gastrins and Celiac-Disease

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

Functioning tumors of the pancreatic islets are now recognized as the source of clinical syndromes affecting the gastrointestinal tract which have a wide variety of catastrophic symptoms. Experiences with thirty-six cases suggest at least four separate diagnostic categories in the ulcerogenic tumor syndrome. These include: a typical history, gastric analysis, and roentgenographic findings with boderline fasting serum gastrin levels; ulcerogenic tumor with evidence of hyperparathyroidism; iatrogenic ulcerogenic syndrome associated with failure of a previous operation for duodenal ulcer; and the classic ulcerogenic syndrome associated with a fulminating ulcer diathesis or diarrhea and high serum gastrin levels. The problems presented at operation include: decisions to be make in the presence of a negative exploration; the finding of a solitary tumor in the wall of the duodenum; solitary pancreatic tumors particularly in the body and tail; ulcerogenic tumors in the very young; liver metastases in the elderly; and the wisdom of removing gross metastases in combination with total gastrectomy. The long-term survival in the ulcerogenic tumor syndrome approximated 50 per cent, with 40 per cent of those having proved malignancy living five years. Evidence of hyperparathyroidism is relatively common in association with both the ulcerogenic and the diarrheogenic tumor syndromes. The association may by a result of a congenital abnormality, metabolic alkalosis, or a direct effect of the islet cell tumor. Parathyroidectomy may be indicated when both the serum calcium and parathormone levels are elevated in the presence of borderline fasting gastrin levels. The latter may return to normal after parathyroidectomy. The evidence of hyperparathyroidism closely parallels the episodes of diarrhea in the diarrheogenic syndrome, and hyperparathyroidism may regress spontaneously after total removal of the pancreatic tumor. Just as routine calcium determinations made the diagnosis of hyperparathyroidism more commonplace, it is suggested that the gastrointestinal syndromes associated with islet cell tumor would receive wider recognition if radioimmunoassays for gastrin as well as secretin, and the other secretin-like polypeptides, were carried out routinely.

Topics: Adenoma, Islet Cell; Age Factors; Celiac Disease; Diagnosis, Differential; Diarrhea; Duodenal Neoplasms; Follow-Up Studies; Gastrins; Humans; Hyperparathyroidism; Liver Neoplasms; Neoplasm Metastasis; Pancreatic Hormones; Pancreatic Neoplasms; Preoperative Care; Secretin; Zollinger-Ellison Syndrome

Topics: Animals; Bacteria; Bacteriolysis; Bile Acids and Salts; Celiac Disease; Dogs; Duodenum; Food; Gastric Juice; Gastrins; Gastrointestinal Motility; Humans; Intestinal Mucosa; Intestine, Small; Lithocholic Acid; Postoperative Complications; Secretory Rate; Vagotomy

Topics: Adenoma, Islet Cell; Angiography; Antacids; Celiac Disease; Diarrhea; Gastric Juice; Gastrins; Humans; Hyperparathyroidism; Malabsorption Syndromes; Pancreatic Neoplasms; Physical Examination; Radioimmunoassay; Radionuclide Imaging; Zollinger-Ellison Syndrome

Topics: Celiac Disease; Cholecystokinin; Digestion; Gastrins; Gastrointestinal Hormones; Homeostasis; Humans; Postgastrectomy Syndromes; Secretin; Vagotomy; Zollinger-Ellison Syndrome

