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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

15 streptozotocin-diabetic wistar rats (an application of a single dose of 64 mg/kg body weight streptozotocin) and a control group of 12 wistar rats with a healthy metabolism have been examined. The majority of B-cells was largely degranulated, insulin was hardly or not to be found with histochemical methods. The A- and B-cells of 11 test animals showed pathological findings: Karyolysis, the dissolution of cell membranes and the decay of cytoplasm which are criteria of necrosis. Besides a round-cell infiltration could be found as a symptom of insulitis. The B-cells showed only single granula under the electron microscope. The endoplasmatic reticulum was only poorly developed and with hardly any ribosomes. There were only very little mitochondria and no GOLGI's apparatus. The cell membrane was smooth and not enlarged by microvilli. Emiocytosis-figures were missing. No changes of nuclei could be noticed. The findings on organelles correlate well with the microscopical results. The exocrine parenchyma contained regions showing the decay of the lobule structure as well as of single acini. The acinus cells were in necrosis. The connective tissue was obviously increased. There were regions in the stroma with a round-cell infiltration as found with a pancreatitis. Both these and the results discussed from our literature show that streptozotocin does not only affect the B-cells of the islets of LANGERHANS, but also the exocrine pancreas and other organs.
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PMID:[Histotopochemical and electronmicroscopical investigations of Wistar-rats with streptozotocin diabetes (author's transl)]. 15 64

17 oral glucose tolerance tests with simultaneous estimation of plasma insulin, were carried out in 15 patients with chronic pancreatitis of which 7 were of calcific type. Among these patients, 10 had obvious diabetes and 3 chemical diabetes. The disorders of glucose regulation were more common in the calcific form of the disease. Serum insulin was then lower and not stimulant. The curves of plasma insulin obtained in non-calcific pancreatitis were variable. In hyperinsulinism, the oral glucose tolerance test showed flat or normal curves. In hypoinsulinism, the glucose tolerance tests were either normal or strongly pathological. This insulinism, as shown by this study of chronic pancreatitis, seems to be linked to an imbalance in the cell distribution of the islets of Langerhans. The role of glucagon appears preponderant.
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PMID:[Study of insulin secretion in chronic pancreatitis]. 18 95

The association of chronic pancreatitis with diabetes is not very common. Men are the usual victims and ethylism the usual cause. The most common age of onset is between 40 and 50. Insulin treatment is much more frequent than for idiopathic diabetics. Diabetic heredity is probable. Calcifying pancreatitis is the most frequent form. Micro and macroangiopathic complications are found. A statistical comparative study with a matched series of idiopathic diabetics reveals no difference in the onset of vascular complications. The rate of triglycerides is statistically lower in pancreatitis (p less than 0.001). The other biological rates are the same (cholesterol, uricemy, alpha 2 macroglobulin). Diabetic stability is no more difficult to obtain than for idiopathic diabetics. In most cases the diet should be wide and alcohol must be prohibited.
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PMID:[Diabetes and chronic pancreatitis. Report of twenty cases (author's transl)]. 23 6

A patient with recurrent pancreatitis was treated by near-total pancreatectomy. The tail of the pancreas, together with the splenic artery and vein, was transplanted into the thigh, with anastomoses of the splenic vessels to the femoral vessels. Two months after operation simultaneously drawn blood samples from both femoral veins showed elevated insulin on the grafted side. Two years after operation the patient is free of symptoms and is not diabetic.
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PMID:Pancreatic autotransplantation following resection. 34 88

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

In diabetic diseases of pancreatic origin we find three typical patterns of insulin secretion. The different insulin secretion allows a clear distinction of a diabetes of the maturity onset type and of the juvenile onset type type on the one hand and of a diabetes caused by a pancreatitis on the other hand. In a pancreatitis we see the expected reduction of the exocrine function. In the so called maturity onset diabetes a slight reduction of excretory functions could be seen. These results suggest that in maturity onset diabetes only a selective defect of the beta-cells exists, while in juvenile onset diabetes a destruction or reduction of beta-cells but an intact excretory function may be assumed.
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PMID:[Endocrine and exocrine functional disorders in pancreatic diabetes]. 39 94

A clinically reliable diabetes mellitus was present in 7.5% of 386 patients with pancreatitis and cholecystopancreatitis. In a number of these patients (6.4%) diabetes mellitus was an immediate aftermath of recurrent pancreatitis. After having carried out sugar tolerance test in 104 patients with pancreatitis and cholecystopancreatitis the authors showed a potential risk of the occurrence of diabetes mellitus. Only administration of simple insulin under a permanent laboratory control should be used. When determining the indications for operation one ought to remember about the possibility of the occurrence of pseudoperitoneal syndrome.
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PMID:[Treatment of acute pancreatitis and cholecystopancreatitis with accompanying diabetes mellitus]. 43 83

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

Pancreatitis was induced in 11 miniature pigs by infusing a bile salt-trypsin solution into the pancreatic duct. Seven animals served as sham-operated controls. Serum ionized calcium, total calcium, albumin, total protein, inorganic phosphorus, urea nitrogen, magnesium, insulin, glucagon, and hematocrit were determined every six to 12 h over a period of one week in both test and control animals. We observed significant decreases in ionized and total calcium, modest decreases in albumin, and significant increases in the inorganic phosphorus, urea nitrogen, and hematocrit in the pancreatitic pigs. The latter two findings were consistent with early acute hypovolemia. Glucagon and insulin appeared to play no role in the hypocalcemia. Glucagon concentrations increased to the same degree in both test and control animals, probably as a result of the stress of being handled and operated on. The highest concentrations of inorganic phosphorus and the lowest concentrations of both ionized and total calcium were seen 18 h after the induction of pancreatitis in the test animals. These findings suggest that parathyrin (parathormone) was not being secreted in adequate amounts, or that the target organs were unresponsive to parathyrin.
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PMID:Biochemical changes in a porcine model of acute pancreatitis. 65 76


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