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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The vicinity of several hormone-producing glands as part of the anatomy of the intestinal tract and the resulting interaction has been confirmed by the discovery of hormonal factors of a specifically gastro-intestinal origin. Today we are mainly interested in the interaction between intermediary metabolism and incretory intestinal function; this is characterized by the joint action of conventional glandular hormones such as insulin and pancreatic glucagon as well as by the incretion of diffuse intestinal organs, hormones such as secretin, pancreozymin, motilin, VIP and GIP. The latter are at present subject of active research with the object of discovering their physiological significance be it as tissue hormones or as humoral agents with a "long distance" impact; their role within pathophysiology is also of interest. GIP ("gastric inhibitory peptide"), apart form acting upon the intestinal tract, also causes a marked rise in insulin production; this GIP possibly is the factor responsible for the difference in glucose tolerance following i. v. or oral administration of glucose, something that scientists have been trying to discover for a long time. We have also endeavored to investigate somatostatin. This substance was originally discovered as a hypothalamic factor with inhibitory action on growth hormone secretion; in the meantime, however, cells containing and possibly also producing somatostatin have also been detected in the intestine and particularly in the islets of Langerhans (D-cells). Since somatostatin inhibits insulin secretion and especially glucagon release as well as the exretory functions of the stomach and of the pancreas, the significance of this hormone possibly is that of a tissue hormone with inhibitory action on adjacent cells. As factor inhibiting both endocrine and exocrine secretory processes it would combine these two complexes. The possible therapeutic significance of somatostatin administration to diabetics would lie in the saving of insulin. A third sector of present-day research deals with the interaction between the calcium metabolism and the hormones involved as well as the intestine. We know that patients suffering from primary hyperparathyroidism are prone to contract stomach ulcers and pancreatitis; patients with a gastrinoma and a hyperfunction of the epithelial bodies suffer from a Zollinger-Ellison-sindrome and this again suggests association with endocrine polyadenomatosis (Wermer syndrome). The inhibitory action of the parathormone antagonist calcitonin on the exocrine functions of the intestinal tract, such as the acid secretion of the stomach and the enzyme secretion of the pancreas, have already given rise to some considerations and experiments relative to treatment. It is to be hoped that because of all the joint observations cited above there will be better intergration of research both from the aspect of gastro-enterology and endocrinology. This might hopefully elucidate some of the unresolved problems ranging from basic research to practical application.
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PMID:[Interaction between gastrointestinal hormones and endocrine regulation]. 0 83

Endoscopic retrograde pancreaticocholangiography (ERPC) has been performed in 140 patients, mainly Blacks and Indians. The first 100 patients have been analysed. The greatest diagnostic yield in this series is in (suspected) obstructive jaundice, where 26 diagnoses were made in 35 patients. In 40 patients with pancreatitis, the widest ducts were seen in 12 patients with calcific pancreatitis, but the procedure was of less help than expected. This was because no patients with continual pain after cessation of alcohol intake were found with operable strictures of the main pancreatic duct. The pancreatic function test with secretin and cholecystokinin-pancreozymin correctly diagnosed 4 patients with non-calcific pancreatitis in whom the ERPC was normal. There was a useful diagnostic yield in patients with unexplained upper gastrointestinal symptoms (15 diagnoses were made in 23 patients).
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PMID:Technique and results of endoscopic retrograde pancreaticocholangiography. A preliminary report on 140 patients. 16 2

Bacterial infections of the pancreas and bacteremia may occur during episodes of pancreatitis. Detection of bacterial infections of the pancreas in the past has required laparotomy. The present study was undertaken to determine whether bacterial infection of the pancreas occurred during nonsuppurative pancreatitis. During endoscopic cannulation of the main pancreatic duct, secretin was administered intravenously and pancreatic juice aspirated from within the duct was cultured. Bacterial infections were detected in 11 of 35 patients with pancreatitis and 3 of 5 with pancreatic cancer. The pancreatic juice was sterile in 25 controls. Cultures from the common bile duct in 9 controls were also sterile whereas 4 of 6 with pancreatitis showed infected bile. The infecting organisms were principally gram-negative and the infections were usually polymicrobial. Antibiotics, where used, successfully eradicated the infecting organisms but did not appear to affect the patient's clinical course.
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PMID:Detection of bacterial infection of the pancreatic ducts in patients with pancreatitis and pancreatic cancer during endoscopic cannulation of the pancreatic duct. 33 75

The diagnosis of both acute and chronic pancreatitis continues to be a challenge despite the development of new techniques and the refinement of old methods. The problem is best approached by the application of a combination of tests which can provide a reasonable degree of sensitivity and specificity applicable to the different forms of pancreatitis. In acute pancreatitis an elevation of serum amylase and amylase/creatinine clearance ratio is diagnostically useful. In chronic pancreatitis, several tests are needed to enhance the diagnostic yield, and such tests can include the secretin-pancreozymin test, ERCP, fecal fat measurement, Lundh test meal, and the administration of the synthetic peptide BZ-Ty-PABA.
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PMID:Laboratory aids in the diagnosis of pancreatitis. 34 Aug 13

