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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of a coffee-antazid-mixture was investigated at 30 patients with diseases of the stomach (17 with duodenal ulcer, 6 with gastric ulcer and 7 with chronic gastritis) in comparison to a commercial coffee. The parameters measured were the gastric basal acid output, the continuous registration of the pH by an intragastric electrode and the serum gastrin concentration before and after the application of the tests substances. 75% of the patients with duodenal ulcer showed a positive effect by means of a greater elevation of the intragastric pH after application of the mixture in comparison to coffee. The effect was strongly correlated to the basal acid ouptput. In the group with gastric ulcer and that with duodenal ulcer under the influence of the mixture the pH after the initial rise decreased to less deeper values. There was a close relationship to the patterns of gastric ulcer as well with chronic gastritis there was an additional facourable effect on the symptoms of abdominal pain which occured after coffee and not after the mixture. The group with chronic gastritis showed no difference between the pure coffee and the coffee-antacid-mixture. A possible relationship of the products of coffee roasting and the adsorptive properties of the antacid is discussed.
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PMID:[Effects of a coffee-antacid-mixture and a commercial coffee with regard to gastrin, pH and gastric secretion (author's transl)]. 1 88

In 5 human subjects, 95% pure cholecystokinin (CCK) given as a background infusion in doses of 42, 84, or 168 pmol kg-1 h-1 did not significantly alter acid secretion in response to graded doses (11-300 pmol kg-1 h-1) of synthetic human gastrin-17-I. The 168 pmol kg-1 h-1 dose of CCK produced maximal pancreatic amylase output. In 3 subjects, 337 pmol kg-1 h-1 of CCK slightly stimulated acid secretion when given alone and tended to reduce acid secretion in response to gastrin, but each of the subjects experienced cramping abdominal pain. The increment in acid secretion produced by CCK alone was similar to that produced by maximally effective doses of carboxyl-terminal octapeptide of CCK. In dogs with gastric and pancreatic fistulas, 168 pmol kg-1 h-1 of CCK produced maximal pancreatic protein output and slightly stimulated gastric acid secretion. In dogs with gastric fistulas and Heidenhain pouches, the lowest dose of CCK that inhibited gastrin-stimulated acid secretion was 674 pmol kg-1 h-1. We conclude that in man and dog 95% pure CCK weakly stimulates gastric acid secretion and inhibits gastrin-stimulated acid secretion but these actions occur only with doses of CCK that are maximal or supramaximal for pancreatic enzyme secretion. Because of the high dose requirement, these effects are unlikely to be physiologically significant.
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PMID:Effect of ninety-five percent pure cholecystokinin on gastrin-stimulated acid secretion in man and dog. 44 32

Elevation in fasting serum gastrin levels was found in three patients being evaluated for persistent upper abdominal pain without radiographic evidence of peptic ulcer disease. Fiberoptic endoscopy of the upper gastrointestinal tract in each patient revealed characteristic changes of chronic atrophic gastritis. Gastric biopsies showed diffuse chronic inflammation in the lamina propria, a decrease in the number of parietal cells, and "intestinalization" of gastric mucosa. Total achlorhydria was demonstrated after a maximal histalog stimulus; however, serum levels of vitamin B12 and Schilling test values were normal in all three patients. Parietal cell antibodies were found in the serum in all patients in a dilution of 1:20 to 1:80. These cases represent autoimmune (type A) chronic atrophic gastritis and should be distinguished from chronic simple (type B) gastritis, in which serum gastrin levels are normal and no parietal cell antibodies are found in the serum. Patients with autoimmune gastritis should be observed at frequent intervals for the occurrence of pernicious anemia or gastric carcinoma.
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PMID:Autoimmune atrophic gastritis with hypergastrinemia. 101 70

A women had hypergastrinaemia associated with the variety of gastritis (Type A) that is associated usually with pernicious anaemia, together with recurring bouts of severe abdominal pain. Fasting serum gastrin levels ranged between 600 and 2750 pg/ml. There was a rise in serum gastrin levels after a standard protein meal, indicative of a large G cell mass, and a fall after intragastric HCI, which led to a trial of treatment with HCI; this gave some symptomatic relief. After surgical antrectomy there was a profound fall of serum gastrin from a pre-operative level of 2500 pg/ml to constant values of 16--25 pg/ml, and complete and lasting relief from the bouts of abdominal pain.
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PMID:Symptomatic hypergastrinaemia with achlorhydria: reflief by antrectomy. 105 75

