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 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence of diabetes due to chronic pancreatitis would appear to be increasing. In western countries this is associated with the known increase in alcohol consumption and AIP. Malnutrition may be etiologic in tropical areas. The incidence of diabetes in chronic pancreatitis is dependent on a number of factors. It is more common in alcohol-induced pancreatitis, rarely occurs after the first attack but tends to increase with time and rises markedly in calcific pancreatitis. Abnormal glucose tolerance occurred in 91% of patients with calcific pancreatitis and 70% of patients with noncalific AIP in our follow up of five to 12 years. This stresses the importance of serial regular glucose tolerance tests in these patients (Table I). The insulin-reserve is severely depleted in most patients who do not yet demonstrate abnormal glucose tolerance, indicating that pancreatitis regularly affects the islets and that nearly all patients are potential diabetics. The beta cells appear to respond better to oral glucose, glucagon or secretin than to i.v. glucose suggesting a selective glucose receptor loss or block to hyperglycemia in chronic pancreatitis. The alpha cells seem to be more resistant to the effects of chronic pancreatitis but true hypoglucagonemia was found in 16% of patients. In addition, stimulated growth hormone secretion may be deficient in pancreatic diabetes. These last two factors, among others, may be responsible for the protracted and even fatal hypoglycemia to which some patients with AIP on insulin therapy are liable. The danger of drug-induced hypoglycemia, coupled with the infrequency of vasculopathy, retinopathy and nephropathy in pancreatic diabetes has induced us to keep these patients hyperglycemic and glycosuric rather than in a sugar-free state, as long as symptoms are contained. Recurrent abdominal pain, marked weight loss and associated steatorrhea often raise special problems in the management of the pancreatic diabetic.
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PMID:Clinical and hormonal aspects of pancreatic diabetes. 80 21

Endoscopic retrograde cholangiopancreatography (ERCP) was carried out in 98 patients with unexplained abdominal pain or known pancreatitis with recurrent pain. Patients with jaundice were excluded from the study. In 38 patients with a clinical diagnosis of pancreatitis, the radiological findings on ERCP were graded according to the criteria of Kasugai et al. Advanced pancreatitis was found in 20 patients (52,5%), moderate changes in 7 (18,4%) and minimal-change pancreatitis in 6 (15,8%). ERCP had normal pancreatic function tests. In 35 patients investigated for unexplained abdominal pain, changes consistent with pancreatitis were found in 7, pancreatic carcinoma in 5, a duodenal ulcer in 2, gallstones in 1 and a duodenal tumour in 1. ERCP was normal in 19 patients. A comparison of the findings on ERCP and the standard secretin-cholecystokinin pancreatic function test was available in 52 patients. There was a good agreement between the two tests in the patients with advanced or moderate pancreatitis as revealed by ERCP, but less agreement in the patients with minimal-change pancreatitis. A few patients with clinical pancreatitis and abnormal ERCP had normal pancreatic function tests. ERCP increases the diagnostic yield in patients suspected of having pancreatitis and is at present the only reliable method of diagnosing pancreatic carcinoma which is not evident by other non-operative techniques. ERCP is also of value in the assessment of the severity of pancreatitis and is a necessary investigation before pancreatic surgery to confirm or exclude cyst formation or the site of duct obstruction. The finding of an unsuspected cyst at ERCP necessitates early operation because of the danger of introducing infection during the procedure.
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PMID:Endoscopic retrograde cholangiopancreatography in the evaluation of pancreatic disease. 98 98

Ten adolescent and young adults with cystic fibrosis (CF) have had well-documented recurrent attacks of acute pancreatitis. The diagnosis of CF in each patient was delayed because they did not have pancreatic insufficiency. The diagnosis of CF was documented by the typical pulmonary involvement and elevated sweat sodium and chloride levels in all cases and a positive family history in six of the ten patients. Two patients were diagnosed as having acute pancreatitis before the diagnosis of CF was made, thus indicating that acute pancreatitis may be the presenting complaint in the young adult with CF. The diagnosis of acute pancreatitis was based on the presence of severe abdominal pain, usually with vomiting, tenderness in the mid-epigastrium, elevated serum and urinary amylase and serum lipase. Attacks were precipitated by fatty meals, alcohol ingestion; postcholecystectomy and tetracycline administration. In some patients no precipitating event could be elicited. Intravenous secretin-pancreozymin stimulation tests revealed a diminished bicarbonate secretion with little effect on the secretion of the zymogen enzymes. A mild attack of pancreatitis occurred after secretin-pancreozymin stimulation. The endocrine pancreatic function tested in four patients was normal as revealed by the glucose tolerance tests and determinations of serum insulin, growth hormone and free fatty acid. Transduodenal pancreatograms were performed in three patients; one showed a normal pancreatic duct, one showed duct obstruction and in the third patient a beady type of narrowing was found. The selenomethionine Se 75 uptake of the pancreas was noted only in the head of the pancreas. This suggests that loss of function occurs initially to a greater extent in the tail and body of the pancreas. Three patients died and showed characteristic lesions of CF.
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PMID:Recurrent acute pancreatitis in patients with cystic fibrosis with normal pancreatic enzymes. 111 Aug 67

