gastrins and Pancreatitis

Gastric acid secretion is a complex phenomenon under nervous and hormonal influence. The stimulation of proton pump (H(+), K(+)-ATPase) in the parietal cell represents the final step of acid secretion and this knowledge has led to the development of a class of drugs, the proton pump inhibitors (PPIs), which are targeted at blocking this enzyme. Chemically, all the available PPIs consist of a benzimidazole ring and a pyridine ring, but vary in the specific side ring substitution. As a class, they are the most potent inhibitors of gastric acid secretion available. Although there are differences among PPIs concerning their pharmacokinetics, pharmacodynamics, influence by food and antacids as well as potential for drug interactions, it is not always evident whether these often subtle differences are clinically relevant. A careful evaluation of the available studies reveals that rabeprazole and esomeprazole achieve more rapid acid inhibition than other PPIs. Also, the effect of rabeprazole is less dependent upon genetic make-up than all other PPIs, giving rise to less inter-subject variability and leading to a more predictable effect. Esomeprazole, by inhibiting its own catabolism, makes all patients slow metabolizers, but could expose them to potential drug interactions. PPIs are the mainstay of medical treatment of gastro-oesophageal reflux disease (GORD), in that they are able to provide 80-85% healing rate of oesophageal lesions, including ulcers, and to reduce the incidence of complications like strictures as well as dysplasia and adenocarcinoma in Barrett's oesophagus (BO). Also relief of symptoms can be achieved in about 80% of cases, even though this benefit is reduced by a factor of approximately 20% in patients with non-erosive reflux disease (NERD). Their effect on Barrett's oesophagus and the extra-oesophageal manifestations of GORD is much less consistent. In general, the tolerability profile of PPIs is good in both short- and long-term clinical trials. This safety profile is similar across the various PPIs used in clinical practice and is extended to children and pregnant women, where they do not present any major teratogenic risk.

Topics: Absorption; Drug Interactions; Gastric Acid; Gastrins; Gastroesophageal Reflux; Heart; Hip Fractures; Humans; Pancreatitis; Pneumonia; Proton Pump Inhibitors; Treatment Failure

The action of acute and chronic administration of ethanol on pancreatic exocrine secretion in humans and several animal species is reviewed. If the data concerning the secretory action of ethanol on the pancreas are to the property assessed, several experimental variables have to be considered. Acute intravenous administration of ethanol inhibits basal and hormonally stimulated pancreatic secretion of bicarbonate and protein in nonalcoholic humans and most species of animals tested. Oral or intraduodenal ethanol causes moderate stimulation of pancreatic bicarbonate and enzyme secretion. Since anticholinergic agents and truncal vagotomy diminish the ethanol-induced inhibition of pancreatic secretion in the intact animal, it is possible that the action of ethanol on the pancreas is at least partly mediated by inhibitory cholinergic mechanisms. The action of ethanol on the pancreas may also be mediated by release of gastrointestinal hormones. Intravenous and oral administration of ethanol releases gastrin in dogs but not in humans. Pancreatic polypeptide is unlikely to be the hormonal mediator of the ethanol-induced inhibition of exocrine pancreatic secretion in humans and dogs, since ethanol does not release pancreatic polypeptide. The main secretory changes induced by chronic alcoholism in humans and dogs are increased basal secretion of pancreatic enzymes and decreased basal bicarbonate output, and these secretory changes may favour the occurrence of protein precipitates which are believed to be the first lesion of chronic pancreatitis in man. A decrease in the concentration of "pancreatic stone protein" in pancreatic juice may favour the development of protein precipitates in chronic alcoholic patients.

Topics: Acute Disease; Alcoholism; Animals; Calcium-Binding Proteins; Cholecystokinin; Chronic Disease; Dogs; Duodenum; Ethanol; Food; Gastric Juice; Gastrins; Gastrointestinal Hormones; Humans; Lithostathine; Nerve Tissue Proteins; Pancreas; Pancreatic Juice; Pancreatic Polypeptide; Pancreatitis; Secretin; Sphincter of Oddi; Stomach

Topics: Diagnosis, Differential; Gastrins; Humans; Pancreatitis; Peptic Ulcer; Secretin

Topics: Acute Disease; Amylases; Antacids; Anti-Ulcer Agents; Calcitonin; Depression, Chemical; Enzyme Inhibitors; Gastric Acid; Gastrins; Hormones; Humans; Pancreas; Pancreatitis; Zollinger-Ellison Syndrome

Topics: Adipose Tissue; Amino Acid Sequence; Animals; Diabetes Mellitus; Gastric Acid; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Diseases; Gastrointestinal Hormones; Glucagon; Glucagon-Like Peptide 1; Glucagon-Like Peptides; Glucose; Humans; Insulin; Pancreatitis; Pepsin A; Peptide Fragments; Peptides; Proinsulin; Radioimmunoassay; Salivation; Splanchnic Circulation

Topics: Animals; Cholecystokinin; Chronic Disease; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Insulin; Insulin Secretion; Pancreatic Hormones; Pancreatic Polypeptide; Pancreatitis

Topics: Achlorhydria; Acromegaly; Adenoma; Adenoma, Islet Cell; Adolescent; Adult; Aged; Calcium; Cushing Syndrome; Diarrhea; Female; Gastric Acid; Gastrins; Glucagon; Humans; Hyperinsulinism; Hyperparathyroidism; Hypoglycemia; Hypokalemia; Male; Middle Aged; Neoplasms, Multiple Primary; Pancreatic Polypeptide; Pancreatitis; Parathyroid Glands; Parathyroid Neoplasms; Pituitary Neoplasms; Syndrome; Thyroid Diseases; Zollinger-Ellison Syndrome

The value of cimetidine in treatment of duodenal ulcer and the Zollinger-Ellison syndrome appears to be well established. The drug has been enthusiastically embraced and widely used by practicing physicians. As with virtually all drugs used in the practice of medicine, cimetidine is not without its adverse effects. In some instances these effects may result from actions of cimetidine on H2-receptors on many widely distributed and diverse cells other than parietal cells, to which its potent acid-inhibiting properties are directed. Other adverse effects of cimetidine may be idiosyncratic, and, therefore, not predictable on a pharmacologic basis. In some instances the mechanisms responsible for cimetidine's adverse effects hav e yet to be defined. An assortment of abnormalities reported in patients receiving cimetidine have been suggested, but not proven, to represent adverse effects of the drug. Considering its extremely wide use, serious toxicity with cimetidine is rare. However, no potent drug, including cimetidine, used in the practice of medicine is without its adverse effects. Recognizing the present and projected extensive and probably long-term use of cimetidine, physicians and surgeons treating patients with cimetidine must maintain continued surveillance in order to detect and clarify potential undesired consequences of cimetidine administration.

Topics: Agranulocytosis; Animals; Bone Marrow; Central Nervous System; Chemical and Drug Induced Liver Injury; Cimetidine; Creatinine; Duodenal Ulcer; Endocrine Glands; Gastric Juice; Gastrins; Guanidines; Humans; Immunity, Cellular; Intrinsic Factor; Liver; Pancreatitis; Receptors, Histamine H2; Risk; Stomach Neoplasms; Transaminases

Topics: Cimetidine; Duodenal Ulcer; Gastric Acid; Gastrins; Guanidines; Humans; Kinetics; Pancreatitis; Time Factors; Zollinger-Ellison Syndrome

Topics: Cholecystokinin; Chronic Disease; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Insulin; Pancreatic Hormones; Pancreatic Polypeptide; Pancreatitis; Secretin

Somatostatin, under physiological conditions, is a regulator of thyroid stimulating hormone, growth hormone, pancreatic islet-cell hormones and gastrin. In pharmacological dosage, gastric acid output, splanchnic blood flow and plasma renin levels, are influenced. A possible therapeutic effect on increased growth hormone secretion, disturbances of carbohydrate metabolism, gastroenteropathies and renal hypertension, is discussed. The clinical application is limited by the short biological half-life of the substance and the unspecific action on several organs.