Collagenous gastritis is a rare condition defined histologically by a superficial subepithelial collagen layer. This study further characterizes the morphologic spectrum of collagenous gastritis by evaluating a multi-institutional series of 40 patients (26 female and 14 male). The median age at onset was 16 years (range 3-89 years), including 24 patients (60%) under age 18. Twelve patients (30%) had associated celiac disease, collagenous sprue, or collagenous colitis. Hematoxylin and eosin slides were reviewed in biopsies from all patients and tenascin, gastrin, eotaxin, and IgG4/IgG immunohistochemical stains were applied to a subset. The distribution of subepithelial collagen favored the body/fundus in pediatric patients and the antrum in adults. There were increased surface intraepithelial lymphocytes (>25 lymphocytes/100 epithelial cells) in five patients. Three of these patients had associated celiac and/or collagenous sprue/colitis, while the remaining two had increased duodenal lymphocytosis without specific etiology. An eosinophil-rich pattern (>30 eosinophils/high power field) was seen in 21/40 (52%) patients. Seven patients' biopsies demonstrated atrophy of the gastric corpus mucosa. Tenascin immunohistochemistry highlighted the subepithelial collagen in all 21 specimens evaluated and was a more sensitive method of collagen detection in biopsies from two patients with subtle subepithelial collagen. No increased eotaxin expression was identified in 16 specimens evaluated. One of the twenty-three biopsies tested had increased IgG4-positive cells (100/high power field) with an IgG4/IgG ratio of 55%. In summary, collagenous gastritis presents three distinct histologic patterns including a lymphocytic gastritis-like pattern, an eosinophil-rich pattern, and an atrophic pattern. Eotaxin and IgG4 were not elevated enough to implicate these pathways in the pathogenesis. Tenascin immunohistochemistry can be used as a sensitive method of collagen detection.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Celiac Disease; Chemokine CCL11; Child; Child, Preschool; Colitis, Collagenous; Collagen; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Immunoglobulin G; Male; Middle Aged; Stomach; Tenascin; Young Adult

To study condition of the stomach, gall-bladder, pancreas, liver in celiac disease (CD) and contribution of their dysfunction to clinical presentation of CD symptoms.. A total of 215 CD patients entered the study (191 females and 24 males) aged under 20 years (n=100), 20 to 50 (n=74) and over 50 years (n=41). The control group consisted of 25 healthy volunteers. Acid-forming function of the stomach, blood serum gastrin level were studied. Bile for biochemical test was obtained at duodenal intubation using 40 ml of 40% glucose solution or 25% magnesium solution as food stimulators, and intravenous injection of cholecystokininpancreosimin. Cholic acid was assayed in bile portions B and C. Two-channel probe was used to obtain duodenal content before meal and after intravenous injection of pancreosimin for tripsin, amylase and lipase assay. Clinical and biochemical blood tests were made as well as puncture biopsy of the liver with histological study of biopsy material.. CD patients were found to have high basal and stimulated acid-forming function, high gastrin concentration in the blood. The morphological examination detected lymphocytic gastritis. There were an inert type of pancreatic enzyme secretion, gall-bladder hypokinesia or atony. Gall-bladder contracted only after intravenous injection of cholecystokinin. Changes in the liver were characterized by hypertransaminasemia, steatohepatitis.. Changes in the stomach in patients with new-onset CD promote formation of ulcer. Decline in excretory pancreatic function, slow enzyme secretion, marked hypokinesia of the gall-bladder, hyperenzymemia and steatohepatitis as manifestations of hepatic pathology result in dramatic disorder of digestion and absorption of food substances.

Topics: Adolescent; Adult; Aged; Amylases; Bile; Biomarkers; Celiac Disease; Female; Gallbladder; Gastric Mucosa; Gastrins; Humans; Lipase; Liver; Male; Middle Aged; Pancreas; Prognosis; Trypsin; Young Adult

The combined evaluation of serum pepsinogens A (PGA) and C (PGC), gastrin-17 (G17) and anti-H. pylori antibodies (anti-H. pylori)(GastroPanel) has recently been proposed as a useful aid for investigating H. pylori-associated gastric mucosal inflammation. Our aim was to evaluate whether GastroPanel can correctly classify children who need or not endoscopy (EGD).. GastroPanel was performed in 554 consecutive children subjected to EGD.. PGC and anti-H. pylori were sensitive (82.5% and 73.1%) and specific (58.1% and 84.0%) indices of H. pylori infection. Antral H. pylori colonization density, inflammation and activity grades were correlated with PGC. PGC and G17 were significantly higher in children with celiac disease (14.9+/-0.88 microg/L and 5.6+/-0.79 pmol/L) than in controls (8.5+/-0.38 microg/L and 2.4+/-0.24 pmol/L). The best cut-offs to distinguish H. pylori infected children from controls were 7.45 microg/L for PGC, 4.2 pmol/L for G17, 18 U for anti-H. pylori and 25 microg/L for PGA. With these cut-offs, GastroPanel had a NPV of 89.6% and a PPV of 66.8%.. A negative GastroPanel result in children with upper abdominal non alarm symptoms, should allow the paediatrician to reasonably rule out the presence of major gastro-duodenal diseases and therefore avoid EGD.

