gastrins and Esophageal-Diseases

Upper-GI diseases are one of the most relevant issue in primary care. Nowadays they are still responsible for about 100 million ambulatory care visits only in the US. The diagnosis of almost every upper-GI condition is still deputed to invasive tests such as upper gastrointestinal endoscopy, gastroesophageal manometry or radiography. The possibility of analysing serum markers like Pepsinogens I and II, produced by gastric mucosa, in order to assess the functional characteristics of the upper GI tract has spread itself since the 80's especially in the diagnosis of peptic ulcer. The discovery of Helicobacter pylori by Marshall and Warren in 1983 and the scientific consecration of its role in the pathogenesis of gastric cancer and peptic ulcer (crystallized in Peleo Correa's Cascade, 1992), led to an increase importance of non-invasive tests, raising the attention towards the assessment of both immunoglobulins anti-H.p. and Gastrin hormone produced by antral G cells, as an implementation of the panel of gastric markers. This narrative review aims to analyze the huge landscape of non-invasive tests for diagnosis of GI diseases, studying the literature of the recent years.

Topics: Antibodies, Bacterial; Biomarkers; Diagnostic Techniques, Digestive System; Dyspepsia; Endoscopy, Gastrointestinal; Esophageal Diseases; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Pepsinogens; Stomach Diseases

Topics: Animals; Biopsy; Cell Differentiation; Cell Division; Colonic Diseases; Culture Techniques; Digestive System; DNA; Epithelial Cells; Esophageal Diseases; Esophagus; Gastric Mucosa; Gastrins; Gene Expression Regulation; Genetic Markers; Humans; Intestinal Diseases; Intestine, Large; Intestine, Small; Neoplasm Transplantation; Oncogenes; Organ Culture Techniques; Stomach; Stomach Diseases

Topics: Animals; Celiac Disease; Child; Duodenal Ulcer; Duodenum; Esophageal Diseases; Gastrins; Gastrointestinal Diseases; Gastrointestinal Hormones; Humans; Intestinal Mucosa; Intestine, Small; Stomach; Zollinger-Ellison Syndrome

Topics: Adult; Biomechanical Phenomena; Esophageal Achalasia; Esophageal Diseases; Esophagitis, Peptic; Esophagogastric Junction; Esophagus; Female; Gastrins; Hernia, Hiatal; Humans; Male; Middle Aged; Muscle Tonus; Muscle, Smooth; Parasympatholytics; Pentagastrin

Topics: Atropine; Barium Sulfate; Deglutition; Esophageal Achalasia; Esophageal Diseases; Esophagus; Gastrins; Gastroesophageal Reflux; Humans; Manometry; Muscle Contraction; Nitroglycerin; Peristalsis; Pressure; Pyridostigmine Bromide; Radiography

Topics: Animals; Cats; Chronic Disease; Creatinine; Dogs; Duodenal Ulcer; Esophageal Achalasia; Esophageal Diseases; Gastric Mucosa; Gastrins; Gastritis; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Peptic Ulcer; Pyloric Antrum; Rats; Scleroderma, Localized; Stomach Neoplasms; Vagotomy; Zollinger-Ellison Syndrome

Topics: Cineradiography; Deglutition Disorders; Esophageal Achalasia; Esophageal Diseases; Esophageal Stenosis; Esophagogastric Junction; Esophagoscopy; Gastrins; Gastroesophageal Reflux; Heartburn; Hernia, Diaphragmatic; Humans; Manometry

Topics: Abdomen; Duodenal Diseases; Duodenal Neoplasms; Duodenal Ulcer; Esophageal Achalasia; Esophageal Diseases; Esophageal Neoplasms; Esophagitis; Esophagoplasty; Esophagus; Female; Gastrins; Gastrointestinal Hemorrhage; Hernia, Diaphragmatic; Humans; Male; Peptic Ulcer; Peptic Ulcer Perforation; Postoperative Complications; Rupture, Spontaneous; Stomach Diseases; Stomach Neoplasms; Stomach Ulcer; Stress, Psychological; Vagotomy