Topics: Acromegaly; Animals; Diabetes Mellitus; Diabetic Retinopathy; Gastric Juice; Gastrins; Growth Hormone; Humans; Hypertension; Islets of Langerhans; Pancreatitis; Renin; Somatostatin; Thyrotropin; Zollinger-Ellison Syndrome

Topics: Animals; Dogs; Gastric Juice; Gastric Mucosa; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Hyperglycemia; Islets of Langerhans; Pancreas; Pancreatitis; Peptic Ulcer; Secretin

Topics: Acute Disease; Alcoholism; Animals; Autoradiography; Bicarbonates; Chronic Disease; Dogs; Enzyme Inhibitors; Ethanol; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Gastrointestinal Hormones; Humans; Pancreas; Pancreatic Juice; Pancreatitis; Proteins; Rabbits; Rats; Secretory Rate; Sphincter of Oddi

Topics: Acetylcholine; Bicarbonates; Calcium; Cyclic AMP; Gastric Juice; Gastric Mucosa; Gastrins; Histamine; Humans; Hypercalcemia; Hyperparathyroidism; Pancreatitis; Pepsin A; Peptic Ulcer; Stimulation, Chemical; Vagus Nerve

Topics: Administration, Oral; Animals; Cholecystokinin; Dogs; Enzymes; Gastrins; Glucagon; Glucose; Hormones; Humans; Injections, Intravenous; Insulin; Islets of Langerhans; Methionine; Pancreas; Pancreatic Juice; Pancreatitis; Secretin; Sulfur Isotopes

Topics: Acute Disease; Adenoma, Islet Cell; Cholecystokinin; Chronic Disease; Gastrins; Humans; Methods; Pancreas; Pancreas Transplantation; Pancreatic Diseases; Pancreatic Neoplasms; Pancreatitis; Radiography; Secretin; Transplantation, Homologous; Zollinger-Ellison Syndrome

Topics: Anemia, Pernicious; Antibodies; Aspirin; Feces; Galactosidases; gamma-Globulins; Gastric Juice; Gastrins; Gastrointestinal Diseases; Glutaminase; Humans; Intestinal Absorption; Intestinal Diseases; Intestines; Metabolism, Inborn Errors; Pancreatic Diseases; Pancreatitis; Radiography; Radionuclide Imaging; Triglycerides

After pylorus-preserving Whipple (PPW), delayed gastric emptying (DGE) is reported in up to 50% of these patients. We analyzed gastric emptying and hormonal adaptation of cholecystokinin (CCK), pancreatic polypeptide (PP), and gastrin following two surgical procedures for chronic pancreatitis (CP): the PPW and the duodenum-preserving pancreatic head resection (DPPHR).. Ten patients underwent DPPHR and 10 underwent PPW for CP. Preoperatively and 10 days and 6 months postoperatively, gastric emptying (paracetamol absorption test) and CCK, gastrin, and PP were measured using a test meal stimulation.. The area under the serum paracetamol time curve for 0 to 120 minutes (AUC) showed no preoperative difference. Ten days postoperatively, the AUC was significantly reduced (P <0.05) after PPW but not after DPPHR. Six months postoperatively, AUC was comparable with the preoperative findings in DPPHR and PPW. The integrated 180-minute PP release was significantly reduced 10 days and 6 months postoperatively in both groups. The integrated 180-minute CCK release was decreased 10 days after PPW, but failed to be significant (P = 0.053). Gastrin levels were postoperatively unchanged.. Following DPPHR we found no delay in gastric emptying. In contrast, DGE occurs early after PPW. Our data may help explain the slower recovery in PPW patients with regard to weight gain and relief from pain, which may be due to the functional alteration of gastric emptying and motility after this type of surgery.

Topics: Acetaminophen; Adult; Cholecystokinin; Chronic Disease; Female; Gastric Emptying; Gastrins; Humans; Male; Middle Aged; Pancreatic Polypeptide; Pancreaticoduodenectomy; Pancreatitis; Postoperative Complications

Topics: Adult; Aged; Arginine; Blood Glucose; Clinical Trials as Topic; Female; Gastric Mucosa; Gastrins; Glucose Tolerance Test; Humans; Insulin; Insulin Secretion; Male; Middle Aged; Pancreatitis; Pylorus

Glucagon is believed to be a pancreas-specific hormone, and hyperglucagonemia has been shown to contribute significantly to the hyperglycemic state of patients with diabetes. This hyperglucagonemia has been thought to arise from α-cell insensitivity to suppressive effects of glucose and insulin combined with reduced insulin secretion. We hypothesized that postabsorptive hyperglucagonemia represents a gut-dependent phenomenon and subjected 10 totally pancreatectomized patients and 10 healthy control subjects to a 75-g oral glucose tolerance test and a corresponding isoglycemic intravenous glucose infusion. We applied novel analytical methods of plasma glucagon (sandwich ELISA and mass spectrometry-based proteomics) and show that 29-amino acid glucagon circulates in patients without a pancreas and that glucose stimulation of the gastrointestinal tract elicits significant hyperglucagonemia in these patients. These findings emphasize the existence of extrapancreatic glucagon (perhaps originating from the gut) in man and suggest that it may play a role in diabetes secondary to total pancreatectomy.

Topics: Aged; Blood Glucose; Case-Control Studies; Cholecystokinin; Chromatography, Liquid; Enzyme-Linked Immunosorbent Assay; Female; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Tract; Glucagon; Glucagon-Like Peptide 1; Glucagon-Secreting Cells; Glucose; Glucose Tolerance Test; Humans; Male; Middle Aged; Pancreatectomy; Pancreatic Neoplasms; Pancreatitis; Peptide Fragments; Proteomics; Radioimmunoassay; Tandem Mass Spectrometry

To investigate whether chronic H pylori infection has the potential to induce pancreatitis in the Mongolian gerbil model, and whether it is dependent on an intact type IV secretion system.. Mongolian gerbils were infected with wild type (WT) H pylori type I strain B128 or its isogenic mutant B128 deltacagY (defective type IV secretion). After seven months of infection, H pylori was reisolated from antrum and corpus and H pylori DNA was analyzed by semi-nested polymerase chain reaction (PCR). Inflammation and histological changes were documented in the gastric antrum, corpus, and pancreas by immunohistochemistry. Cytokine mRNA, gastric pH, plasma gastrin, amylase, lipase, and glucose levels were determined.. The H pylori infection rate was 95%. Eight infected animals, but none of the uninfected group, developed transmural inflammation and chronic pancreatitis. Extensive interstitial fibrosis and inflammation of the pancreatic lobe adjacent to the antrum was confirmed by trichrome stain, and immuno-histochemically. Pro-inflammatory cytokine mRNA was significantly increased in the antral mucosa of all infected gerbils. In the corpus, only cytokine levels of WT-infected animals and those developing transmural inflammation and pancreatitis were significantly increased. Levels of lipase, but not glucose or amylase levels, were significantly reduced in the pancreatitis group. H pylori DNA was detected in infected antral and corpus tissue, but not in the pancreas.. H pylori infection is able to induce chronic pancreatitis in Mongolian gerbils independently of the type IV secretion system, probably by an indirect mechanism associated with a penetrating ulcer.