Topics: Adolescent; Antibodies, Bacterial; Celiac Disease; Child; Child, Preschool; Endoscopy, Gastrointestinal; Female; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Diseases; Helicobacter Infections; Helicobacter pylori; Humans; Infant; Logistic Models; Male; Pepsinogen A; Pepsinogen C; Sensitivity and Specificity

Conventional endoscopic and radiographic methods fail to identify a probable source of gastrointestinal blood loss in about one third of males and post-menopausal females and in most women of reproductive age with iron deficiency anemia (IDA). Such patients, as well as subjects refractory to oral iron treatment, are often referred for hematologic evaluation.. Patient clinic, screened for non-bleeding gastrointestinal conditions including celiac disease (antiendomysial antibodies), autoimmune atrophic gastritis (hypergastrinemia with strongly positive antiparietal cell antibodies) and H. pylori infection (IgG antibodies confirmed by urease breath test).. The mean age of all subjects was 39+/-18 years, and 119 of 150 were females. We identified 8 new cases of adult celiac disease (5%). Forty IDA patients (27%) had autoimmune atrophic gastritis of whom 22 had low serum vitamin B12 levels. H. pylori infection was the only finding in 29 patients (19%), but was a common co-existing finding in 77 (51%) of the entire group. Refractoriness to oral iron treatment was found in 100% of patients with celiac disease, 71% with autoimmune atrophic gastritis, 68% with H. pylori infection, but only 11% of subjects with no detected underlying abnormality. H. pylori eradication in previously refractory IDA patients in combination with continued oral iron therapy resulted in a significant increase in hemoglobin from 9.4+/-1.5 (mean +/- 1SD) before, to 13.5+/-1.2 g/ dL (p<0.001 by paired t test) within 3 to 6 months.. The recognition that autoimmune atrophic gastritis and H. pylori infection may have a significant role in the development of unexplained or refractory IDA in a high proportion of patients should have a strong impact on our daily practice of diagnosing and managing IDA.

Topics: Adolescent; Adult; Aged; Amoxicillin; Anemia, Iron-Deficiency; Antibodies, Bacterial; Autoantibodies; Autoimmune Diseases; Bacterial Proteins; Breath Tests; Celiac Disease; Child; Clarithromycin; Comorbidity; Drug Therapy, Combination; Female; Ferrous Compounds; Gastrins; Gastritis; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Male; Middle Aged; Omeprazole; Parietal Cells, Gastric; Prospective Studies; Urease; Vitamin B 12 Deficiency

The authors provide the data obtained during examination of 36 children with celiac disease and 18 children with lactase deficiency. The children's age ranged from 8 months to 15 years. All the children underwent spot biopsy of the gastric and duodenal mucosa followed by immunomorphological PAP-staining of the biopsy specimens and count of the number of gastrin- and somatostatin-producing cells. Gastrin in the blood serum was measured by radioimmunoassay. The children with celiac disease manifested an increase of the number of somatostatin-producing cells in the duodenum and decrease of their number in the pyloric part of the stomach, seen in the acute phase of the disease. The number of gastrin-producing cells remained unchanged. The level of gastrin declined in the acute phase and increased during a remission. The alterations described were found to be related to the atrophic processes in the small intestinal mucosa. In lactase deficiency, no significant alterations were established in the number of pyloric and duodenal endocrine cells or in blood gastrin level.

