Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Postprandial gastric function in pancreatic insufficiency. 3 48

The influence of severe exocrine pancreatic disease on the acid-neutralizing capacity of the duodenum was studied in five patients with pancreatic insufficiency (PI) and six control subjects using duodenal perfusion-marker technique. Hydrochloric acid (0.1 N containing 1% PEG) was infused at constant rates (1.2, 4.5 and 7.0 ml/min) into the duodenum just distal to the duodenal bulb. Samples were aspirated from the tip of the duodenal perfusion tube located at the ligament of Treitz. All samples were analyzed for volume, pH, titrable acidity, PEG and [14C]PEG (gastric marker) determination. Patients with PI demonstrated significantly diminished ability to neutralize various acid loads as compared to controls who virtually completely neutralized acid loads in the range of maximal gastric acid secretion. Exogenous secretin did not significantly improve percent acid neutralized in PI. These data clearly indicate that patients with PI have significantly impaired ability to neutralize even small loads of acid in the duodenum.
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PMID:Impaired acid neutralization in the duodenum in pancreatic insufficiency. 3 15

An episode of severe small intestinal hemorrhage occurred in a cystic fibrosis patient having pancreatic insufficiency and receiving timed-release aspirin therapy for disabling hypertrophic pulmonary osteoarthropathy. The increased acidity of small intestinal contents due to decreased bicarbonate secretion observed in patients with pancreatic insufficiency may alter the luminal environment and result in mucosal erosions and/or ulcerations in association with the presence of aspirin. Thus, physicians should be aware of the possibility that timed-release aspirin causes small intestinal hemorrhage in such patients.
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PMID:Possible hazard of timed-release aspirin in a patient with pancreatic insufficiency. 31 79

The failure of standard oral pancreatic enzyme replacement therapy to correct malabsorption in patients with advanced pancreatic insufficiency is likely due to acid-peptic inactivation of ingested enzymes. Theoretically, the use of cimetidine, an H2-receptor antagonist, in conjunction with oral enzymes, would permit greater transgastric passage of ingested enzymes with resulting improvement in intraluminal lipolysis. To test this hypothesis, we studied the effects of orally administered cimetidine in two groups of patients by utilizing a previously validated double-marker perfusion technique. Cimetidine, in varying doses, had no effect on postprandial exocrine pancreatic function in 16 duodenal ulcer patients without pancreatic disease. In six patients with pancreatic insufficiency, cimetidine produced a pronounced decrease in the output of gastric acid and secretory volume, resulting in reduction of postprandial acidity and intragastric volume. These actions of cimetidine should retard or prevent inactivation of ingested enzymes and also increase their intragastric concentration, with resulting enhancement of luminal duodenal enzyme activity. Supplemental cimetidine may thus be useful in the medical management of patients who fail to respond to routine pancreatic extract therapy alone.
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PMID:Rationale for the use of cimetidine in pancreatic insufficiency. 34 Aug 5

Calcitonin (CT) inhibits gastric acid and pancreatic enzyme secretion when infused intravenously. Therefore, in two patients showing excessively elevated CT-blood levels due to medullary thyroid carcinoma and in two patients with bone diseases before and under CT-treatment, gastric and pancreatic secretion were measured. Spontaneous (BAO) and pentagastrin stimulated acid as well as hormonally stimulated pancreatic enzyme secretion revealed normal in all subjects and tests. The findings are in favour of adaptation mechanisms of gastric parietal and pancreatic acinar cells against the inhibitory action of chronically elevated CT. Therefore, long term treatment with CT is no likely to induce impaired acidity or exocrine pancreatic insufficiency.
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PMID:[Gastric and exocrine pancreatic function in patients with medullary thyroid carcinoma and with bone diseases under treatment with calcitonin (author's transl)]. 70 15

Fat malabsorption in patients with chronic alcoholic pancreatitis and cystic fibrosis may lead to vitamin and essential fatty acid deficiency in addition to steatorrhea. In clinical practice it can be difficult to achieve complete correction of malabsorption and elimination of steatorrhea. The earliest treatment methods used the oral administration of porcine pancreatic enzyme preparations. These conventional enzymes, however, were unstable in the acidic intragastric environment. Subsequently, medications to neutralize or reduce gastric acidity (H2-blockers, antacids, or bicarbonate) were added to improve the stability of the conventional enzymes. Enteric-coated enzyme preparations were then developed that would release only in an alkaline milieu, protecting the enzymes from acid denaturation. The newest and potentially most exciting modalities for the treatment of fat malabsorption are acid-stable lipases, obtained either from a fungal source or through the expression of cloned genes for the enzymes utilizing recombinant DNA techniques. The advantages and disadvantages of the various medications for the therapy of fat malabsorption in pancreatic insufficiency are reviewed.
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PMID:Enzyme therapy for malabsorption in exocrine pancreatic insufficiency. 266 33