Topics: Air; Anemia, Pernicious; Angiography; Barium; Biopsy; Cholangiography; Colonic Diseases; Contrast Media; Cytodiagnosis; Duodenal Diseases; Endoscopy; Enema; Esophageal Diseases; Gastrins; Gastroenterology; Gastrointestinal Diseases; Gastrointestinal Neoplasms; Gastroscopy; Glucose; Glucuronidase; Gold Isotopes; Insulin; Liver Diseases; Methionine; Pancreatic Diseases; Peptic Ulcer; Peptides; Rectal Neoplasms; Rose Bengal; Selenium; Silicones; Stomach Neoplasms; Vagotomy

Apart from the complication of gastrointestinal vasculitis it is not known whether the upper gastrointestinal (UGI) tract has any special disease characteristics in rheumatoid arthritis (RA). However, oesophageal motility disorders have been reported in 30% of RA patients. Hypergastrinaemia has been found in 23-43% of RA patients, usually in combination with a decreased gastric acid output. Another finding suggestive of a decreased secretory state, namely a decreased level of pepsinogen A, was found in RA patients with the sicca syndrome and in patients with active disease. The risk for peptic ulcer disease with regard to nonsteroidal anti-inflammatory drugs (NSAID) is possibly higher in RA patients than in patients with other rheumatic diseases. These findings suggest that in RA patients intrinsic factors play a role in the pathogenesis of the oesophageal motility disorders, in hypergastrinaemia and hypopepsinogenaemia and the related decreased gastric secretory state, and possibly in the increased susceptibility to NSAID-related ulcers. However, there are also indications that oesophageal motility disorders, hypergastrinaemia, and NSAID-related ulcers in RA are the result of extrinsic factors, mainly the use of NSAIDs. The effects of NSAIDs and gold compounds on infection with Helicobacter pylori, a possible pathogenetic factor in ulcer disease, is discussed. It is clear that the discussion about intrinsic and extrinsic factors as a cause of the UGI manifestations in RA remains an intriguing but difficult subject for further studies.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Arthritis, Rheumatoid; Esophageal Diseases; Esophageal Motility Disorders; Gastric Acid; Gastrins; Helicobacter pylori; Humans; Pepsinogens; Peptic Ulcer; Stomach Diseases

Barrett's epithelium refers to the presence of ectopic mucosal types in the squamous-lined oesophagus. Previous studies have documented argentaffin and argyrophil-positive cells as well as gastrin-like immunoreactivity in oesophageal tissue extracts from patients with Barrett's mucosa. In the present study, 125 oesophageal biopsies obtained under direct vision at endoscopy from 22 patients with Barrett's oesophagus were systematically studied using fluorescence and peroxidase antiperoxidase single and double-staining immunocytochemical methods employing highly specific antibodies to localize the following peptide-containing cell types in Barrett's mucosa: gastrin, somatostatin, gastric inhibitory polypeptide, motilin, neurotensin and pancreatic glucagon. In addition, EC cells were localized using a cytochemical silver staining method. The results of this study indicate that EC cells and gastrin- and somatostatin-containing endocrine cells are detectable in Barrett's epithelium.

Topics: Adolescent; Adult; Aged; Barrett Esophagus; Enterochromaffin Cells; Esophageal Diseases; Esophagus; Female; Gastric Inhibitory Polypeptide; Gastrins; Glucagon; Humans; Immunoenzyme Techniques; Male; Middle Aged; Motilin; Neurotensin; Peptides; Somatostatin

We present the patterns for the diagnosis, checking the clinical, radiological, endoscopical and histological data of 35 patients suffering from Barrett's Esophagus (BE) (columnar metaplasia lining the lower esophagus). The clinical characteristics are those of a severe esophagitis of long evolution, although metaplasia itself is asymptomatic, and its features depend on the inflammation degree. Radiology can bring out some data as GE reflux, hiatal hernia, ulcers or stricture, and perhaps double contrast may show any sign by means of which endobrachyesophagus (EBE) can be suspected. Endoscopy provides us with accurate data about EBE, ulcers, stricture and inflammation. Histology reveals the type of columnar metaplasia (junctional or cardial, gastric fundic, intestinal or specialized, or composite). Acquired or congenital etiology can be clarified by an immunohistochemical method, Peroxidase anti-Peroxidase (PAP), showing the presence of gastrin secretory cells (G cells) in the congenital cases.