Topics: Amylases; Animals; Cytokines; DNA, Bacterial; Female; Gastrins; Gerbillinae; Glucose; Helicobacter Infections; Helicobacter pylori; Hydrogen-Ion Concentration; Lipase; Pancreatitis; Radioimmunoassay; RNA, Messenger

We have investigated the involvement of cholecystokinin (CCK) receptor subtypes in haemodynamic changes in the pancreas of anaesthetized rats during submaximal and supramaximal stimulation with the CCK analogue, caerulein.. For submaximal stimulation, caerulein (0.4 nmol/kg/h) was infused intravenously, while acute pancreatitis was induced by intraperitoneal injections of high doses of caerulein (3 x 25 nmol/kg). Pancreatic blood flow was measured by hydrogen clearance.. Low caerulein doses increased pancreatic blood flow by 26 +/- 8% and vascular conductance by 24 +/- 4%. This effect was mimicked by the CCK2 agonist gastrin-17. All effects were abolished by a CCK2 antagonist while a CCK1 antagonist remained inactive. Conversely, amylase output by caerulein was abolished by CCK1 receptor blockade, but not by inhibition of CCK2 receptors. During caerulein-induced pancreatitis, vascular conductance increased by 109 +/- 26% and remained elevated throughout the experiment; vascular flow initially increased by 62 +/- 27% and then returned to baseline. The vascular effects were prevented by a CCK2 receptor antagonist, while the induction of pancreatitis was due to CCK1 receptor stimulation.. Caerulein increases pancreatic vascular flow via activation of CCK2 receptors. This effect occurs both at submaximal and at supramaximal levels of exocrine stimulation.

Topics: Animals; Bradykinin B2 Receptor Antagonists; Ceruletide; Female; Gastrins; Indoles; Pancreas, Exocrine; Pancreatitis; Rats; Rats, Sprague-Dawley; Receptor, Cholecystokinin A; Receptor, Cholecystokinin B; Receptors, Cholecystokinin; Regional Blood Flow; Stimulation, Chemical

The duodenum is abnormally acidic in cystic fibrosis (CF) due to decreased bicarbonate ion secretion that is dependent on the CF gene product CFTR. In the CFTR null mouse, the acidic duodenum results in increased signaling from the intestine to the exocrine pancreas in an attempt to stimulate pancreatic bicarbonate ion secretion. Excess stimulation is proposed to add to the stress/inflammation of the pancreas in CF. DNA microarray analysis of the CF mouse revealed altered pancreatic gene expression characteristic of stress/inflammation. When the duodenal pH was corrected genetically (crossing CFTR null with gastrin null mice) or pharmacologically (use of the proton pump inhibitor omeprazole), expression levels of genes measured by quantitative RT-PCR were significantly normalized. It is concluded that the acidic duodenal pH in CF contributes to the stress on the exocrine pancreas and that normalizing duodenal pH reduces this stress.

Topics: Acids; Amylases; Animals; Chimera; Cystic Fibrosis; Cystic Fibrosis Transmembrane Conductance Regulator; Duodenum; Enzyme Inhibitors; Gastrins; Gene Expression; Hydrogen-Ion Concentration; Mice; Mice, Inbred C57BL; Mice, Knockout; Oligonucleotide Array Sequence Analysis; Omeprazole; Pancreas; Pancreatitis; Reverse Transcriptase Polymerase Chain Reaction

To evaluate the effect of early intrajejunal nutrition (EIN) on the natural course, entero-hormone secretion and its efficacy on dogs with acute pancreatitis.. An acute pancreatitis model was induced by injecting 1 ml/kg of combined solution (2.5% sodium taurocholate and 8,000-10,000 BAEE units trypsin/ml) into the pancreas via pancreatic duct. Fifteen dogs were divided into parenteral nutrition (PN) group and EIN group. Two groups were isonitrogenous and isocaloric. EIN was used at postoperative 24 h. Serum glucose, calcium, amylase and lysosomal enzymes were determined before and 1, 4, 7 d after acute pancreatitis was induced. All the dogs were injected 50 uCi 125I-BSA 4 h before sacrificed on the 7th day. The 125I -BSA index of the pancreas/muscle, pancreas/blood, and pancreas pathology score (PPS) were determined. The peripheral plasma cholecystokinin (CCK), secretin (SEC) and gastrin were measured by ELISA and RIA, and was quantitative analysis of pancreatic juice and amylase, pancreatolipase and HCO3-, Cl-, Na+ and K+ performed by an autochemical analyzer at 30, 60, 120 and 180 min after beginning PN or EIN on the first day.. There was no difference between two groups in the contents of serum calcium, amylase and lysosomal enzymes, 125I-BSA index of pancreas/muscle and pancreas/blood and PPS. The contents of CCK and gastrin in EIN were higher than those in PN group at 60 and 120 min (P<0.05). The content of SEC post-infusion of nutrition solution was higher than that of pre-infusion of nutrition solution in both groups, and only at 60 min SEC in EIN group was higher than that in PN group. The content of gastrin in EIN was higher than that in PN group at 120 and 180 min (P<0.05). The changes of pancreatic juice, amylase, pancreatolipase and HCO3-, Cl-, Na+ and K+ between two groups did not reach significantly statistical difference (P>0.05).. EIN does not stimulate entero-hormone and pancreatic juice secretion, and enzyme-protein synthesis and release. EIN has no effect on the natural course of acute pancreatitis.

Topics: Acute Disease; Amylases; Animals; Blood Glucose; Calcium; Cholecystokinin; Dogs; Gastrins; Iodine Radioisotopes; Jejunum; Lysosomes; Pancreatic Juice; Pancreatitis; Parenteral Nutrition; Secretin; Serum Albumin, Bovine

The histopathology of Fibrocalculous Pancreatic Diabetes (FCPD) has been extensively studied, but there are no reports on alteration in patterns of hormone secreting cells using immunohistochemistry in islets of FCPD patients. In this study, we report on the histopathology and immunohistochemistry of islets of FCPD patients and its possible correlation with the clinical picture. Pancreatic biopsies were carried out in six patients with FCPD at the time of surgery for abdominal pain. Routine histopathology and immunohistochemistry studies were carried out with six primary antibodies namely insulin, glucagon, pancreatic polypeptide (PP), somatostatin, vasoactive intestinal peptide and gastrin. Histopathology of the pancreas showed a spectrum of changes ranging from moderate to severe atrophy, fibrosis of the parenchyma and degeneration of the ducts. Nesidioblastosis was present in three patients. Immunohistochemical studies showed a decrease in the number of islets but some patients showed evidence of hyperplasia. There was an overall decrease in the percent of insulin cells and the positivity in the islets correlated with plasma C-peptide levels and the duration of diabetes. There was no consistent relationship with glucagon with some patients showing increased and other decreased positivity. There was a marked decrease in PP and somatostatin positivity, the significance of which is not clear. The reduction, but partial preservation of insulin positivity is consistent with the ketosis resistance shown by patients with Fibrocalculous Pancreatic Diabetes.

