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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

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

Uremia results in complex metabolic disturbances of exocrine pancreatic function which increase with the severity of renal insufficiency. This uremic pancreopathy is not identical with the pancreatitis of classical type. Its important clinical indicator is an elevation of serum lipase activity (more than 60% in nondialyzed renal insufficiency; hyperlipasemia was also detectable in chronic hemodialyzed patients (45%). The pathogenesis is heterogenous, its concept based on clinical and experimental studies involves several components: hormonal alterations (calcitonin etc.), catabolic protein metabolism in uremia, systemic disturbances (hemodynamics, hypoxia, acidosis etc.), direct impairment of the pancreatic cells induced by uremic toxins.
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PMID:[Uremic pancreopathy. Clinical and experimental studies of its pathogenesis]. 45 76

Differences in metabolic homeostasis in 12 patients with initial vs. eight patients with repeated attacks of acute pancreatitis have been compared during the acute phase of the disease. As a group, subjects with a previous history of pancreatitis had significantly lower glucagon concentrations (P less than 0.002) for the over all 24-hour study period. Conversely, the serum concentrations of blood sugar, insulin, growth hormone, gastrin, cortisol, nonesterified fatty acids, triglycerides and cholesterol failed to distinguish between the two patient groups. Likewise, immunoreactive plasma parathyroid hormone and calcitonin levels were comparable in both patient populations. Of the measurements considered, it would appear therefore that plasma immunoreactive glucagon is the best indicator of previous pancreatic inflammation. Evaluation of parenchymal integrity during an episode of acute pancreatitis would be of prognostic and therapeutic value in this disease.
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PMID:First 24 hours of acute pancreatitis. A biochemical and endocrine evaluation of initial versus repeated attacks. 69 15

Serum calcitonin (Ct) levels, serum calcium, and urine amylast were analyzed in 29 patients with an acute pancreatitis collected at random. In two of the patients the acute pancreatitis complicated a primary hyperparathyroidism. It was found that the calcitonin levels in serum were usually elevated during the acute phase of the pancreatitis. During this phase of the disease 22 of 27 examined patients had Ct-values above the upper normal limit of 1 mug/ml. The patients with normal Ct-values also had moderately elevated amylast values and a less pronounced pancreatitis. Normal Ct-values were usually found in patients more than 10 days after the onset of symptoms. Serum calcium was mostly within normal limits. However, a slight fall in serum calcium or low values was recorded in six patients with a pronounced disese. One patient with hyperparathyroidism normalized a previously elevated serum calcium during the calcitonin release.
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PMID:Serum calcitonin in acute pancreatitis in man. 83 66

Calcitonin was administered to 4 patients presenting with acute pancreatitis as well as to 6 patients presenting with postoperative pancreatitis. Prophylactic administration was performed in 3 cases consecutive to pancreatic interventions. Following calcitonin all patients showed considerable improvement of clinical course. Although 8 patients recuperated completely 2 patients died from independent complications. After prophylactic administration of calcitonin the postoperative course was uncomplicated without demonstrable increase in serum amylase. It is emphasized that only early case histories are reported; their verification will depend upon the results of a controlled survey presently being performed.
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PMID:[Preliminary observations on the clinical use of calcitonin. Treatment and postoperative prevention of pancreatitis]. 95 24

Calcitonin was measured in four patients with acute pancreatitis with hypocalcemia. A marked elevation of this hormone was noted in each case and persisted over several days. The peak level of calcitonin preceded the maximum fall in calcium. Among the various factors affecting calcium balance in pancreatitis, calcitonin probably plays an important role.
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PMID:Hypercalcitoninemia in acute pancreatitis. 112 85

Elevated concentrations of serum parathyroid hormone and hypocalcemia occur following the induction of experimental pancreatitis in the pig, but only when the thyroid gland is present. Prior thyroidectomy completely eliminates these changes. Serum magnesium concentrations remained normal throughout the experiments despite the occurrence of hypocalcemia. These data support the hypothesis that calcitonin or another thyroid-related substance plays a role in the mechanism of the hypocalcemia which accompanies experimental pancreatitis in the pig.
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PMID:Increased parathyroid hormone secretion and hypocalcemia in experimental pancreatitis: necessity for an intact thyroid gland. 114 41

We describe an adult patient who developed persistent hypercalcemia while bedridden for more than three months with pancreatitis and sepsis. On the basis of hypercalciuria, suppressed serum intact PTH, suppressed serum 1,25-dihydroxy vitamin D3 and no clinical evidence of malignancy, the diagnosis of immobilization hypercalcemia was established His hypercalcemia improved during treatment with saline, calcitonin and/or etidronate. With active mobilization and weight-bearing exercises, serum calcium finally normalized. We discuss clinical and laboratory features as well as current modalities of treatment of this rare form of hypercalcemia in adults.
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PMID:Immobilization hypercalcemia in an adult patient with pancreatitis and sepsis: case report. 148 89

Indirect evidence suggests a causative role for intraperitoneal free fatty acids (FFA) in hypocalcemia associated with pancreatitis. We examined the effects of intraperitoneal injection of four naturally occurring FFAs on serum calcium in rats. Two saturated FFAs, stearate and palmitate, induced little or no hypocalcemia. Two unsaturated FFAs, oleate and linoleate, caused dramatic hypocalcemia in treated versus control rats (6.3 +/- 1.4 and 5.3 +/- 0.7 mg/dl, respectively, versus 10.1 +/- 0.6). Dose-response studies demonstrated that minute quantities of oleate (100 microliters per 250 g rat) caused marked hypocalcemia (7.2 +/- 0.3 mg/dl). Treated versus control rats also revealed a decrease in ionized calcium (3.15 +/- 0.2 versus 5.6 +/- 0.05 mg/dl) and magnesium (1.4 +/- 0.15 versus 2.0 +/- 0.10), an appropriate increase in PTH levels (1670 +/- 451 versus 396 +/- 235 pg/ml), and a fall in calcitonin levels (70.4 +/- 21.3 versus 47.5 +/- 16.4 pg/ml) but no change in albumin or phosphate levels. In vitro, the Ksp of calcium dioleate was shown to be 5.3 x 10(-8) m3/liter3; thus under physiologic conditions 100 microliters oleate binds 7.2 mg calcium, or approximately twice the total ECF ionized calcium in the rat. The amounts of intraperitoneal FFA that can easily be achieved in pancreatitis complex pathophysiologically significant amounts of calcium and may lead to severe hypocalcemia.
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PMID:Intraperitoneal free fatty acids induce severe hypocalcemia in rats: a model for the hypocalcemia of pancreatitis. 207 38


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