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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

Pancreatitis has been described previously following renal transplantation, but not in association with chronic renal failure. Analysis of 168 patients with renal transplants revealed five who developed pancreatitis, three of whom died. All five were on treatment with prednisone and azathioprine. Four patients were seen with definite attacks of pancreatitis and chronic, stable renal failure from a variety of causes. None had received immunosuppressive agents, prednisone nor thiazide diuretics, but two were on regular frusemide. One patient was on maintenance dialysis, which could not be related directly to the pancreatitis. In either group alcohol ingestion, cholethiathiasis, or hypercalcaemia was not a factor. This diagnosis of pancreatitis was established on clinical grounds and serum amylast levels of greater than 900 iu/1. Similar serum amylast elevation was not found ina random group of patients with chronic renal failure. Hyperlipidaemia was not present in any patient with pancreatitis. Although hypercalcaemia and primary hyperparathyroidism was not found in the transplant and non-transplant subjects, elevated serum parathormone levels have been described in uraemic patients with normocalcaemia. Hyperparathyroidism may be a factor in the development of pancreatitis in reanl failure. Pancreatitis carries a significant mortality risk in renal transplantation. The four non-transplanted patients have survived, despite recurrent attacks of pancreatitis.
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PMID:Pancreatitis and renal disease. 31 21

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

Although parathormone primarily determines normal ionized serum calcium concentration [Ca++] over the long term, it has little impact in the acute situation. Nonhormonal changes in [Ca++] have been related to acute changes in serum pH, but these have been believed small. With use of an experimental model of acute pancreatitis, we measured changes in [Ca++] and related them to changes in other serum constituents known to affect it. All 18 animals studied experienced a decrease in total serum calcium concentration [CaT]. Changes in [CaT] correlated only with changes in protein-bound calcium concentration [CaP] (r = 0.98, p less than or equal to 0.0005). They did not correlate independently with changes in albumin, globulin, or total protein concentration. [CaP] varied as a function of albumin, globulin, and phosphate concentration and pH according to the equation: [CaP] = 17.9 +/- 0.89 [albumin] = 0.68 [globulin] - 2.5 pH + 0.12 [phosphate]. Calculated values for [CaP], when this equation was used, correlated strongly with observed values for [CaP] (r = 0.81, p less than or equal to 0.0005). Measured [Ca++] increased in the animals early during pancreatitis and then returned to baseline levels. A few animals experienced ionized hypocalcemia. [Ca++] correlated only with changes in pH (r = 0.87, p less than or equal to 0.02). The calculated response slope was delta [Ca++]/delta pH = -2.9. It is concluded that pH has a greater effect on [Ca++] than previously recognized. The major determinant of [CaT] during periods of rapid physiologic change appears to be [CaP] while that for [Ca++] is pH.
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PMID:The role of pH in altering serum ionized calcium concentration. 340 67

Pancreatitis is accepted as an uncommon complication of parathyroid surgery, but it has been suggested that up to 35% of patients may experience hyperamylasaemia after parathyroidectomy indicating subclinical inflammation of the pancreas. A series of 26 patients undergoing parathyroidectomy were studied by preoperative biochemical analyses repeated 24 and 48 h postoperatively allowing changes in calcium metabolism and serum and urinary amylase levels to be documented. Of the patients, 21 also underwent a CT scan of the pancreas between 24 and 48 h after operation. Despite highly significant changes in serum parathormone, calcium and phosphate levels postoperatively, there was no evidence in any patient of acute pancreatic inflammation or hyperamylasaemia. Twenty-one patients underwent unilateral neck exploration, and we suggest that the absence of any detectable amylase elevation supports the suggestion that such elevation may reflect an increase in salivary isoamylase as a result of extensive neck dissection, rather than reflecting a subclinical pancreatitis. The development of postparathyroidectomy pancreatitis appears to be an all or nothing phenomenon of unknown aetiology.
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PMID:Does subclinical pancreatic inflammation occur after parathyroidectomy? 754 Aug 15

Pancreatitis occurred in 13 (5.6%) of 234 patients (76 men, 158 women; mean age 63 [2-83] years) who were operated on for primary hyperparathyroidism (pHPT) between 1987 and 1992. The pancreatitis patients had a significantly higher median level of parathormone (340 pg/ml), of serum calcium (3.2 mmol/l) and of thyroid weight (1.7 g) than the remaining 221 patients (135 pg/ml; 2.9 mmol/l; 1.0 g, respectively: P < 0.05 for each). In ten patients pHPT had been diagnosed during an attack of pancreatitis: pancreatitis had been the diagnostic clue to pHPT. After conservative treatment of the pancreatitis and parathyroidectomy seven of the ten patients were free of symptoms during the follow-up. In one patient pancreatitis recurred postoperatively and two patients died of the consequences of haemorrhagic necrotizing pancreatitis. Cholelithiasis, as another possible causative factor for pancreatitis, was present in five of the 13 patients (38%). None of the patients was an alcoholic. These data indicate that there is a positive correlation between advanced pHPT and pancreatitis. Pancreatitis may be the expression of much advanced hyperparathyroidism which has been diagnosed too late.
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PMID:[Pancreatitis in primary hyperparathyroidism (pHPT) is a complication of advanced pHPT]. 819 41

