlorhydria and a low pepsinogen I without hypergastrinemia (type-B gastritis) were common in those with polypoid-type early gastric carcinoma.

Topics: Aged; Female; Gastric Acid; Gastrins; Humans; Hyperplasia; Japan; Male; Middle Aged; Pepsinogens; Polyps; Stomach Neoplasms

An infant presented with hematemesis and gastric outlet obstruction. Preoperative diagnosis of duodenal duplication cyst was based on a collaboration of radiological studies. At exploration the patient was found to have a gastric polyp that had intussuscepted into the duodenum leading to obstruction and hypergastrinemia secondary to gastric mucosa in the duodenal alkaline environment.

Topics: Gastric Outlet Obstruction; Gastrins; Hematemesis; Humans; Hyperplasia; Infant; Male; Polyps; Stomach Neoplasms

To evaluate the characteristics of the gastric mucosa in women with fundic glandular polyps, we examined gastric acid secretion, fasting serum levels of pepsinogen I and gastrin, and gastric histology in 11 female patients with fundic polyps, and compared the results with 30 female controls without endoscopic abnormalities and 50 female patients with gastric foveolar hyperplastic polyps. No significant difference was found in gastric and secretion and fasting serum levels of pepsinogen I and gastrin between the patients with fundic glandular polyps and the control subjects. Histological examination showed that atrophic gastritis was generally not found in the patients with fundic glandular polyps. In contrast, gastric acid secretion and fasting serum levels of pepsinogen I were significantly lower and serum gastrin levels were significantly higher in the patients with foveolar hyperplastic polyps than in the other two groups. Also, patients with foveolar hyperplastic polyps had a higher prevalence and further advanced atrophic gastritis in the fundus than did the other two groups. Our investigations demonstrated that fundic glandular polyps arise from gastric mucosa without atrophic gastritis, whereas foveolar hyperplastic polyps develop from mucosa affected by atrophic gastritis, especially type A gastritis.

Topics: Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Middle Aged; Pepsinogens; Polyps; Stomach Neoplasms

The immunoreactive gastrin (IRG) and somatostatin (IRS) contents in gastric mucosa were measured from the same biopsy specimen of the same patients with duodenal ulcer (DU) at the active stage and healing stage, and compared to those of patients with fundic gland polyposis (FP) and endoscopically normal subjects whose gastric mucosa had only slight atrophic change (Control). The IRS in both the antrum and the gastric body of DU were significantly lower than those of the other two groups, and those showed no difference between the two stages. In all groups, there was a significant positive relation between the IRG and IRS in the antrum. In DU, particularly at the active stage, the relative decrease of the IRS against the IRG was prominent compared to the other two groups. In FP, which has similar background gastric mucosa and ability of acid output to those of DU, it was found that somatostatin was secreted sufficient to control gastrin secretion and acid output. Whereas in DU, secretion of somatostatin was reduced and, particularly at the active stage, it was considered that somatostatin, which could control increased gastrin secretion and increased acid output, was not secreted.

Topics: Adult; Duodenal Ulcer; Female; Gastric Fundus; Gastric Mucosa; Gastrins; Humans; Male; Polyps; Radioimmunoassay; Somatostatin; Stomach Neoplasms

To assess the functional and morphological characteristics of the gastric mucosa of patients with fundic hyperplastic polyps (FP), the determination of gastric acid secretion, serum gastrin levels, serum pepsinogen 1 (PG1) levels and histological examination were undertaken in 24 patients with FP, 34 with foveolar hyperplastic polyps (HP) and 62 controls, who had no gastric lesions. The following were the results of our investigation. 1) There were no differences between the patients with FP and the controls as to gastric acid secretion, serum gastrin levels, and serum PG1 levels. On the other hand, hypochlorhydria, hypergastrinemia and hypopepsinogenemia were common in those with HP. 2) Histological examination using gastric biopsy specimens showed almost normal gastric mucosa in patients with FP. However, severe atrophic gastritis of the fundus was common in patients with HP. 3) It was shown that there were definite differences between the patients with FP and those with HP with regard to the gastric function and morphology, although both types of gastric polyp were histologically classified as hyperplastic.

Topics: Adolescent; Adult; Female; Gastric Acid; Gastric Fundus; Gastric Mucosa; Gastrins; Humans; Hyperplasia; Male; Middle Aged; Pepsinogens; Polyps; Stomach Neoplasms

Topics: Gastrins; Humans; Neoplasm Recurrence, Local; Polyps; Prognosis; Stomach Neoplasms