Topics: Adolescent; Adult; Atrophy; Biopsy; Blood Glucose; Chronic Disease; Diabetes Mellitus; Female; Gastrins; Glucagon; Humans; Hyperplasia; Immunohistochemistry; Insulin; Islets of Langerhans; Male; Middle Aged; Pancreas; Pancreatic Ducts; Pancreatic Polypeptide; Pancreatitis; Vasoactive Intestinal Peptide

Continuous enteral feeding, the old-new therapeutic modality in the treatment of patients with acute pancreatitis and those with complications is considered to bypass the cephalic, the gastric, and (at least in part) the intestinal phase of pancreatic secretion. The aim of this study was to test the GI hormonal changes and gallbladder motility during CJF in patients with pancreatic pseudocysts following acute pancreatitis, with or without octreotide pretreatment.. In 15 patients with pancreatic pseudocysts, an 8-French (8F) nasojejunal catheter was positioned into the jejunum distal to the ligament of Treitz during duodenoscopy. On test d 1, blood samples were taken for CCK, gastrin, insulin-like immunoreactivity (IRI), glucagon, and glucose measurements prior to and at 20, 40, 60, and 120 min following jejunal saline infusion at a rate of 2 mL/min. The gallbladder volumes were determined simultaneously by ultrasonography. On test d 2, CJF (175 kcal/h) was started by the same route and at the same infusion rate. Analogous measurements were performed as indicated above. On test d 3, 100 microg of octreotide was administered subcutaneously and the previous procedure was repeated. The plasma level of CCK and glucagon and the serum levels of IRI and gastrin were determined by bioassay and radioimmunoassay (RIA), respectively.. Significant changes in hormone levels were not observed during jejunal saline perfusion. However, the levels of CCK (5.7+/-0.9 pmol), gastrin (10.6+/-1.3 pmol/L), IRI (27.2+/-5.8 microIU/mL), glucagon (322.8+/-32.4 pg/mL), and glucose (5.8+/-1.0 mmol/L) were significantly increased at 20 min during CJF vs the saline controls (2.0+/-0.3 pmol, 6.8+/-1.1 pmol/L, 7.8+/-0.4 microIU/mL, 172.8+/-33.4 pg/mL, and 4.5+/-0.5 mmol/L, respectively) and remained elevated at 40, 60, and 120 min. Octreotide pretreatment eliminated the increases in CCK, gastrin, IRI, and glucagon levels observed during CJF alone. The significant decrease in gallbladder volume during CJF was also prevented by octreotide pretreatment.. Continuous jejunal feeding (CJF) elicited significant increases in gastrointestinal (GI) regulatory hormone (cholecystokinin [CCK], gastrin, IRI, and glucagon) levels and evoked a consecutive gallbladder contraction. These biological responses are eliminated by octreotide pretreatment. Further clinical studies are needed to assess the eventual therapeutic effect of octreotide during CJF in patients with pancreatic pseudocyst.

Topics: Adult; Aged; Cholecystokinin; Enteral Nutrition; Female; Gallbladder; Gastrins; Humans; Jejunum; Male; Middle Aged; Muscle Contraction; Octreotide; Pancreatic Pseudocyst; Pancreatitis

Patients with chronic pancreatitis and exocrine insufficiency have lower intraduodenal pH compared to controls. It has been assumed that abnormal low intraduodenal pH in these patients not only results from impaired pancreatic bicarbonate secretion but also from an increased gastric acid load to the duodenum.. We have tested this hypothesis by combined intragastric and intraduodenal 24 h pH monitoring in nine chronic pancreatitis patients with exocrine pancreatic insufficiency and nine healthy control subjects during standardized test conditions. Postprandial gastrin and cholecystokinin release were also determined.. Median 24-h intraduodenal pH (5.90 vs. 6.00) and intragastric pH (1.60 vs. 1.70) were not significantly different between patients and controls. However, in the 2-h postprandial periods intraduodenal pH was below five for a significantly higher percentage of time in chronic pancreatitis patients compared to controls (lunch: 14.5% vs. 0.17%, P=0.011; dinner: 24.1% vs. 5.75%, P=0.05). The post-dinner intragastric pH was below three for a significantly higher percentage of time in chronic pancreatitis patients vs. controls (72.2 vs. 48.9%, P=0.04). Postprandial gastrin release was not significantly different between the two groups. Postprandial secretion of cholecystokinin (CCK), as enterogastrone, was significantly (P < 0.01) reduced in chronic pancreatitis patients (78 +/- 13 pmol/L, 120 min) compared to controls (155 +/- 14 pmol/L, 120 min).. Median intraduodenal and intragastric pH are not significantly decreased in patients with chronic pancreatitis and exocrine insufficiency but the postprandial time with an acidic pH in the duodenum (pH < 5) and in the stomach (pH < 3) is significantly (P

Topics: Adult; Case-Control Studies; Cholecystokinin; Chronic Disease; Duodenum; Exocrine Pancreatic Insufficiency; Female; Gastric Mucosa; Gastrins; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Pancreatitis; Postprandial Period; Time Factors

Topics: Adult; Female; Gastrins; Gastritis; Humans; Insulinoma; Pancreatic Neoplasms; Pancreatitis; Syndrome

In patients suffering from chronic pancreatitis with concomitant atrophic antral gastritis, gastrinemia is less whereas the response of pancreatic enzymic secretion to pentagastrin is more potent than in patients suffering from chronic pancreatitis without atrophic alterations in the gastroduodenal mucosa. The pancreas-stimulating effect of pentagastrin administered in a dose of 6 micrograms/kg is approximately equal to the action of 0.5 U/kg pancreozymine and noticeably yields to the effect of 1.5 U/kg pancreozymine (according to the criteria for output of intraduodenally secreted lipase and trypsin). The same diagnostic dose of pentagastrin used commonly for gastric secretion studies not only stimulates pancreatic enzyme secretion but also enhances the activity of beta-cells of Langerhans' islets of the pancreas in accordance with insulinemia and blood C-peptide determined by RIA.

Topics: C-Peptide; Cholecystokinin; Chronic Disease; Dose-Response Relationship, Drug; Gastrins; Gastritis, Atrophic; Humans; Insulin; Islets of Langerhans; Pancreas; Pancreatitis; Pentagastrin; Recurrence

We have investigated the relationship between cholecystokinin levels and abdominal pain in patients with chronic pancreatitis. The baseline and postprandial cholecystokinin levels were measured in 15 patients with chronic pancreatitis (8 with and 7 without abdominal pain) and in a reference group of 8 healthy subjects. The baseline, 30 and 60 min postprandial plasma cholecystokinin levels were significantly (p less than 0.05) higher in the patients with pain as compared with the other two groups. No correlation was observed between increased cholecystokinin levels and impairment of the exocrine pancreatic function as assessed by the NBT-PABA test. The increased cholecystokinin levels might be an important factor in the genesis of pain in chronic pancreatitis.