Topics: Adolescent; Celiac Disease; Child; Child, Preschool; Digestion; Duodenum; Gastrins; Humans; Infant; Lactose Intolerance; Pylorus; Somatostatin

Untreated celiac disease is characterized by gastrointestinal endocrine cell hyperplasia (ECH). This study investigated the constitutive nature of the ECH. Ten duodenal biopsies showing villous atrophy from adult celiacs were evaluated against ten sex- and age-matched controls. The mean number of endocrine cells per unit length of mucosa in the celiacs was compared with the control group using the Student t test. These values, respectively, were as follows: Churukian-Schenk method, 52.4 versus 29.6 (P = 0.001); Fontana-Masson, 32.5 versus 18.4 (P = 0.016); chromogranin, 33.4 versus 23.6 (P = 0.017); serotonin, 44.7 versus 26.7 (P = 0.006); somatostatin, 5.0 versus 5.4 (P = 0.631); and gastrin, 0.37 versus 0.37 (P = 1.000). There was thus ECH as shown by the first four stains with, in some areas, the endocrine cells continuously abutting against each other to form linear profiles. With respect to specific hormonal products, only serotonin showed ECH. These results suggest that the ECH in celiac disease is not a haphazard process but, instead, a selective proliferation of certain endocrine cell types.

Topics: Adult; Aged; Biopsy; Celiac Disease; Cell Division; Chromogranins; Digestive System; Duodenum; Endocrine Glands; Female; Gastrins; Humans; Hyperplasia; Immunohistochemistry; Male; Middle Aged; Serotonin; Somatostatin

Topics: Celiac Disease; Child, Preschool; Chronic Disease; Diarrhea, Infantile; Eating; Fasting; Female; Gastrins; Humans; Infant; Male; Reference Values

The individual daily intake of gluten was calculated in 45 patients with dermatitis herpetiformis (DH) on the basis of a depth interview about food habits. Gastric and small intestinal morphology and function were studied concurrently. Mean daily gluten intake was estimated to be 15 g, a figure which corresponds well to the average gluten intake in Sweden. There was a significant correlation between the degree of morphological mucosal changes of the small intestine and the quantity of gluten ingested. All patients with jejunal villous atrophy consumed more than 10 g gluten daily and all but one patient with normal jejunal villous structure had a gluten intake of less than 10 g/d. The findings suggest a dose-dependent effect of gluten on the intestinal mucosa. Conversely, the daily gluten intake was not correlated to gastric morphology, gastric acid secretion, serum gastrin levels or serum parietal cell antibodies. Patients with reduced ability to secrete gastric acid did not differ from the remaining patients in this respect. Whereas the coeliac-like enteropathy in DH seems to be caused by ingested gluten, the frequently occurring achlorhydric atrophic gastritis must be assumed to be of different immunopathogenesis.

Topics: Achlorhydria; Adolescent; Adult; Aged; Celiac Disease; Dermatitis Herpetiformis; Duodenum; Feeding Behavior; Female; Gastric Acid; Gastric Mucosa; Gastrins; Glutens; Humans; Intestinal Mucosa; Jejunum; Male; Middle Aged

Topics: Celiac Disease; Child; Child, Preschool; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Humans; Intestinal Mucosa; Jejunum

Jejunal biopsies and the postprandial response of pancreatic polypeptide (PP), gastrin, gastric inhibitory polypeptide (GIP), and somatostatin have been examined in nine patients with celiac disease before and 1 year after gluten withdrawal. All presented initially with total villous atrophy of the jejunal mucosa. After gluten withdrawal five showed marked mucosal regeneration on light microscopy examination (responders) and four only moderate or no regeneration (nonresponders). Before treatment the celiac patients had enhanced gastrin response and normal PP response compared with normal controls. After gluten withdrawal the integrated gastrin release was reduced to normal in the responders (275 versus 114; p less than 0.05) but remained elevated in the nonresponders (231 versus 204). Postprandial PP release was similar before and after treatment regardless of the degree of mucosal regeneration. In the responders the integrated release of GIP was increased (180 versus 241; p less than 0.05), and the somatostatin release was enhanced (-2.6 versus 8.4; p less than 0.05) after gluten withdrawal. We conclude that the postprandial release of GIP and somatostatin increases and that the release of gastrin decreases when the intestinal mucosa is regenerated in celiacs on a gluten-free diet. The release of PP after food is not influenced by mucosal regeneration.