This randomized controlled trial was conducted to compare the efficacy of intravenous infusion of octreotide (a synthetic long-acting somatostatin analogue) with vasopressin in 48 cirrhotic patients with endoscopically proven bleeding esophageal varices. Twenty-four patients received a continuous infusion of octreotide 25 micrograms/h for 24 h after an initial bolus of 100 micrograms and another 24 patients received a continuous infusion of vasopressin 0.4 U/min for 24 h. Bleeding was initially controlled after 6 h of drug infusion in 88% (21/24) and 54% (13/24) of the patients treated with octreotide and vasopressin respectively (p = 0.03). Complete control of bleeding after 24 h of drug infusion was achieved in 15 (63%) patients receiving octreotide and in 11 (46%) patients receiving vasopressin (p > 0.05). Side effects during drug infusion such as headache, chest pain and abdominal pain were significantly lower in the octreotide group (3/24) than in the vasopressin group (11/24). Serum gastrin and insulin levels fell significantly following octreotide infusion, but plasma glucose levels remained unchanged. Mortality related to bleeding esophageal varices was no different between the two groups. This report showed that octreotide infusion was more effective and had fewer side effects than vasopressin in initial controlling of acute esophageal variceal bleeding until an elective endoscopic sclerotherapy could be performed.
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PMID:A randomized controlled trial comparing octreotide and vasopressin in the control of acute esophageal variceal bleeding. 148 8

Antral gastrin cell hyperfunction is a rare condition, often associated with severe duodenal ulcer disease. In children, clinical and functional characteristics of this syndrome are poorly known. Two cases are described here: one child had melena and the other had moderate abdominal pain, both without peptic ulceration. Basal and postprandial increase of gastrin levels showed a response over the upper normal range, indicating gastrin cell hyperfunction. Acid hypersecretion, both basal and after pentagastrin stimulation, was also found in the two children, confirming the biological effect of their sustained hypergastrinemia. Gastrin cell counts were within the normal range, while the number of somatostatin D cells was significantly reduced. This report stresses the importance of diagnosing antral gastrin cell hyperfunction in children because this unrecognized condition may manifest with serious complications (bleeding) or nonspecific abdominal symptoms.
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PMID:Antral gastrin cell hyperfunction in children. A functional and immunocytochemical report. 168 24

All 95 portal venous sampling (PVS) procedures performed in patients with Zollinger-Ellison syndrome in the past 10 years at the authors' institution were reviewed. It was possible to catheterize at least one branch of the pancreaticoduodenal venous arcade in all but two procedures (98%). The highest concentration of gastrin was found in a selective sample from the pancreaticoduodenal venous arcade or the transverse pancreatic vein in 56 of 91 procedures (62%). Selective sampling of pancreatic head veins yielded a gastrin gradient sufficient for localization in 60 patients (63%). Among 55 solitary sporadic gastrinomas identified at surgery, PVS allowed correct localization of the tumor in 32 (58%); if selective samples had not been obtained, only eight (15%) would have been localized (P less than .0005). Sensitivity was the same for tumors in the gastrinoma triangle (64%) and the body or tail of the pancreas (60%). There were no false-positive results. The overall complication rate was 20%, but most complications were abdominal pain lasting 3 days or less. Six patients (6%) had serious complications.
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PMID:Zollinger-Ellison syndrome: technique, results, and complications of portal venous sampling. 172 89

The authors reported a case of giant solitary pancreatic gastrinoma. A 29-year-old woman complaining of upper abdominal pain and loss of weight of 6 months duration. Four months later she noticed moving abdominal tumor. At the surgery a tumor was identified on pancreatic body measuring 20 centimeters of dimension and it was completely removed. A partial pancreatectomy with pancreatic tail preservation was performed in addition to this the Wirsung duct was joined on pancreatic head. No abdominal metastasis was found. The gastrointestinal transit was re-established by end-to-side Roux-en-Y jejunum-pancreatic anastomosis. The final diagnosis was confirmed by immunohistochemical test (immunoperoxidase). The follow-up was made until 40th postoperative month and after surgery the plasma level of gastrin was 120 pg/ml but at present day is normal. The authors concluded that it was a benign giant solitary pancreatic gastrinoma.
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PMID:[Giant solitary gastrinoma of the pancreas]. 184 39