Topics: Abdominal Pain; Adult; Cholecystokinin; Chronic Disease; Female; Food; Gastrins; Humans; Male; Pancreatitis; Radioimmunoassay

We investigated the time courses of the plasma ethanol, acetaldehyde, gastrin and cholecystokinin (CCK) levels after the ingestion of ethanol (1g/kg, 21.5%, whisky) in healthy male adult volunteers. The ethanol level reached a peak at 15 to 45 minutes after the ingestion and then decreased almost linearly. The acetaldehyde level of the group who became flushed after drinking (the F group) peaked earlier than that of the other group whose faces became only slightly flushed (the N group). The gastrin level increased significantly and remained elevated for about 3 hours. In three of the nine subjects, the CCK level increased 75 minutes after drinking. As a result, the absorption of the ingested ethanol is more rapid than 15 minutes, followed by a quick catabolism of the absorbed ethanol to acetaldehyde, but the catabolic action of acetaldehyde in the F group is later than that in the N group. The plasma gastrin level is certified to increase after the ingestion of ethanol and this is not mediated by acetaldehyde because the intra-venous infusion of acetaldehyde was not increased the plasma gastrin level in dogs. CCK which stimulate the pancreatic enzymes may be considered to have a possibility relating to the development of alcoholic acute pancreatitis but the ingestion of ethanol showed no increase of the plasma CCK level. But we cannot deny the possibility of the individual differences in the hormonal reaction in these experiments.

Topics: Acute Disease; Adult; Alcohol Drinking; Animals; Cholecystokinin; Dogs; Ethanol; Female; Gastrins; Humans; Pancreatitis

A disturbed intraduodenal milieu and pancreatic scarring in advanced chronic pancreatitis (CP) may lead to changes of gut and pancreatic hormones. In the present study, the gastroduodenal mucosal content of several regulatory peptides was determined in 8 patients with severe calcific CP and 8 healthy volunteers. In addition, hormone release into the bloodstream was estimated after intraduodenal acid/glucose stimulation in the control subjects and 8 CP patients each with or without secondary diabetes mellitus (DM), and in 8 patients with juvenile DM, so that disturbed gut hormone release could be attributed either to CP or DM. While VIP release into the circulation was similar in all participants, mucosal levels of VIP and substance P were significantly elevated in the duodenal bulb and descending duodenum of CP patients. The somatostatin content of gastroduodenal mucosa in CP was at least as high as in normals. Gastrin was significantly more abundant only in the duodenal bulb of CP patients, while plasma gastrin was normal. Duodenal CCK concentrations tended to be elevated in the duodenal bulb, but not significantly. The release of secretin seemed to be higher in type-1 diabetics than in CP patients. The mucosal pattern of GIP was nearly identical in CP patients and controls. Compatible with this finding, the GIP release did not show any peculiarities in CP with or without DM or in DM. Basal and stimulated plasma levels of motilin were abnormally high in CP. Pancreatic polypeptide plasma levels were normal in DM, but significantly reduced in CP, especially in CP with DM. Fasting PP and stimulated pancreatic enzyme outputs were linearly related.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Chronic Disease; Diabetes Mellitus; Female; Gastric Inhibitory Polypeptide; Gastric Mucosa; Gastrins; Gastrointestinal Hormones; Glucagon; Glucagon-Like Peptides; Humans; Intestinal Mucosa; Male; Middle Aged; Motilin; Neurotensin; Pancreatic Polypeptide; Pancreatitis; Secretin; Somatostatin; Substance P; Vasoactive Intestinal Peptide

Exocrine and endocrine stomach was studied serially in 13 patients who had gastrobulbar preserving pancreatoduodenectomy (GPPD). In most of them, acid output temporarily increased just after operation but recovered. Gastrin response level decreased transiently but returned to the preoperative level. A negative correlation was observed between the acid and gastrin levels, which suggests that the negative feedback mechanism between parietal cells and G cells was maintained. Acid and gastrin levels in GPPD were higher than those in conventional pancreatoduodenectomy (cPD) but not remarkably different from those of the controls. No peptic ulcer was detected after the operation. These findings indicated that GPPD poses little problem concerning offensive factors. Postoperative ulcer formation is considered to be prevented by the authors' procedure, which is devised to best preserve defensive mechanisms so that duodenectomy is minimized and the gastrointestinal continuity is reconstructed physiologically from mouth to anus by end-to-end duodenoduodenestomy, end-to-side pancreatojejunostomy, and end-to-side choledochojejunostomy.

Topics: Adult; Aged; Chronic Disease; Duodenal Neoplasms; Duodenum; Female; Gastric Acid; Gastric Mucosa; Gastrins; Humans; Male; Middle Aged; Pancreatectomy; Pancreatitis; Postoperative Period

Pancreatic specimens of nine patients suffering from multiple endocrine neoplasia type I (MEN I) were investigated with regard to tumor frequency and growth pattern, islet hyperplasia and endocrine cell neoformation, immunocytochemical hormone profile of the tumors, and correlation to clinical symptoms. The majority of the 201 tumors were microadenomas (diameter less than 0.5 cm), which frequently displayed a trabecular growth pattern. Microadenomatosis was considered the most distinct feature of the MEN I pancreas. Additional larger tumors (diameter greater than 1.0 cm) were found in five patients. Whereas islet hyperplasia appears not to belong to the spectrum of the pancreatic lesions in MEN I, nesidioblastosis was occasionally observed. Immunocytochemical screening revealed that among hormone-positive tumors (approximately 80% of the tumors), pancreatic polypeptide tumors (PPomas), glucagonomas, and insulinomas were the most frequent. The high incidence of PPomas in these pancreases probably accounts for the elevated serum PP levels found in many MEN I patients. Somatostatinomas, gastrinomas, vasoactive intestinal polypeptide tumors (VIPomas), and neurotensinomas were rare. Clinically overt hyperinsulinism, observed in two patients and associated with a large insulinoma, was cured by tumor resection. Eight of nine patients presented a Zollinger-Ellison's syndrome (ZES), but only in two patients were gastrin-producing tumors found. The source of gastrin in MEN I patients with a ZES, in whom no gastrinoma could be detected, remains unclear.

Topics: Adult; Aged; Female; Gastrins; Glucagon; Histocytochemistry; Hormones; Humans; Immunoenzyme Techniques; Insulin; Male; Middle Aged; Multiple Endocrine Neoplasia; Neurotensin; Pancreatectomy; Pancreatic Neoplasms; Pancreatic Polypeptide; Pancreatitis; Somatostatin; Staining and Labeling

Acid and gastrin production after pyloric-preserving pancreaticoduodenectomy was evaluated in six patients. Five patients had low-normal basal and stimulated acid output; the sixth patient was achlorhydric. Fasting gastrin levels were less than 90 to 105 pg/mL (normal range) in five patients, three of whom had stimulated gastrin levels that remained below this range. Two patients had stimulated gastrin levels of 510 pg/mL and 205 pg/mL, respectively, within 15 minutes of eating; however, both levels returned to normal by 120 minutes' time. The sixth patient had mildly elevated fasting (105 pg/mL) and stimulated gastrin levels (160 to 200 pg/mL) throughout the test period. The results suggest that pyloric-preserving pancreaticoduodenectomy does not lead to either gastric hyperacidity or persistent hypergastrinemia.

Topics: Achlorhydria; Duodenum; Female; Gastric Acidity Determination; Gastrins; Humans; Male; Middle Aged; Pancreatectomy; Pancreatic Neoplasms; Pancreatitis; Pylorus; Radioimmunoassay

A patient with a calcifying chronic pancreatitis was found to have a neuroendocrine islet cell tumour (a previously unreported association). The tumour secreted both gastrin and ACTH leading to clinical manifestations of both the Zollinger-Ellison syndrome and Cushing's syndrome.