Topics: Adult; Celiac Disease; Female; Food; Gastric Inhibitory Polypeptide; Gastrins; Glutens; Hormones; Humans; Intestinal Mucosa; Jejunum; Male; Middle Aged; Pancreatic Polypeptide; Somatostatin

Topics: Adolescent; Celiac Disease; Child; Child, Preschool; Gastrins; Humans; Infant; Infant, Newborn

Increased basal and/or pentagastrin-stimulated gastric acid secretion was observed in 31 of 40 cystic fibrosis (CF) patients as compared to 13 age-matched control volunteers. Fasting serum gastrin level for 20 CF patients of 67.7 +/- 11.1 pg/ml (ranging from 10 to 145 pg/ml) was normal. Meal-stimulated serum gastrin concentrations were not significantly higher for seven CF patients as compared to nine normal subjects. In a rat bioassay, serum extracts from six CF patients produced gastric acid secretion comparable to 250 ng/ml of pentagastrin; significantly (p less than 0.01) greater than the responses produced by serum extracts from six normal subjects. There was no significant correlation of severity of pulmonary disease or steatorrhea with acid secretory results. Fourteen of 16 CF patients biopsied had evidence of proximal small intestinal injury which correlated with basal acid output elevation. Gastric acid hypersecretion in CF patients is due to nongastrin secretagogues and is a cause of proximal small intestinal injury.

Topics: Adolescent; Adult; Animals; Celiac Disease; Child; Child, Preschool; Cystic Fibrosis; Duodenum; Female; Gastric Acid; Gastrins; Humans; Infant; Intestinal Diseases; Lung Diseases, Obstructive; Male; Pentagastrin; Rats; Rats, Inbred Strains; Time Factors

In adult coeliac sprue patients, intraduodenal instillation of a hypertonic glucose-citric acid solution may release gastrointestinal hormones of the proximal (secretin, gastric inhibitory polypeptide, motilin) and distal (enteroglucagon, neurotensin) small intestine and, indirectly, of the pancreas (glucagon, insulin, pancreatic polypeptide). Characteristic plasma hormone profiles can be measured radioimmunologically. The reduced secretin response reflects most sensitively the impaired function of the small intestine. Exposure of the distal small bowel to greater nutrient loads leads to markedly and constantly elevated plasma levels of enteroglucagon. Only after complete functional as well as morphologic mucosal restoration, the increased enteroglucagon concentrations return to normal. On the other hand, the neurotensin response, which is likewise enhanced in active coeliac sprue, is sooner corrected during treatment. Gastrointestinal hormones with predominantly neurocrine action, such as vasoactive intestinal peptide (VIP), are apparently less affected by coeliac sprue. Pancreatic hormones are involved in the pathophysiology of sprue only indirectly, e. g. via diminished glucose absorption.

Topics: Adult; Blood Glucose; Celiac Disease; Female; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Glucagon; Glucagon-Like Peptides; Humans; Insulin; Insulin Secretion; Male; Middle Aged; Motilin; Neurotensin; Pancreatic Polypeptide; Secretin; Vasoactive Intestinal Peptide

Topics: Brain; Celiac Disease; Digestive System Physiological Phenomena; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Glucagon-Like Peptides; Humans; Obesity; Pancreas; Pancreatic Neoplasms; Pancreatic Polypeptide; Secretin; Somatostatin; Substance P

Gastric acid secretion in nineteen children with celiac disease remained almost unchanged and the level of fasting serum gastrin was comparable with that of a control group of the same age. The absorption of vitamin B12 was significantly decreased, most clearly in the infants with celiac disease as compared with their controls. The serum B12 level, however, was decreased only in the oldest children. The results suggest that the mucosal lesion in the small intestine is most extensive in the youngest children, but the absorption defect of vitamin B12 becomes clinically significant only after a long duration of the disease and not in childhood.