Topics: Adult; Aged; Barrett Esophagus; Chromaffin System; Enterochromaffin Cells; Esophageal Diseases; Esophagoscopy; Esophagus; Female; Gastrins; Humans; Male; Middle Aged; Radiography

A 61-year-old man with a 20-year history of recurrent gastric peptic ulcerations had an adenocarcinoma of the esophagus resected. The carcinoma was associated with columnar cell-lined (Barrett's) esophagus with carcinoma in situ. The patient had hypergastrinemia (gastrin level, 1,000 pg/dl), and at autopsy two months after the operation, a 3-mm pancreatic adenoma was discovered. In addition to the rarity of this clinical constellation, the case is of interest in suggesting that hypergastrinemia does not protect against peptic esophagitis and its sequelae.

Topics: Adenocarcinoma; Esophageal Diseases; Esophageal Neoplasms; Esophagitis, Peptic; Gastrins; Humans; Male; Middle Aged; Zollinger-Ellison Syndrome

An intravenous bolus of pentagastrin significantly increased the amplitude and duration of oesophageal body contractions in seven patients with diffuse oesophageal spasm (DES) when compared with five normal subjects (P greater than 0.05). In order to determine whether this stimulation also occurred at physiological gastrin concentrations, the effect of an intravenous infusion of gastrin heptadecapeptide (G17), 25 pmol/kg-h, on oesophageal contractions was studied in DES patients. G17 had no significant effect on the amplitude and duration of oesophageal contractions compared with a saline control. This dose of G17 was near the D50 for gastric acid secretion and produced a rise in serum gastrin concentration comparable with a meal. G17 infusions at doses of 100 and 200 pmol/kg-h increased the amplitude and duration of oesophageal contractions, but the corresponding serum gastrin concentrations were higher than postprandial levels. Thus, endogenous fluctuations in serum gastrin heptadecapeptide, alone, are unlikely to alter oesophageal contractions in DES patients.

Topics: Adult; Aged; Dose-Response Relationship, Drug; Esophageal Diseases; Esophagus; Female; Gastrins; Humans; Infusions, Parenteral; Male; Middle Aged; Muscle Contraction; Pentagastrin; Spasm

Immunocytochemical techniques using antigastrin antibody were employed to localize G cells in ectopic gastric mucosa of metaplastic and congenital origins and to compare their distribution with that in normal gastric mucosa. Five examples of Barrett's esophagus, 8 Meckel's diverticula, and 2 small bowel duplications were studied. Although G cells were absent in the gastric mucosa from all cases of Barett's esophagus, four Meckel's diverticula and one small bowel duplication contained G cells. In all instances of congenitally derived ectopic gastric mucosa where G cells were demonstrable, the gastric mucosa showed areas of antropyloric differentiation, whereas in the remaining cases the ectopic gastric mucosa was exclusively of the body-fundic type. It is concluded that the presence of G cells within ectopic gastric mucosa of Meckel's diverticula and small bowel duplications in foci of antropyloric differentiation reflects their developmental origin, whereas the absence of G cells in Barrett's esophagus is in keeping with its metaplastic derivation.

Topics: Choristoma; Esophageal Diseases; Esophagus; Gastric Mucosa; Gastrins; Histological Techniques; Humans; Intestinal Neoplasms; Intestine, Small; Meckel Diverticulum; Metaplasia

Present knowledge about gastrointestinal peptide hormones is discussed from three points of view: (a) diagnostic significance of these hormones; (b) states characterized by over-production or deficiency of peptide hormones; (c) clinical application and perspectives of gastrointestinal hormones. The data in the literature are subjected to a critical analysis; in addition, the author's own experiments are discussed.

Topics: Anemia, Pernicious; Celiac Disease; Cholecystokinin; Duodenal Ulcer; Duodenum; Esophageal Diseases; Gastrins; Gastrointestinal Hormones; Humans; Peristalsis; Pyloric Stenosis; Secretin; Spasm; Zollinger-Ellison Syndrome

Topics: Esophageal Diseases; Esophagogastric Junction; Gastrins; Humans; Peptic Ulcer; Pressure

Topics: Animals; Cholecystokinin; Esophageal Diseases; Esophagogastric Junction; Esophagus; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Pressure; Secretin

Topics: Adolescent; Adult; Aged; Esophageal Diseases; Esophagogastric Junction; Female; Gastrins; Gastrointestinal Diseases; Humans; Male; Middle Aged; Secretory Rate