Topics: Adenoma, Islet Cell; Adrenocorticotropic Hormone; Aged; Calcinosis; Chronic Disease; Gastrins; Humans; Male; Pancreatic Neoplasms; Pancreatitis; Zollinger-Ellison Syndrome

It has been claimed that plasma cholecystokinin (CCK) concentrations are raised in patients with pancreatic insufficiency. We have measured plasma CCK concentrations in 32 patients with pancreatic insufficiency (22 alcoholic pancreatitis and 10 cystic fibrosis) and in 30 normal subjects by radioimmunoassays using antibodies with different specificities. Antibody 1703 binds to COOH-terminal forms of CCK containing at least 14 amino acid residues and does not cross-react with gastrins. Antibody T204 binds to all CCK-peptides containing the sulfated tyrosyl region and shows low cross-reactivity with sulfated gastrins but no binding to nonsulfated gastrins. Antibody 5135 binds to all COOH-terminal CCK-peptides and shows full cross-reactivity with gastrins. In patients with pancreatic insufficiency, plasma CCK concentrations (1.2 +/- 0.1 pmol/liter, antibody 1703; 2.0 +/- 0.2 pmol/liter, antibody T204; 12.5 +/- 1.4 pmol/liter, antibody 5135) were not significantly different from those in normal subjects (1.1 +/- 0.1 pmol/liter, antibody 1703; 2.2 +/- 0.3 pmol/liter, antibody T204; 10.5 +/- 0.9 pmol/liter, antibody 5135). Furthermore, plasma CCK concentrations in patients with pancreatic insufficiency due to alcoholic pancreatitis (1.2 +/- 0.1 pmol/liter, antibody 1703; 1.9 +/- 0.2 pmol/liter, antibody T204; 14.0 +/- 1.9 pmol/liter, antibody 5135) were not significantly different from those in patients with cystic fibrosis (1.2 +/- 0.2 pmol/liter, antibody 1703; 2.4 +/- 0.4 pmol/liter, antibody T204, 9.1 +/- 1.0 pmol/liter, antibody 5135). Cross-reactivity with gastrin accounted for almost all CCK-like-immunoreactivity measured with antibody 5135.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Alcoholism; Antibodies; Antibody Specificity; Binding Sites, Antibody; Cholecystokinin; Cross Reactions; Cystic Fibrosis; Diabetes Mellitus; Exocrine Pancreatic Insufficiency; Female; Gastrins; Humans; Male; Middle Aged; Pancreatitis; Radioimmunoassay

Topics: Adult; Chronic Disease; Female; Gastrins; Humans; Male; Middle Aged; Pancreatitis

Topics: Duodenal Ulcer; Gastrins; Humans; Pancreatic Function Tests; Pancreatitis; Peptic Ulcer Hemorrhage; Secretin; Stomach Ulcer

Topics: Acute Disease; Amylases; Animals; Cholangiopancreatography, Endoscopic Retrograde; Chronic Disease; Gastrins; Pancreas; Pancreatitis; Somatostatin; Swine

Topics: Acute Disease; Adult; Aged; Female; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Insulin; Male; Middle Aged; Pancreatic Polypeptide; Pancreatitis; Vasoactive Intestinal Peptide

Controversial data have been reported on gastric acid secretion in patients with chronic pancreatitis. Moreover, studies on gastroduodenal morphological changes in patients with this disease and with other alcohol-related conditions have given different results. Basal and penta-gastrin-stimulated gastric secretion, histological changes of gastric and duodenal mucosa, and basal and meal-stimulated gastrin were measured in 21 patients with chronic alcoholic pancreatitis and in the following pair-matched groups: 21 chronic alcoholics and 21 control subjects (nonulcer dyspepsia), and in 19 patients with proven liver cirrhosis of alcoholic origin. No patient suffered from peptic ulcers. Moreover, gastric secretion was also measured in 51 patients with proven duodenal ulcers and in 34 healthy subjects. Basal acid output in patients with chronic pancreatitis was significantly higher (p less than 0.05) than in the other groups, except for the patients with duodenal ulcers. Peak acid output values in patient with chronic pancreatitis were similar to those measured in patients with duodenal ulcer, and they were higher than in the healthy subject group and in patients with liver cirrhosis, but statistical significance was not attained for patients with nonulcer dyspepsia. An increased frequency of duodenitis was found in patients with chronic pancreatitis, whereas an increased frequency of gastric metaplasia in the duodenal bulb was observed in all the patients with alcohol-related conditions considered. No relevant differences among the considered groups were found relating to gastric histological changes. Basal and meal-stimulated gastrin were similar in all the studied groups. This study suggests that in patients with chronic pancreatitis there is increased gastric secretion and probably an increased capacity for secretion of acid. Moreover, in patients with chronic pancreatitis, duodenitis seems to be frequent, but it probably is not directly related to chronic alcohol consumption.

Topics: Adult; Alcoholism; Chronic Disease; Duodenum; Female; Gastric Juice; Gastrins; Humans; Male; Middle Aged; Pancreatitis; Stomach

Topics: Acute Disease; Animals; Dogs; Fat Emulsions, Intravenous; Female; Gastrins; Male; Pancreatitis; Parenteral Nutrition; Parenteral Nutrition, Total; Trypsin

In order to further investigate hormonal changes and possible metabolic consequences in acute pancreatitis, 10 cases with a mild form of the disease was studied. The influence of tissue injury per se on the hormones in question was assessed from comparison with the hormone levels in the course of myocardial infarction (MI) in 9 cases. Insulin and glucose showed no consistent changes. Glucagon was suppressed on admission, 22 +/- 10 pg . ml-1, compared with the ultimate concentration, 40 +/- 20 pg . ml-1 (p less than 0.05), and with the initial value in MI, 74 +/- 32 pg . ml-1 (p less than 0.01). Serum calcitonin (CT) was strongly elevated initially, 348 +/- 313 pg . ml-1, compared with the ultimate level, 24 +/- 7 pg . ml-1 (p less than 0.001), and with the normal initial level in MI, 43 +/- 44 pg . ml-1 (p less than 0.01). Serum CT elevations were time-related to a slight reduction in corrected serum Ca, which might reflect a biological expression of this substance. In pancreatitis, parathyroid hormone (PTH) remained normal and unchanged throughout the study, whereas patients with MI had an increased level of this hormone on admission, 0.19 +/- 0.08 microgramEq . 1(-1), compared with the ultimate concentration, 0.09 +/- 0.03 microgram/q . 1(-1) (p less than 0.02) and with the initial concentration in pancreatitis, 0.11 +/- 0.06 microgramEq . 1(-1) (p less than 0.05). Supranormal PTH levels were found in more than half of the infarction patients on days 0 and 1.

Topics: Acute Disease; Adult; Aged; Calcitonin; Calcium; Female; Gastrins; Glucagon; Hormones; Humans; Insulin; Male; Middle Aged; Myocardial Infarction; Pancreatitis; Parathyroid Hormone

Of 114 patients with chronic pancreatitis, 19 (16.7%) has gastric or duodenal ulcers. Patients with moderate pancreatic exocrine dysfunction tended to show high acid output and low serum gastrin levels, while those with severe dysfunction had slightly lower acid output and higher serum gastrin levels. The higher the degree of pancreatic fibrosis, the higher tended to be the acid output and serum gastrin levels. Not all patients with ulcers developed hypergastrinemia. The mechanism of acid hypersecretion and ulcer formation in patients with chronic pancreatitis cannot be explained solely by pancreatic deterioration, fibrosis or gastrin release; a decrease in the production and release of gastric inhibitory hormone should be taken into consideration.