Topics: Gastric Mucosa; Gastrins; Humans; Polyps; Stomach Neoplasms

A consecutive series of 357 endoscopic gastric biopsies was investigated after staining of histological sections with the Grimelius silver method. Argyrophil cells were classified according to the type of mucosa (fundic, antropyloric or intestinalized) in which they were located. Cases of argyrophil cell hyperplasia detectable on a qualitative basis were selected and their associations with various gastroduodenal disorders of the patients as well as with functional and pathological findings of the gastric mucosa were investigated. Hyperplasia of fundic argyrophil cells was more frequent in patients with atrophic gastritis of the fundic mucosa and a relatively well preserved antral mucosa as well as in patients with hyperplastic polyps. In contrast, it was infrequent in patients with duodenal ulcer and gastric stump. Hyperplasia of antropyloric argyrophil (non-G) cells was most frequent in patients with gastric peptic ulcer or with hyperplastic polyps as well as in those with atrophic gastritis of the fundic mucosa irrespective of the concomitant condition of antral mucosa. Hyperplasia of metaplastic argyrophil cells was more frequent in intestinal metaplasia of the antral mucosa than in that of fundic mucosa. Moreover, it was more frequent in patients with gastric cancer.

Topics: Adolescent; Adult; Aged; Biopsy; Female; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Diseases; Gastroscopy; Humans; Hyperplasia; Intestinal Mucosa; Male; Metaplasia; Middle Aged; Peptic Ulcer; Polyps; Silver; Staining and Labeling; Stomach Neoplasms

The relation of gastric polyps to acid-secreting mucosa was examined in 120 patients with gastric polyps. Studies were made by the endoscopic Congo red test developed in this clinic. In 23 patients (19.1%) gastric polyps were located in acid-secreting mucosa and may have arisen from normal oxyntic mucosa. These polyps were of two histological types: oxyntic gland polyps containing many parietal cells, and nonoxyntic gland polyps without parietal cells. Only the former type appeared to secrete acid, judging endoscopically from the change of Congo red from red to blue-black on the surface of the polyps after administration of gastrin.

Topics: Adult; Aged; Congo Red; Female; Fiber Optic Technology; Gastric Juice; Gastric Mucosa; Gastrins; Gastroscopy; Humans; Male; Middle Aged; Polyps; Stomach Neoplasms

Sessile polyps in the antrum were found in 12 of 51 patients with pernicious anaemia. During gastroscopy, mucosal biopsies for gastrin determination were taken from the antrum and fundus and from the polyps. Patients with high gastrin concentration in the antral mucosa showed high serum gastrin concentrations, while most patients with low antral gastrin concentrations also had low serum gastrin values. On an average, the gastrin concentrations in the antrum were approximately 10 times, and those in the fundus approximately 100 times, higher than the corresponding values obtained in a reference group. The gastrin content in the polyps was not different from that in the surrounding antral mucosa. This study suggests that the polyps are not due to a functional hypertrophy of the antral mucosa caused by locally increased production of gastrin.

Topics: Adult; Aged; Anemia, Pernicious; Female; Gastric Mucosa; Gastrins; Humans; Male; Middle Aged; Polyps; Stomach Neoplasms

Topics: Animals; Chronic Disease; Dogs; Duodenal Ulcer; Gastrins; Histamine Release; Humans; Hydrogen-Ion Concentration; Polyps; Stomach Neoplasms

The mean concentration of gastrin in serum was determined in healthy fasting persons (n = 27), it amounted to 56.8 pg/ml (SD = 19.8 PG/ML). The values of gastrin in serum of patients, who were grouped by endoscopicbioptic criteria of antral mucosa and who exceptionally showed diffuse inflammation of gastric mucosa, amounted to 73.2 pg/ml in patients with mild superficial gastritis (n = 24), to 73.4 pg/ml in those with severe superficial gastritis (n = 55), to 82.3 pg/ml in patients with chronic atrophic gastritis (n = 11) and to 70.7 pg/ml in those with chronic atrophic gastritis and intestinal metaplasia (n = 17). The concentration of serum gastrin in patients with additional pathological processes of gastric or duodenal mucosa was also determined. Patients with gastric resection according to Billroth II (n = 15) revealed gastrin values of 47.8 pg/ml, those with duodenal ulcer (n = 5) of 58.5 pg/ml, with gastric ulcer (n = 50) of 61.3 pg/ml, with polyps in stomach (n = 10) of 109.6 pg/ml and with neoplasms of the stomach (n = 27) of 77.7 pg/ml. Gastrin values were not correlated to age or sex. The difference between the mean gastrin concentrations of the mentioned groups of patients however is not marked enough and the range of values is too wide to characterize those groups by specific gastrin levels. The determination of gastrin in serum of fasting patients is not helpful for diagnosis of gastritis without antibodies to intrinsic factor or for diagnosis of certain localized pathological conditions in stomach or duodenum obviously.

Topics: Adolescent; Adult; Aged; Duodenal Ulcer; Female; Gastrectomy; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Metaplasia; Middle Aged; Polyps; Stomach Diseases; Stomach Neoplasms; Stomach Ulcer

Topics: Adult; Aged; Anemia, Pernicious; Female; Gastrins; Humans; Male; Middle Aged; Polyps; Pyloric Antrum; Stomach Neoplasms