Serum gastrin concentration was measured in newborns and infants with no gastrointestinal disorders, in the fasting state and after food stimulation. Mean fasting concentration in 14 newborns aged 1 to 12 days (130 . 4 pg/ml +/- 11 . 4 SE) was significantly higher than the mean value in 23 infants aged 1.5 to 22 months (101.4 +/- 6.6 pg/ml). Ingestion of the usual milk meal resulted in a definite rise of the serum gastrin level in the 5 subjects tested (3 newborns and 2 infants). The mean fasting serum gastrin level in 6 babies with hiatus hernia and gastro-oesophageal reflux was found to be no different from the corresponding value in 8 age-matched controls. However, a conspicuously raised fasting gastrin concentration was observed in one infant with lower oesophageal dyskinesia. The results indicate that the release of gastrin and the reactivity of the hormone-producing sites to food stimulation in early life are similar to those in adult humans. No defect of gastrin release was shown in patients with gastro-oesophageal reflux.

Topics: Animals; Esophageal Diseases; Gastrins; Gastroesophageal Reflux; Hernia, Hiatal; Humans; Infant; Infant, Newborn; Milk

Topics: Animals; Esophageal Diseases; Esophagogastric Junction; Gastrins; Humans; Motor Neurons; Muscle, Smooth; Parasympathetic Nervous System; Pressure

To determine the pathogenesis of esophageal dysfunction in scleroderma and Raynaud's disease, the lower esophageal sphincter (LES) was tested with: (a) methacholine acting directly at the cholinergic receptor on the muscle; (b) edrophonium, a cholinesterase inhibitor, enhancing the effect of released acetylcholine; and (c) gastrin I, acting through the release of acetylcholine. 10 patients with Raynaud's disease and 22 patients with scleroderma were compared with 20 normals and 20 patients with isolated LES incompetence. The mean basal LES pressure in normals was significantly greater than that recorded in both patients with scleroderma and Raynaud's disease. Six patients having scleroderma with normal peristalsis had an LES pressure significantly greater than that noted in 16 patients having scleroderma with abnormal peristalsis. In all groups, the per cent increase in LES pressure was similar when tested by direct muscle stimulation by methacholine. The response to agents that acted indirectly through intact cholinergic nerves differed in these groups. The LES response to gastrin I distinguished patients with normal peristalsis from those with abnormal peristalsis. The patients with normal peristalsis, either with scleroderma or with Raynaud's disease showed only a partial reduction in their response to gastrin I. The response to gastrin I was markedly reduced only in patients with abnormal peristalsis. These data indicate that in patients with scleroderma and Raynaud's disease, the LES response to direct muscle stimulation by methacholine was intact while the response to gastrin I and edrophonium was diminished.

Topics: Adult; Edrophonium; Esophageal Diseases; Esophagus; Gastrins; Humans; Manometry; Methacholine Compounds; Middle Aged; Raynaud Disease; Scleroderma, Systemic

Topics: Esophageal Achalasia; Esophageal Diseases; Esophagogastric Junction; Esophagus; Gastrins; Gastroesophageal Reflux; Humans; Muscle, Smooth

Topics: Adult; Antacids; Cerebral Palsy; Child; Esophageal Diseases; Esophagogastric Junction; Gastrins; Gastroesophageal Reflux; Hernia, Diaphragmatic; Humans; Infant; Infant, Newborn; Manometry; Muscle Spasticity

Intraluminal manometric studies were carried out in 19 patients with untreated achalasia and in 20 normals. Lower esophageal sphincter (LES) pressure was 50.5 +/-4.6 mm Hg in patients with achalasia as compared with 19.4 +/-1.3 mm Hg in the normal group. In both groups, the LES pressure was lowered when exogenous 0.1 N HCl was placed into the stomach. Although the nadir of pressure attained with acid suppression was the same, the per cent inhibition was significantly greater in patients with achalasia. Serum gastrin levels were the same in the two groups studied. The patients with achalasia, pre- and postpneumatic dilatation, showed a supersensitivity to exogenous intravenous gastrin I, as compared with normals. These data suggest that high, acid-suppressible levels of LES pressure, in patients with achalasia, are due to supersensitivity to endogenous gastrin.

Topics: Adolescent; Adult; Aged; Child; Esophageal Achalasia; Esophageal Diseases; Esophagus; Gastrins; Humans; Manometry; Methacholine Compounds; Middle Aged; Pressure