Although in most patients with duodenal ulcer disease the ulcer heals after 8 weeks of treatment with standard doses of H2 blockers or other agents, in about 10% the ulcer does not heal. These patients are considered 'refractory' to treatment. Reasons often cited for non-healing include poor patient compliance, cigarette smoking, and non-steroidal anti-inflammatory drug (NSAID) use. Gastric acid hypersecretion also appears to be an important factor in non-healing with standard doses of antisecretory agents. We have defined idiopathic gastric acid hypersecretion as a basal acid output of greater than 10 mmol/h in the absence of an elevated fasting serum gastrin level (or a negative secretin test if gastrin level greater than 100 pg/ml) to exclude persons with Zollinger-Ellison syndrome. Among the acid/peptic-related disorders in which idiopathic gastric acid hypersecretion should be considered are refractory duodenal ulcer, refractory gastro-oesophageal reflux disease (especially patients with oesophagitis), postbleeding duodenal ulcer, and certain rare disorders such as hereditary angioedema. Some children with atypical abdominal pain may also be hypersecretors of gastric acid. Once identified, patients with refractory duodenal ulcer or gastro-oesophageal reflux disease are treated with incremental doses of ranitidine titrated against the level of gastric acid secretion that remains during therapy. Ranitidine was selected to avoid the dose-related antiandrogenic effects and potential hepatic cytochrome P450 system-related drug interactions that may occur with cimetidine. In most cases of refractory duodenal ulcer, doubling the standard dose of ranitidine (to 300 mg b.d.) is sufficient to achieve symptomatic relief and mucosal healing. Higher doses appear to be necessary for refractory oesophagitis. To date, no side effects have been associated with high doses of ranitidine (up to 1800 mg/day) for periods of longer than 6 months. Idiopathic gastric acid hypersecretion is an important factor in explaining why not all patients respond to a 'standard' ulcer-healing dose of H2 blocker, and it provides a rationale for use of higher-dose therapy as a safe and effective alternative to omeprazole or to combination drug therapy in refractory acid/peptic disease.
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PMID:Idiopathic gastric acid hypersecretion: treatment implications for refractory acid/peptic disorders. 188 34

Prior to the 17th century, there was considerable confusion regarding the process of digestion. Although some physicians were certain that it was initiated by acid in the stomach, both the source and the nature of the acid were unclear. In the early 19th century, Prout confirmed the active secretion of hydrochloric acid by the stomach and related it to the symptoms of dyspepsia. Jacob Helm and, subsequently, Beaumont studied digestion in humans with gastric fistulas and each commented extensively on the physiologic manifestation of digestion. The role of the vagus nerves in the control of gastric acid secretion was identified in the early and mid-19th century by Brodie, and subsequently elaborated upon by Pavlov. By the early 20th century, Latarjet and Jaboulay in France, performing operations for abdominal pain and tabes, reported the effects of vagotomy on acid secretion and gastric motility. In 1943, Dragstedt, in the United States, reported the cure of duodenal peptic ulcer disease by supradiaphragmatic vagotomy. He later observed the substantial delays in emptying of the stomach, which necessitated the introduction of concomitant gastric drainage procedures, such as gastrojejunostomy and pyloroplasty. In 1902, Bayliss and Starling had described the existence of a chemical regulator of function--secretin--which they termed a hormone. Shortly thereafter, Edkins reported results of studies that supported the presence of an acid regulatory hormone, gastrin, in the antrum of the stomach. Unfortunately, controversy marred this observation, and the action of gastrin was for more than 30 years ascribed to histamine. Komarov, in 1938, confirmed the existence of gastrin and its stimulatory effects on acid secretion. Physiologic recognition of the roles of vagal stimulation and antral gastrin in the secretion of acid from the stomach resulted in the development of the operation of vagotomy and antrectomy for peptic ulcer disease. Studies of the pylorus and the motility of the stomach resulted in an appreciation of the genesis of the postgastrectomy syndromes. By the middle of the 20th century, a clear appreciation of the morphologic characteristics of the parietal cell and its ability to secrete hydrochloric acid was under way. The complex metabolic process of the cell was correlated with the major morphologic transformation necessary to generate secretion of hydrochloric acid. The development of sophisticated research technology allowed the appreciation of the complex intracellular processes necessary to allow the generation of a 2.5 million-fold gradient of hydrogen ion secretion.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:From Prout to the proton pump--a history of the science of gastric acid secretion and the surgery of peptic ulcer. 215 87


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