Topics: Adolescent; Celiac Disease; Child; Child, Preschool; Gastric Acidity Determination; Gastrins; Humans; Infant; Intestinal Absorption; Vitamin B 12

Topics: Animals; Cattle; Celiac Disease; Child; Child, Preschool; Eating; Fasting; Gastrins; Humans; Infant; Insulin; Milk

The response of serum immunoreactive gastric inhibitory polypeptide (IR-GIP), gastrin (IRG) and insulin (IRI) to a mixed standard meal was measured in 15 controls, 6 patients with coeliac disease, 26 patients with chronic pancreatitis and partial duodenopancreatectomy (Whipple's procedure). Serum levels of IR-GIP, IRG and IRI were significantly reduced in patients with coeliac disease. The serum glucose increase was significantly smaller only during the first hour after the meal. Since small intestinal GIP- and G-cells are situated mainly in the glands of duodenal and jejunal mucosa their absolute number is not significantly reduced in coeliac disease. It is suggested that the release of IR-GIP and duodenal IRG is influenced by the rate of absorption of nutrients. In patients with chronic pancreatitis the IR-GIP release is significantly greater than in controls, the IRG release normal and the IRI response delayed. After Whipple's procedure the IR-GIP response is increased significantly while the IRG secretion is abolished. This demonstrates that the duodenum is not necessary for GIP release and that pancreatic and jejunal gastrin are without clinical significance.

Topics: Adult; Aged; Celiac Disease; Chronic Disease; Duodenum; Eating; Female; Gastrins; Gastrointestinal Hormones; Humans; Insulin; Insulin Secretion; Jejunum; Male; Middle Aged; Pancreatectomy; Pancreatitis

Topics: Bile Acids and Salts; Celiac Disease; Diarrhea; Gastrins; Gastrointestinal Motility; Humans; Intestine, Small; Syndrome; Vagotomy

Twenty-nine patients with chronic pancreatitis had a significantly greater IR-GIP response to a test meal than 15 controls. This increased response was not related to the degree of steatorrhoea or glucose intolerance. It was most marked in a group of patients with moderately impaired IRI release and medium steatorrhoea. From this is concluded that the IR-GIP response to a test meal is determined by at least two factors: 1. feedback control via insulin secretion, 2. assimilation of fat. In chronic pancreatitis endocrine insufficiency may induce an exaggerated GIP response and severe exocrine insufficiency may prevent fat induced GIP release. Gastrin is not involved in the different GIP response in patients with chronic pancreatitis.

Topics: Adult; Celiac Disease; Chronic Disease; Eating; Female; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Humans; Insulin; Male; Pancreatitis

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

One hundred and twelve consecutive patients selected for surgical treatment for duodenal ulcer disease were treated by a graded gastrectomy according to the Moynihan modification of the Billroth II partial gastrectomy. A large partial gastrectomy (R) (2/3-3/4 gastrectomy) was done in patients who after maximal stimulation with histamine showed a high acid output (MAO greater than 30 mEa/hr), and a small resection (r) (1/3-1/2 gastrectomy) in low secretors (MAO less than 30 mEq/hr). The material was prospectively controlled by admission to hospital at 3 months, 1 year and 5 years postoperatively. The preoperative values of MAO found in R and r were 42.8 and 21.5 mEq/hr (p less than 0.001), respectively. The postoperative MAO values at the 3-month control were 4.5 and 3.0 mEq/hr by R and r, respectively, which shows that the grading of resection had been successful. Atrophic gastritis increased in frequency from 4% at the time of operation to 72% at the 1-year control...

Topics: Adolescent; Adult; Aged; Anemia; Biopsy; Body Weight; Celiac Disease; Child; Duodenal Ulcer; Female; Folic Acid Deficiency; Follow-Up Studies; Gastrectomy; Gastric Juice; Gastric Mucosa; Gastrins; Histamine; Humans; Male; Middle Aged; Norway; Postgastrectomy Syndromes; Prospective Studies; Recurrence; Work Capacity Evaluation

Topics: Adult; Celiac Disease; Diarrhea; Esophagitis; Female; Gastrins; Humans; Hyperparathyroidism; Male; Middle Aged; Neoplasm Metastasis; Radiography; Zollinger-Ellison Syndrome