A dynamic study of scintigraphy of the pancreas using 75Se-selenomethionine in diabetic patients was performed. Patients were selected who complained of abdominal pain or diarrhea or both and whose pancreatic exocrine functions were thought to be disturbed. Selenium-75-selenomethionine (3 muCi/kg body weight) was injected intravenously and radioactivity (cpm) was recorded by a scinticamera for 10 min successively up to 120 min. After 20-30 min the increase of radioactivity in the selected area of the displayed pancreas usually reached a plateau. Pancreozymin (1 Harper unit/kg) and secretin (1 harper unit/kg) were administered intravenously and decrease of radioactivity in the same area was followed for 60 min to examine pancreatic exocrine function. After 75Se-selenomethionine injection, the angle of the initial increase of radioactivity, the height of the plateau, and the reactive decrease of radioactivity after pancreozymin and secretin were analyzed in each case. Radioactivity recorded on data tape was reproduced for each 10-min period on a cathode-ray tube display. Areas of interest were selected for dynamic analyses. To supplement the diagnosis by visual image of a scintigram of the pancreas, the scintigram was quantified in the present study and the dynamic curves of radioactivity in the selected area of the displayed pancreas were studied for a total of 3 hr. Application of the dynamic study of the pancreas scintigraphy and the additional data analyses seemed useful for the early detection of pancreatic exocrine dysfunction in diabetic patients in whom the ordinary laboratory pancreatic exocrine function tests gave uncertain results.
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PMID:Dynamic study of exocrine function of the pancreas in diabetes mellitus with scintigraphy using 75Se-selenomethionine. 111 83

Variations in pancreatic duct diameter at CT scanning and serum pancreatic amylase response following secretin administration were studied in 29 patients with pancreas divisum and unexplained upper abdominal pain. Eleven healthy individuals were used as controls. At endoscopic retrograde pancreatography (ERP) six patients had signs of marked and six moderate pancreatitis, whereas there were no pancreatitis changes in 17 of the patients. At CT scanning patients with marked pancreatitis (ERP) had significantly increased pancreatic duct diameter as compared to patients without signs of pancreatitis. The duct was visualized in 52% of all patients before and 71% after secretin stimulation the corresponding figures for healthy controls, being 18% both before and after secretin. In patients without signs of pancreatitis, it was demonstrated in 5/17 (29%) before and 11/17 (65%) after secretin, whereas it was seen in 10/12 (83%) pancreatitis patients both before and after the hormonal provocation. In five of the nonpancreatitis patients in whom the duct was measurable before and at all study intervals (10, 20, and 50 min) after secretin, there was a significant duct dilation response both at 10 min and when comparing the maximal duct diameter after secretin to the initial values. In contrast secretin did not affect the duct caliber in pancreatitis patients. Serum pancreatic amylase increased significantly after secretin administration to healthy controls and nonpancreatitis patients but was uninfluenced in the marked and moderate pancreatitis groups, respectively. However, when all pancreatitis patients were grouped together, the amylase levels were significantly elevated by secretin. In conclusion, secretin provocation caused duct dilation at CT scanning in pancreas divisum patients without signs of pancreatitis at ERP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dynamic CT scanning of pancreatic duct after secretin provocation in pancreas divisum. 169 12

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

In a prospective study the pancreatic duct diameter was measured sonographically before and after secretin stimulation in 20 healthy controls and 59 patients with upper abdominal pain, weight loss, and/or diarrhea. Whereas healthy controls and patients without pancreatic disease after secretin stimulation showed a distinct pancreatic duct dilatation of more than 90% of basal duct diameter, no distinct secretin-induced duct enlargement was observed in most patients with chronic pancreatitis. Patients with circumscript pancreatic duct stenosis even had a marked and longer-lasting duct dilatation after stimulation. In patients with anomalies of the pancreatic duct system, no uniform response was found after secretin injection. In this study the sonographic secretin test showed a sensitivity of 92% and a specificity of 95% for diagnosis of chronic pancreatitis. The results confirm that this diagnostic method can be recommended as a reliable screening test for pancreatic disease.
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PMID:Significance of a sonographic secretin test in the diagnosis of pancreatic disease. Results of a prospective study. 264 57

Pancreas divisum is the most common anatomical variant of pancreatic ductal anatomy. It has been suggested that obstruction at the accessory papilla in subjects with pancreas divisum can be assessed by measurement of ductal diameter by ultrasonic examination after a maximal secretory stimulus with i.v. secretin. We have prospectively assessed this test in 44 individuals; nine healthy controls, nine patients with abdominal pain and normal pancreatic anatomy, 17 patients with pancreas divisum and abdominal pain but no other evidence of pancreatitis, and nine patients with pancreas divisum and either chronic or recurrent acute pancreatitis. We have found no correlation between ductal anatomy and response to i.v. secretin. Secretin provocation tests do not indicate which patients have accessory papillary stenosis and do not add support to the hypothesis of obstruction leading to pancreatitis in patients with pancreas divisum.
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PMID:Pancreatic duct dilatation after secretin stimulation in patients with pancreas divisum. 266 Jan 34

Two patients with chronic abdominal pain and fasting hypergastrinemia had increases in serum gastrin of 440 and 300 pg/ml after injection of 2 U/kg Secretin-KABI. Both subsequently proved to have pentagastrin-fast achlorhydria. Intragastric instillation of 0.1 N HCl suppressed serum gastrin concentration by greater than 60%. In both, the pancreas was normal by sonography or computed tomography (CT) scan and at laparotomy in one. Both are currently asymptomatic 12 and 18 months later. We conclude that achlorhydria may be associated after injection of Secretin-KABI with a false-positive rise in fasting serum gastrin concentration of greater than 200 pg/ml and that gastric analysis for hypochlorhydria should be performed before secretin provocation testing.
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PMID:False-positive secretin-KABI provocation test associated with achlorhydria. 341 78


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