Pancreatic enzyme therapy may be beneficial to all patients with chronic pancreatitis, even those in whom the condition is very mild. The goal of enzyme therapy should be to restore normal gastrointestinal physiology as completely as possible. Monitoring of body weight is recommended as the main measure of treatment efficacy. Most pancreatic enzyme preparations presently employed are porcine in origin and must meet certain standards of quality for human consumption. The amount of active lipase in the duodenum determines the quantity of enzymes to be given. An appropriate diet is also important for relieving symptoms of pancreatic insufficiency and improving nutritional status. Although administration of large amounts of proteases has provided pain relief in some patients, the rationale for using enzymes to relieve pain in chronic pancreatitis has not been generally accepted. Gastric acid plays a role in malabsorption, since administered enzymes may be destroyed by gastric acid. Also, acidic conditions in the duodenum decrease the efficacy of pancreatic enzymes administered with meals. Histamine-H2-receptor antagonists may decrease gastric acidity but there are certain drawbacks to long-term use of these agents. The use of enteric-coated microspheres overcomes many of the problems associated with enzyme destruction. Patients with chronic pancreatitis display considerable individual variation in their treatment requirements. Therapy must be tailored to meet the need for adequate disease control as well as for social and emotional acceptability by the patient. The attending physician and the patient share the responsibility for maintaining appropriate therapy.
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PMID:Theory and practice in the individualization of oral pancreatic enzyme administration for chronic pancreatitis. 270 51

Operative death following pancreatoduodenectomy results essentially from a pancreatojejunal anastomosis leakage. Pancreaticogastrostomy has been used infrequently. Seventeen patients (12 with malignant tumors and 5 with chronic pancreatitis) have undergone pancreaticogastrostomy following pancreatoduodenectomy. There was no operative mortality rate and no pancreaticogastrostomy leakage. Our data agree with data concerning pancreaticogastrostomy published in literature; cumulative mortality rate including our results is 4.5% (6 out of 134 patients) with only one transient benign pancreatic fistula reported. Many advantages offered by this method can explain these positive results including trypsine neutralization by gastric acidity and the possibility of nasogastric aspiration on contact with the anastomosis. Furthermore, permeability of the pancreatic duct can be easily verified by endoscopic examination. However, external pancreatic insufficiency does not seem to occur in long-term follow-up. These results suggest that this simple and safe method merits a more widespread application.
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PMID:Pancreaticogastrostomy following pancreatoduodenectomy. 334 12

In order to avoid inactivation in the stomach, pancreatic enzymes have been prepared as pH-sensitive, enteric-coated microspheres (Pancrease). An in vitro study was performed to evaluate the pH-related dissolution of Pancrease and to confirm its resistance to gastric acidity. Two assay methods were used with three different batches of Pancrease: (a) Enzyme absorbency at 280 nm was measured at unit pH intervals from pH 1 to pH 8 and at 0.5 pH intervals from the start of dissolution to pH 8. (b) Proteolytic activity was measured at pH 6.8. Significant enzyme dissolution started at pH 5.5 and was maximal at pH 6.0. At pH 6.8, the pH of simulated intestinal fluid, dissolution was complete in less than 15 min. At pH 5.0, no dissolution occurred within the first 10 min and only 13% dissolution was observed after 2 h. At pH 7.0, 100% dissolution was seen within 10 min. Results of the two assay methods were comparable with all three enzyme batches assayed. This study confirmed the gastroresistance of Pancrease. Because of the enteric coating of Pancrease, liberation of enzymes occurs in the duodenum and jejunum, providing maximal enzymatic efficacy in exocrine pancreatic insufficiency.
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PMID:Pancrease gastroresistance: in vitro evaluation of pH-determined dissolution. 340 58

Pancreatic enzyme replacement may fail to achieve a beneficial effect because of enzyme inactivation by gastric acid. In this controlled randomized study, 8 hospitalized patients with severe exocrine pancreatic insufficiency and considerable steatorrhoea (greater than 15 g faecal fat/day) were treated with a conventional pancreatic enzyme preparation (Pankreon 700; 3 X 3 dragees daily), with (300 mg) and without cimetidine before meals, and with a new pH-sensitive enzyme preparation (Kreon; 3 X 6 capsules daily) comprising acid-protected granules. Both conventional enzyme replacement plus cimetidine, and acid-protected pancreatin were significantly (p less than 0.05) more effective than conventional enzyme therapy alone. Since both regimens are equally potent in overcoming gastric acid-induced enzyme inactivation, it is concluded that therapy with acid-protected pancreatin may simplify and improve treatment of exocrine pancreatic insufficiency in the presence of gastric hyper- or normo-acidity.
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PMID:Therapy of pancreatogenic steatorrhoea: does acid protection of pancreatic enzymes offer any advantage? 354 9


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