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Biomedical subjects

P T Regan

Publications and source records attributed to P T Regan.

12 recordsLinked to original sources
PubMed1979

Postprandial gastric function in pancreatic insufficiency.

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.

Duodenum↗
PubMed1979

Medical treatment of acute pancreatitis.

Standard medical management of acute pancreatitis includes measures to relieve pain and maintain intravascular volume, nasogastric aspiration of gastric contents, and prompt recognition and treatment of complications. Despite many years of investigation, no specific drug or nonoperative procedure is of proven benefit in this common disease.

Acute Disease↗
PubMed1979

Reduced intraluminal bile acid concentrations and fat maldigestion in pancreatic insufficiency: correction by treatment.

Malabsorption of bile acids is known to occur in patients with pancreatic insufficiency particularly when due to cystic fibrosis. Abnormal biliary secretion or intraluminal acidic precipitation of bile acids could contribute to the steatorrhea of pancreatic insufficiency. To measure bile acid outputs and duodenal concentrations of bile salts and lipids simultaneously, we performed intestinal intubation and perfusion studies during feeding of a solid test meal in 6 healthy controls and 8 adult patients with advanced acquired exocrine pancreatic insufficiency. The effects of various treatment regimens were also investigated. Postprandial bile acid secretion was similar in all treatment groups. However, significant (P less than 0.05) reductions in micellar concentrations of bile acids and fatty acids were observed in untreated pancreatic insufficiency. These abnormalities were directly related to pH-induced precipitation of bile acids and were corrected only by the addition of cimetidine to standard pancreatin therapy. Thus, in pancreatic insufficiency, treatment with pancreatin plus cimetidine enhances fat digestion and absorption by reducing both acid-peptic inactivation of lipase and acidic precipitation of bile acids.

Administration, Oral↗
PubMed1978

Pancreatic insufficiency and Ménétrier's disease. Report of a case with clinical response to pancreatic enzyme replacement.

A patient with exocrine pancreatic insufficiency and hypoalbuminemic edema was shown also to have a protein-losing gastropathy secondary to giant hypertrophic gastritis (Ménétrier's disease). Despite continuation of excessive gastric protein loss, the manifestations of hypoproteinemia were reversed by oral pancreatic enzyme replacement therapy. We speculate that impaired intraluminal proteolysis exaggerated the consequences of gastric protein loss.

Gastritis↗
PubMed1978

Rationale for the use of cimetidine in pancreatic insufficiency.

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.

Adult↗
PubMed1978

A reappraisal of clinical, roentgenographic, and endoscopic features of the Zollinger-Ellison syndrome.

Recent experience with 40 patients with the Zollinger-Ellison syndrome at all Mayo Clinic suggests that traditional clinical criteria for diagnosis are often absent or invalid. Patients are younger have a shorter duration of symptoms, and often present without prior gastric surgery. Clinical, roentgenographic, and endoscopic findings indistinguishable from those of idiopathic duodenal ulcer or erosive duodenitis were the only presenting features in half of the patients in this series. Therefore, increased diagnostic use of serum levels of gastrin and gastric analysis appears desirable, particularly in patients selected for elective surgical treatment of duodenal ulcer disease, because specific therapeutic approaches may be required.

Adolescent↗
PubMed1977

Comparative effects of antacids, cimetidine and enteric coating on the therapeutic response to oral enzymes in severe pancreatic insufficiency.

To provide a rational basis for pancreatic enzyme replacement therapy, we evaluated, in six patients with advanced pancreatic insufficiency, the effects of various treatment regimens on fecal fat and nitrogen balance and on duodenal recovery of ingested pancreatic enzymes after a solid test meal. The combination of cimetidine (an H2-receptor antagonist) and pancreatin, each given by mouth, produced significantly higher postprandial duodenal recoveries and concentrations of trypsin and lipase (P less than 0.05). Steatorrhea was reduced in all patients and abolished in four of the six. In the dosages used, neither enteric-coated enzymes nor supplemental neutralizing antacids were more effective than pancreatin alone in decreasing steatorrhea or improving duodenal enzyme delivery. Cimetidine may be a useful adjunct to oral pancreatic extract therapy in some patients with severe pancreatic insufficiency who fail to respond to pancreatic enzyme replacement alone.

Administration, Oral↗
PubMed1977

[The medical management of malabsorption (author's transl)].

A broad overview of the modalities available for the medical treatment of malabsorptions is presented with emphasis on practical applications. The more common disorders, such as sprue, lactase deficiency, and pancreatic insufficiency, are generally managed successfully with specific dietary and drug regimens. Nonspecific dietary therapy is available for patients to whom specific therapy cannot be offered.

Anti-Bacterial Agents↗
PubMed1977

Scleroderma and intestinal perforation.

We report four cases of scleroderma and intestinal perforation. There were three instances of colonic perforations, two associated with fecal impaction and stercoral ulceration and one with evidence of vasculitis. The fourth patient was an unusual instance of spontaneous perforation of the small intestine in scleroderma.

Adolescent↗