Topics: Chronic Disease; Duodenal Ulcer; Female; Gastric Acid; Gastrins; Humans; Male; Middle Aged; Pancreas; Pancreatitis; Stomach Ulcer

To determine the frequency of gastrointestinal symptoms in primary hyperparathyroidism, we retrospectively analyzed 100 consecutive patients seen at Emory University Hospital from Jan 1, 1977 through March 1, 1979. At the time of diagnosis, 28 patients complained of nausea, 19 of vomiting, 29 of abdominal pain, and 33 of constipation. One patient presented with acute pancreatitis and 14 had ulcer disease (two gastric and 12 duodenal ulcers). Hypercalcemia increases gastric acid secretion and may account for associated ulcer disease and the ulcer-like pain in primary hyperparathyroidism. The mechanisms causing the other gastrointestinal symptoms in hypercalcemia remain to be elucidated. These symptoms abate on correction of hyperparathyroidism.

Topics: Constipation; Female; Gastrins; Gastrointestinal Diseases; Humans; Hypercalcemia; Hyperparathyroidism; Male; Pancreatitis; Peptic Ulcer

Fasting serum gastrin and gastrin response to a protein meal were measured in a group of patients with chronic pancreatitis and in controls. No significant differences were found between the two groups of subjects. In patients with chronic pancreatitis no relation was found between gastrin release and the severity of pancreatic exocrine insufficiency.

Topics: Adult; Alcoholism; Chronic Disease; Fasting; Female; Food; Gastrins; Humans; Male; Middle Aged; Pancreatitis

Plasma gastrin levels were measured by radioimmunoassay before and after a test meal associated with 40 ml ethanol in 21 patients presenting with chronic calcifying pancreatitis, in 10 apparently normal subjects drinking since at least 5 years 100 g alcohol a day, in 14 subjects presenting hepatic alcoholic cirrhosis and in 18 apparently normal non alcoholic controls. Post-stimulation gastrin concentration were higher in chronic pancreatitis patients or in normal alcoholics (peak post-stimulation value: 74 +/- 41 and 74 +/- 43 pg/ml respectively) than in cirrhotics or non alcoholic controls (45 +/- 26 and 41 +/- 15 pg/ml respectively) (m +/- SD).

Topics: Adult; Alcoholism; Chronic Disease; Ethanol; Fasting; Food; Gastrins; Humans; Liver Cirrhosis, Alcoholic; Male; Middle Aged; Pancreatitis

Abnormalities in postprandial gastric function could contribute to the maldigestion of pancreatic insufficiency. To measure simultaneously postprandial gastric secretion and emptying and correlate these measurements with intraluminal duodenal changes, we performed intestinal intubation and duodenal perfusion during feeding of a solid-liquid test meal in 10 healthy controls and 10 patients with documented pancreatic insufficiency before and after replacement therapy. In pancreatic insufficiency, intraduodenal pH was significantly decreased late in the postprandial period while simultaneously measured duodenal acid loads were normal, confirming that reduced bicarbonate output rather than increased acid delivery was responsible for higher duodenal acidity in these patients. Significant (P less than 0.05) reductions in postprandial acid, pepsin, and total secretory outputs were noted in untreated patients only during the first postprandial hour. Absolute gastric emptying rates were lower in patients (P less than 0.05) than in healthy subjects, but fractional rates of emptying were similar. Fasting and postprandial hypergastrinaemia were consistently observed in the patients with pancreatic disease. There are postprandial disturbances of secretory function but no primary gastric motor defect in patients with exocrine pancreatic insufficiency.

Topics: Duodenum; Eating; Female; Gastric Emptying; Gastric Juice; Gastrins; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Pancreatin; Pancreatitis

In 21 female Beagle dogs an experimental pancreatitis was induced by injection of bile into the pancreatic duct system. Beside controls, dogs received 62.5 micrograms/h cyclic somatostatin (SRIF) a continuous i.v. infusion starting with a bolus of 250 micrograms 15 minutes before or 2 hours after bile injection. Following blood parameters were determined: lipase, amylase, blood count, minerals, glucose, insulin, gastrin, secretin and CCK. Two controls died within 24 hours, the others were sacrificed after 48 hours. All pancreata were examined morephologically. The controls developed all clinical signs of acute hemorrhagic pancreatitis, whereas all SRIF-treated dogs were in much better general condition. Lipase and amylase increased in all groups. In the controls insulin, gastrin and secretin remained unchanged and CCK rose slightly. SRIF-treatment diminished insulin, CCK and the test meal-induced increase of secretin. At autopsy the pancreata of the controls were nearly entirely apoplectic. The SRIF-treated dogs showed less damage of the pancreas and no severe hemorrhagic necrosis was noted. The beneficial effect of SRIF cannot only be due to an interaction with intestinal hormones. An additional direct protective effect on the exocrine parenchyma is proposed to exist.

Topics: Acute Disease; Animals; Blood Glucose; Cholecystokinin; Dogs; Fasting; Female; Gastrins; Insulin; Pancreatitis; Secretin; Somatostatin

Secretin releasing response to intraduodenal acid infusion was investigated in 15 cases of diseased control, 7 cases of duodenal ulcer, 5 cases of chronic pancreatitis, and 6 cases of diabetes mellitus. Plasma secretin levels in response to duodenal acidification were less in duodenal ulcer and the appearance of the maximal peak was delayed compared with that found in control. It is suggested that the secretin release was impaired in duodenal ulcer in spite of hypersecretion of gastric acids. In chronic pancreatitis, secretin releasing response to acidification was markedly impaired, in addition, inhibition of secretin release by bicarbonate was diminished due to a lack of bicarbonate flow from the pancreas. On the other hand, although the response of secretin release in diabetes mellitus was also lower compared with that in control group, the capacity of secretin response showed values in-between control subjects and chronic pancreatitis. This research was supported in part by grant from the Ministry of Education, Science and Culture in Japan.

Topics: Adolescent; Adult; Chronic Disease; Diabetes Mellitus; Duodenal Ulcer; Female; Gastric Juice; Gastrins; Humans; Male; Middle Aged; Pancreatitis; Secretin

Topics: Adult; Cholecystitis; Chronic Disease; Duodenal Obstruction; Female; Gastrins; Humans; Male; Middle Aged; Pancreatitis; Peptic Ulcer

Differences in metabolic homeostasis in 12 patients with initial vs. eight patients with repeated attacks of acute pancreatitis have been compared during the acute phase of the disease. As a group, subjects with a previous history of pancreatitis had significantly lower glucagon concentrations (P less than 0.002) for the over all 24-hour study period. Conversely, the serum concentrations of blood sugar, insulin, growth hormone, gastrin, cortisol, nonesterified fatty acids, triglycerides and cholesterol failed to distinguish between the two patient groups. Likewise, immunoreactive plasma parathyroid hormone and calcitonin levels were comparable in both patient populations. Of the measurements considered, it would appear therefore that plasma immunoreactive glucagon is the best indicator of previous pancreatic inflammation. Evaluation of parenchymal integrity during an episode of acute pancreatitis would be of prognostic and therapeutic value in this disease.

