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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

A patient with acute pancreatitis developed subcutaneous fat necrosis of the anterior abdominal wall secondary to leakage of pancreatic enzymes through a rent in the peritoneum following paracentesis. The same patient also had another subcutaneous complication of pancreatitis, namely, nodular liquifying panniculitis of the lower extremities. The diagnosis was made by the typical histological findings of subcutaneous fat necrosis, foci of necrotic cells with a "ghost-like" appearance, and basophilic-staining calcium soaps deposited around the necrotic cells.
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PMID:Subcutaneous fat necrosis after paracentesis: Report of a case in a patient with acute pancreatitis. 13 3

States of hypersecretion of PTH may occur primarily, or in response to other physiologic abnormalities. Primary hyperparathyroidism must be considered in the differential diagnosis of hypercalcemia, nephrolithiasis, metabolic bone disease, and pancreatitis and peptic-ulcer disease. The clinical manifestations of this disease have become more subtle with improved detection. The serum calcium level is almost always elevated, and when it it accompanied by relatively high serum PTH levels or increased urinary cAMP excretion, the diagnosis is usually secure. Findings of hypophosphatemia, decreased renal tubular reabsorption of phosphorus, hypercalciuria, and characteristic roentgenographic changes support the diagnosis of hyperparathyroidism, but are not prerequisites for that diagnosis. Most cases will come to operation, and experienced intraoperative assessment is necessary for the correct distinction between multiglandular disease and that involving only a single gland. We expect that a clearer understanding of the histopathologic features of these diseases, and improvement in the methods for measurement of PTH will be the main areas of advancement in the diagnosis of hyperparathyroidism in the next few years.
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PMID:Diagnosis of hyperparathyroidism. 19 30

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

Studies of coagulation were performed prospectively in 41 patients with mild to moderately severe acute pancreatitis. Six patients (15%) presented with coagulation data suggestive of defibrination; two of them had clinical signs of bleeding. No other cause than pancreatitis was found in these 6 patients to account for coagulation abnormalities. Comparing the patients who presented defibrination to those who did not, no difference was observed in clinical course and admission values of serum amylase, fibrinogen, urea, calcium, glucose, transaminase levels, white blood cell count and arterial partial pressure of oxygen. Platelets counts and serum creatinine levels were respectively lower and higher in the first group of patients.
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PMID:[Defibrination syndrome during acute pancreatitis: 6 cases. Prospective studies of coagulation in 41 patients (author's transl)]. 46 Nov 54

Sweat electrolytes were carried out in 84 adult patients with calcific pancreatitis, 51 with noncalcific pancreatitis, and the results compared to 37 adult controls. Of the patients with calcific pancreatitis, 33.5% had sweat sodium levels greater than 90 mEq/liter and 14.4% a level greater that 120 mEq/liter. Patients with noncalcific pancreatitis also had a high incidence of elevated sweat sodium levels. Sweat potassium levels were less discriminating, and there appeared to be high sweat calcium levels in a few patients so tested. The reasons for the elevated sweat sodium levels in pancreatitis is not readily apparent, and the possible relationship to heterozygous forms of cystic fibrosis is discussed.
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PMID:Sweat electrolytes in chronic pancreatitis. 62 82

Total protein, alpha1-antitrypsin, alpha2-macroglobulin, amylase, methemalbumin, tryptic amidase activity, radioimmunoassayable elastase 2, and three lysosomal hydrolases were determined in the ascites fluid from patients with acute pancreatitis. In eight patients methemalbumin was detected in ascites and serum, supporting the diagnosis of hemorrhagic pancreatitis. Significant levels (4-45 microgram/ml) of tryptic amidase activity were detected in ascites samples from all patients. Evidence is presented which demonstrates that the tryptic amidase activity is due to alpha2-macroglobulin-bound trypsin. Pancreatic elastase 2, determined with a new sensitive and specific radioimmunoassay, ranged from 400 to 2100 ng/ml in serum and from 650 to 4460 ng/ml in ascites fluid. Substantial amounts of alpha2-macroglobulin-bound trypsin and elastase 2, entering the circulation from the peritoneal cavity, might be responsible for certain serious complications seen in acute pancreatitis. However, with the exception of serum calcium and methemalbumin and the ascites fluid methemalbumin and total protein, none of the biochemical parameters studied showed a distinct correlation with the patient's outcome.
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PMID:Studies on the ascites fluid of acute pancreatitis in man. 62 83

We report on eight cases of parathyroid carcinoma seen at the Bowman Gray School of Medicine, Winston-Salem, NC, since 1969. Diagnosis of a parathyroid disorder was made on the basis of elevated serum calcium levels and associated disorders such as renal calculi, peptic ulcer disease, pancreatitis, and demineralization of bone. Six of the involved glands were on the left side. In seven patients, the disease was localized to the gland or adjacent structures; one patient had cervical lymph node invasion. Except for the last patient, in whom radical neck dissection and wide excision was done, local excision with adequate margins was the only procedure done. The patient with metastases died of his disease four years later. One patient died of myocardial infarction two years later, but had been normocalcemic in the interval between operation and death, and one patient is hypercalcemic and has had two local recurrences within a 3 1/2 year period. The other five patients are alive and well. The routine use of automated serum level determinations of all hospitalized patients has led to early detection of this malignancy, while it is still a stage I lesion in many instances. On the basis of this material, we conclude that radical neck dissection can no longer be advocated as a routine measure in the treatment of parathyroid carcinoma.
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PMID:Carcinoma of the parathyroid. 62 71

A retrospective and prospective study was made of 82 attacks of acute pancreatitis occurring in 80 patients. Attacks were defined as mild (55) or severe (27) according to clinical criteria. Severe attacks were associated with significantly low levels of uncorrected calcium and calculated ionized calcium, both at the time of admission and 48 h later. Patients with severe attacks were found to have lower levels of parathyroid hormone than either those with mild attacks or other patients who had undergone an abdominal operation. These results indicate that severe pancreatitis is associated with true hypocalcaemia, and that deficiency of circulating parathyroid hormone may be a factor in its production.
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PMID:The nature of hypocalcaemia in acute pancreatitis. 63 40

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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