Cope showed in 1957 that pancreatitis may be the presenting symptom in hyperparathyroidism. Since then, the literature has reported a coincidence of primary hyperparathyroidism and pancreatitis between 1% and 19%, but the true relationship has not been fully established. When severe pancreatitis follows parathyroidectomy, a condition familiar to parathyroid surgeons, reports are mostly anecdotal and by many authors considered to be coincidental. We present the case history of a 58-year-old man with a longstanding history of untreated primary hyperparathyroidism who developed severe pancreatitis immediately after removal of a 400-mg parathyroid adenoma. He was the first in a series of 108 operated patients to develop this complication. His preoperative levels of parathormone and serum calcium were the highest in our material. We believe that pancreatitis after parathyroidectomy is a real but rare complication that might be predicted by preoperative high values of serum calcium and parathormone.
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PMID:Severe pancreatitis after parathyroidectomy. 1083 Dec 71

The purpose of this investigation is to study the state of Ca regulation mechanism at chronic alcohol pancreatitis and to compare with the activity changes of pancreatic lipase and its inhibitor at this disease. Content of Ca and regulating hormones (parathormone and calcitonin), activity of pancreas lipase and inhibitory blood ability in connection with it were determined in 30 patients with chronic alcohol pancreatitis without complications and in 20 persons with complicated disease course. Ca blood content fluctuates within normal level. But the median Ca contents in the group of patients with complications were significantly higher than in the control group. No changes in the level of pathormones and the increased Ca content were observed in the blood of the patients. The direct correlation between Ca and calcitonin and inverse correlation between Ca and parathormone were kept. According to correlation analysis of definite indexes the regulatory mechanisms of Ca metabolism in patients were intact. The increased calcitonin blood content in patients with chronic alcohol pancreatitis has apparently a compensatory character. This fact is confirmed by direct correlation with inhibitory ability of blood with respect to lipase.
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PMID:[Hormonal regulation of calcium metabolism in chronic alcoholic pancreatitis]. 1227 90

Pancreatitis due to hypercalcemia is very rare in children, and its pathogenetic role is still debated. The following report describes a case of acute pancreatitis secondary to hypercalcemia in a 6-year-old boy with pseudohypoparathyroidism treated with calcium and vitamin D. Pseudohypoparathyroidism is characterized by parathormone (PTH) resistance, high PTH levels and hypocalcemia which need to be corrected with calcium and vitamin D supplementation. The patient was admitted for severe abdominal pain and vomiting associated with high plasma amylase, lipase and calcium levels. Hypercalcemia due to vitamin D and calcium overtreatment was probably responsible for the acute pancreatitis in this case. High serum calcium levels seem to sensitize patients to pancreatitis, even if the mechanism through which it happens is not completely understood. Moreover, the importance of concomitant predisposing factors, either acquired or especially genetic, needs to be further defined. Even though a rare occurance in childhood, hypercalcemia should be considered as a cause of pancreatitis and it should be examined together with the other etiologies that may contribute to the development of this disease.
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PMID:Iatrogenic acute pancreatitis due to hypercalcemia in a child with pseudohypoparathyroidism. 2393 39

A parathyroid adenoma present in an ectopic site, in the anterior mediastinum, is a rare cause of persistent hyperparathyroidism. Though its occurrence in the mediastinum is unusual, existence has been noted in literature for more than a century. We describe a case of a 35-year-old male presenting with complaints of pain abdomen, clinically diagnosed as acute necrotizing pancreatitis, with raised serum calcium. Patient received symptomatic treatment for the pancreatitis which subsided. However, high levels of serum calcium persisted. Suspecting hyperparathyroidism, ultrasound neck was done, revealing apical thoracic mass. CT scan of neck revealed a large heterogeneous enhancing mass in superior mediastinum. Fine Needle Aspiration (FNA) of the mass done endoscopically was confusing as it showed features suggestive of a cystic teratoma. However, persistently raised calcium levels along with raised parathormone warranted a Technetium - 99 (Tc-99m) sestamibi scan which revealed positive uptake involving right inferior parathyroid extending to superior mediastinum. The mass was surgically excised and it was diagnosed as a parathyroid adenoma. This case helps bring to light the necessity to consider ectopic parathyroid adenoma as an important differential diagnosis in mediastinal tumour with persistent hypercalcaemia, and as a cause of hyperparathyroidism.
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PMID:Ectopic Parathyroid Adenoma Presenting as a Mediastinal Mass. 2865 91


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