Topics: Acute Disease; Adult; Amylases; Blood Glucose; Calcitonin; Calcium; Cholesterol; Fatty Acids, Nonesterified; Female; Gastrins; Glucagon; Growth Hormone; Humans; Hydrocortisone; Insulin; Male; Middle Aged; Pancreatitis; Parathyroid Hormone; Recurrence; Triglycerides

Angiographic findings in one giant cell carcinoma, one cystadenocarcinoma, one poorly vascularized mucinous cystadenocarcinoma, as well as in two avascular (gastrin- and glucagon-producing) islet-cell tumors of the pancreas are described. Two hypervascularized islet-cell tumors are presented for comparison and a case of tumorous chronic pancreatitis in a child is reported because ot its rarity. The aggressiveness of the giant cell carcinoma of the pancreas was demonstrated by its expansive growth. In the case of cystadenocarcinoma angiography revealed the tumor with hepatic metastases not diagnosed at explorative laparotomy. The relative hypovascularity in the case of mucinous cystadenocarcinoma was unusual. Both avascular islet-cell tumors simulated a pancreatic pseudocyst and the final diagnosis was made only by immunoassay. Chronic pancreatitis in a child presented with marked hypervascularization.

Topics: Adenoma, Islet Cell; Adult; Aged; Angiography; Carcinoma; Celiac Artery; Chronic Disease; Contrast Media; Cystadenoma; Diagnosis, Differential; Female; Gastrins; Glucagon; Hepatic Artery; Humans; Male; Middle Aged; Pancreatic Cyst; Pancreatic Neoplasms; Pancreatitis; Zollinger-Ellison Syndrome

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

On the basis of some experimental observations of hypergastrinemia in animals chronically intoxicated with ethanol, both fasting and after meals serum gastrin were determined in patients affected by chronic alcoholic pancreatitis. A significant increase in serum gastrin levels was observed in patients with chronic pancreatitis compared with controls, both in basal conditions and following food stimulation. The physiopathological hypotheses and possible aetiopathogenetic implications suggested by such gastrin behaviour are discussed.

Topics: Adult; Aged; Alcoholism; Chronic Disease; Gastrins; Humans; Male; Middle Aged; Pancreatitis

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

Fasting and after meals serum gastrin levels were determined in healthy subjects and patients with different gastroenterological diseases (duodenal and gastric ulcer, hiatal hernia with gastroesophageal reflux, Billroth II gastric resection, atrophic gastritis, Zollinger-Ellison, Ménétrier, chronic calcifying pancreatitis, gastric carcinoma and lymphoma). The results pointed to the usefulness of evaluating both fasting levels and "gastrin curve" after meals as an expression of the rapidity of response of hormone-secreting gastric cells. Calculation of the I.G.O. (Integrated Gastrin Output) must also be carried out to provide a parameter from which the overall ability of G cells to secrete in response to feeding can be assessed.

Topics: Duodenal Ulcer; Gastrins; Gastritis; Gastroesophageal Reflux; Gastrointestinal Diseases; Hernia, Hiatal; Humans; Pancreatitis; Stomach Neoplasms; Zollinger-Ellison Syndrome

A total of 1 035 routine serum gastrin investigations was undertaken with a commercially available kit. Levels in 49 normal subjects were similar to those found in 200 patients with duodenal ulcertaion, in 42 patients with gastric ulcers, in 9 patients with carcinoma of the stomach, in 55 patients with chronic alcohol-induced pancreatitis, and in 27 with iron deficiency anaemia. Significantly raised levels of serum gastrin were found in 32 patients with megaloblastic anaemias, where the rise in serum gastrin concentration correlated with a fall in maximal acid output, and in 14 patients with complete vagotomies. It is suggested that a level of less than 2 mEq/h of acid after insulin and a raised serum gastrin level are useful criteria of completeness of vagotomy.

Topics: Adult; Anemia, Hypochromic; Anemia, Megaloblastic; Duodenal Ulcer; Female; Gastric Juice; Gastrins; Gastrointestinal Diseases; Humans; Male; Pancreatitis; Stomach Neoplasms; Stomach Ulcer; Vagotomy

Topics: Alcoholism; Amylases; Anemia, Pernicious; Atrophy; Bicarbonates; Gastrins; Gastritis; Humans; Pancreas; Pancreatic Juice; Pancreatic Neoplasms; Pancreatitis; Secretin; Zollinger-Ellison Syndrome

Variables of calcium metabolism were measured in 11 patients with clearly documented acute pancreatitis. Total and ionized calcium levels were either low or in the low-normal range as were phosphorus and total magnesium levels. Parathyroid hormone levels were high, and there was a significant inverse correlation with ionized calcium. Gastrin levels were normal, calcitonin values were uniformly below the detection limit of the assay, and pancreatic glucagon levels were elevated. The hypocalcemia of acute pancreatitis was probably not caused by abnormalities of glucagon, calcitonin, or gastrin secretion. Furthermore, parathyroid hormone secretion was apparently not impaired. Hypomagnesemia possibly played a minor role. This study suggests that the hypocalcemia of acute pancreatitis is secondary to extraskeletal calcium sequestration or an as yet unidentified defect of bone metabolism, or both.

Topics: Acute Disease; Calcitonin; Gastrins; Glucagon; Homeostasis; Hypocalcemia; Magnesium; Pancreas; Pancreatitis; Parathyroid Hormone; Phosphorus; Prospective Studies; Triglycerides

Topics: Alkaline Phosphatase; Amylases; Bilirubin; Duodenal Neoplasms; Duodenum; gamma-Glutamyltransferase; Gastrins; Humans; Intestinal Absorption; Iron; Leucyl Aminopeptidase; Lipase; Pancreas; Pancreatic Neoplasms; Pancreatitis; Postoperative Complications

Topics: Animals; Dogs; Duodenal Obstruction; Female; Gastrins; Male; Pancreas; Pancreatic Juice; Pancreatitis

Topics: Adolescent; Adult; Aged; Anemia, Pernicious; Female; Gastrins; Humans; Male; Middle Aged; Pancreatitis; Radioimmunoassay; Secretin; Zollinger-Ellison Syndrome

Topics: Adult; Aged; Cholecystokinin; Chronic Disease; Duodenal Ulcer; Duodenum; Female; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Histamine; Humans; Injections, Intravenous; Male; Middle Aged; Pancreatitis; Secretin; Secretory Rate; Stomach

Topics: Animals; Dogs; Ethanol; Gastrins; Pancreatic Ducts; Pancreatic Juice; Pancreatitis; Pressure

Topics: Bicarbonates; Cholecystokinin; Enteritis; Gallbladder Diseases; Gastric Acidity Determination; Gastrins; Gastritis; Pancreas; Pancreatitis; Pyrazoles; Secretin; Stimulation, Chemical; Stomach Ulcer

Topics: Age Factors; Animals; Chronic Disease; Cystic Fibrosis; Depression, Chemical; Dogs; Gastrins; Injections, Intravenous; Pancreatitis; Secretin; Sex Factors; Vagus Nerve

Topics: Amylases; Bicarbonates; Bilirubin; Cholecystokinin; Chronic Disease; Duodenum; Gastrins; Humans; Lipase; Methods; Pancreatic Juice; Pancreatitis; Peptides; Secretin; Stimulation, Chemical; Stomach; Trypsin

Topics: Amino Acids; Autonomic Nervous System Diseases; Cholecystitis; Duodenal Ulcer; Fatty Liver; Gastric Acidity Determination; Gastrins; Gastritis; Humans; Pancreatitis; Proctitis; Stomach Ulcer