In Germany alcohol is responsible for 40--60 per cent of cases with chronic or chronic relapsing pancreatitis. The histologic lesions for a long time remain clinically asymptomatic. Their degree depends on the duration and the total amount of alcohol which is ingested. Promoters of alcoholic damage to the pancraes are a high intake of fat and protein and a genetic disposition. Acute application of alcohol leads to an inhibition of pancreatic secretion when the entrance of gastric acid into the duodenum is prevented. Otherwise a weak stimulation occurs with release of secretin. Chronic application of alcohol after a few months abolishes the initially seen inhibition and leads to an increase of enzyme secretion of the gland. The raised concentration of protein in the pancreatic juice is the cause of precipitation of protein plugs, and thus probably leads to the alterations which are typical for chronic pancreatitis.
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PMID:[Effect of alcohol on the human and animal pancreas (author's transl)]. 35 68

Glucagon can depress normal animal and human pancreatic exocrine secretions and modify experimentally-induced pancreatitis in animals. It has yet to be demonstrated that glucagon has any efficacy in the treatment of the diseased pancreas in man. Glucagon might act on the exocrine pancreas by 1. reducing pancreatic blood flow, 2. decreasing gastric secretion, 3. lowering serum calcium levels by the release of calcitonin, 4. acting to inhibit the secretin mechanism, 5. causing a hyperglycemia and 6. degranulating pancreatic acinar cells. While a reduction in pancreatic blood flow, an inhibition of the secretin mechanism and a hyperglycemia seemed to have been ruled out as possible mechanisms of action, there is too little available data to effectively speculate on the mechanism(s) of action of glucagon on the exocrine pancreas.
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PMID:The effect of glucagon on the exocrine pancreas. A review. 36 5

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.
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PMID:Effect of somatostatin on bile-induced acute hemorrhagic pancreatitis in the dog. 39 59

Severe pancreatitis and a pseudocyst occurred in a patient following accidental ingestion of an anticholinesterase insecticide, a substance not previously known to produce pancreatitis. Experiments were done to elucidate the mechanism. In one group of dogs the pancreatic duct was perfused and intraductal pressures were measured. The cholinesterase inhibitor 0,0-diethyl-0-(2-isopropyl-6-methyl-4-pyrimidinyl)phosphorothioate (25 mg/kg) caused a significant increase in the mean intraductal pressure from 12 +/- 2.4 to 27.8 +/- 5.9 cm saline. In a second group of dogs pancreatic secretory rates were measured. Anticholinesterase (75 mg/kg) in combination with secretin infusion (1 U/kg/hr) caused a significant increase in the secretin stimulated flow rate from 0.13 to 0.56 cc/min. Atropine (75 microgram/kg) abolished the anticholinesterase induced pressure and secretory rate increases. In a third group of dogs administration of cholinesterase inhibitor 75 mg/kg and secretin infusion 2 U/kg/hr resulted in acute pancreatic interstitial edema, acinar cell vacuolization, hyperamylasemia and hyperlipasemia. These results suggest that occurrence of pancreatitis as a complication of anticholinesterase insecticide intoxication is the result of hypersecretion and pharmacologic ductal obstruction.
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PMID:Pancreatitis as a complication of anticholinesterase insecticide intoxication. 42 52

Precise relationships between pancreatic ductal obstruction and pancreatic secretory capacity have not been established. In this study, we describe the quantitative relationships between the lengths of opacified ducts obtained at retrograde pancreatography and the secretory capcity of the gland for volume, bicarbonate, lipase, and trypsin. Forty-five patients (17 with pancreatic cancer, 6 pancreatitis, 5 other malignancies, and 17 nonmalignant, nonpancreatic disease found at laparotomy) were studied with a method of duodenal intubation and perfusion with basal saline perfusion alone or with continuous intravenous infusion of secretin or of cholecystokinin-pancreozymin. Secretory outputs of volume, bicarbonate, and enzymes compared with the length of opacified ducts showed a significant (P less than 0.05) linear relationship for patients with pancreatic cancer, pancreatitis, and other cancers. The resulting data imply that obstruction of the pancreatic duct is important in decreasing secretion of the pancreas in pancreatic disease. The relationship between obstruction and pancreatic secretion demonstrates that a decrease in exocrine pancreatic secretion cannot be detected until more than 60% of the total length of the main pancreatic duct has been obstructed.
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PMID:The relationships between pancreatic ductal obstruction and pancreatic secretion in man. 43 Nov 21

A follow-up investigation of 20 patients, surgically treated for acute haemorrhagic necrotising pancreatitis, was performed in an average of 2 3/4 years after the operation. Twelve patients showed manifest diabetes mellitus, four further cases had a suspicious oral glucose tolerance test. Only one patient was insulin dependent. A secretin-pancreozymin test performed in 15 patients showed a dissociated or global pancreatic insufficiency in 13 cases. The extent of the endocrine and exocrine functional disturbance did not correlate with the extent of surgery. Postoperative functional defects were readily improved therapeutically in most cases. Only in patients who continued to consume alcohol were there digestive disturbances. The results indicate that the functional state of the remaining pancreas does not only depend on the extent of surgery but also on the extent of already existing or persisting toxic inflammatory damage and on the regenerative capacity of the remaining parenchyma.
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PMID:[Long-term results after operative treatment of acute haemorrhagic necrotising pancreatitis (author's transl)]. 51 Jan 95


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