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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypercalcemia causes acute pancreatitis in humans, a phenomenon reproduced experimentally in cats and guinea pigs. Because the rat is the most frequently used animal for the study of experimental pancreatitis, the present studies were performed to evaluate the effects of hypercalcemia in the rat. In in vitro studies, pancreatic lobules were prepared from fasted Wistar rats (200-250 g) and incubated in HEPES bicarbonate-buffered medium (pH 7.4) containing 0, 0.6, 1.2, 2.5, 5, and 10 mM CaCl2 with or without carbachol 10(-6) M. Amylase was measured in the medium after 30 min to 3 h, and expressed as percent of total amylase. In in vivo studies, fasted male Wistar rats (300-400 g) received calcium (CaCl2; 0.6 mmol/kgh) into the tail vein for 12 h. Control animals received NaCl 0.9% infusion. Histologic slides (H&E-stained) were evaluated in a blinded fashion. Pancreatic lobules showed a higher basal amylase output when incubated in higher calcium medium. The largest, significant difference (2.6-fold) was between 0.6 and 5 mM medium CaCl2 (p < 0.05). Carbachol-stimulated amylase release was again higher with increasing medium calcium with the most pronounced difference (1.3-fold) between 0.6 and 2.5 mM CaCl2 (p < 0.05). In vivo calcium-treated animals showed accumulation of zymogen granules in the cytoplasm, cytoplasmic vacuolization, focal acinar cell depolarization, acinar necrosis, and edema. Calcium causes amylase release from rat pancreatic lobules in vitro. Higher medium calcium levels both significantly increase amylase release from unstimulated and carbachol stimulated lobules. Twelve-hour in vivo calcium infusion leads to accumulation of zymogen granules in acinar cells and acinar injury.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A rat model to study hypercalcemia-induced acute pancreatitis. 752 Sep 26

A 67-year-old man was hospitalized with the chief complaint of diffuse abdominal pain for 3 days. Hypercalcemia and acute pancreatitis was found by laboratory examination. Abdominal CT scans showed swelling of the pancreas, multiple liver tumors and osteolytic lesions of bone. Upper mediastinal lobulated mass was suspected from chest x-ray examination, then small cell lung cancer (SCLC) was proved by bronchoscopic and pathological examination. The final diagnosis is SCLC with liver and bone metastasis associated with hypercalcemia and acute pancreatitis. After pancreatitis subsided, the patient was put on chemotherapy. Unfortunately, due to immunocompromise, he died of pneumonia and sepsis. There was no reasonable explanation regarding to the cause of acute pancreatitis except hypercalcemia, which might be due to SCLC with bone metastasis. This is the first report of such a complication in a patient with SCLC.
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PMID:[Small cell lung cancer with liver and bone metastasis associated with hypercalcemia and acute pancreatitis--a case report]. 764 Nov 15

A totally thyroidectomized patient with thyroid and parathyroid carcinomas, which had developed after neck irradiation in childhood, became hypercalcemic due to pulmonary metastases. The hypercalcemia was ameliorated by intermittent iv administration of bisphosphonate for 3.5 years, but this gradually became refractory to the bisphosphonate treatment. After right thoracotomy for resection of pulmonary metastases, acute necrotizing pancreatitis developed. The patient was therefore placed on total parenteral nutrition supplemented with T4 and a restricted dose of magnesium. Thyroxine(T4) (30 micrograms/day, iv) was not sufficient to maintain euthyroidism, but a higher dose (60 micrograms/day) elicited mild hyperthyroidism to the same extent as that elicited by an oral dose of 100 micrograms/day. The present case showed that the appropriate iv dose of T4 in this thyroidectomized patient with acute pancreatitis was about 60% of the oral dose. Furthermore, bisphosphonates (pamidronate and alendronate) and magnesium depletion were very effective in controlling the hypercalcemia.
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PMID:Appropriate intravenous doses of L-thyroxine and magnesium in a thyroidectomized patient with thyroid and parathyroid carcinomas receiving total parenteral nutrition during acute necrotizing pancreatitis. 778 23

A patient with familial benign hypercalcaemia (FBH) who developed relapsing pancreatitis is presented. She underwent distal partial pancreas resection with surgical removal of pancreatic duct stones, and a pancreaticojejunostomy. No further causes for the pancreatitis were found. The present case is remarkable since it is an example of the occurrence of pancreatitis in a previously known patient with hypercalcaemia, and it underlines the severity of the pancreatitis when it occurs in this syndrome.
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PMID:Acute pancreatitis in a patient with familial benign hypercalcaemia. 796 63

Possible new indications for the use of octreotide are discussed. In October 1988, octreotide received FDA-approved labeling for use in the management of carcinoid syndrome and vipomas. Since that time, research results and clinical experience have accumulated that suggest a potentially much broader therapeutic role for octreotide. Reports continue to be published on the use of octreotide for treating pituitary tumors, gastroenteropancreatic tumors, diabetes mellitus, AIDS-associated diarrhea, autonomic neuropathy, pancreatitis, pancreatic pseudocysts and ascites, complications of pancreatic surgery and transplantation, ileostomy-associated diarrhea, enterocutaneous fistulas, pancreatic fistulas, dumping syndrome, short bowel syndrome, and gastrointestinal bleeding. Other emerging indications for the use of octreotide include psoriasis, hypercalcemia, cancer-related pain, polycystic ovary syndrome, and certain cancers. In children, octreotide has been studied for use in treating hyperinsulinemic hypoglycemia of infancy. Along with the common adverse effects of octreotide, such as pain at the injection site and nausea, less frequent effects, such as cholelithiasis, gallbladder hypercontractility, and gastritis have now been described. Much of what has been learned is based on small uncontrolled studies and case reports, since the rarity of many of the conditions for which octreotide has shown promise has tended to preclude larger studies. As clinical experience with octreotide accumulates and better-designed trials are completed where possible, a broader therapeutic role for octreotide is likely to be recognized.
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PMID:Emerging indications for octreotide therapy, Part 1. 804 37

The relation between hypercalcemia and pancreatitis, first described in patients with hyperparathyroidism, is controversial. Other causes of hypercalcemia also have been associated with pancreatitis. In this report, the authors describe a patient with pancreatitis and the milk-alkali syndrome who had the classic triad of hypercalcemia, alkalosis, and renal insufficiency. The authors also review the literature for all the reported cases of pancreatitis associated with hypercalcemia.
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PMID:Case report: milk-alkali syndrome and pancreatitis. 807 35

Acute pancreatitis in patients on CAPD treatment is an infrequent, but serious complication. We studied the records of all CAPD patients with acute pancreatitis in the Netherlands from 1979 until May 1992. The incidence of acute pancreatitis during CAPD treatment was 0.46 per 100 treatment-years. In all patients at least one risk factor was present. Hypercalcaemia was the most frequently observed risk factor in our patients. The clinical picture consisted of abdominal pain and vomiting, with normal temperature and normal peristalsis. Plasma amylase was elevated in 18 episodes. Dialysate amylase concentrations exceeded 100 U/l in seven of ten episodes. The dialysate could either be clear, haemorrhagic, or cloudy. Positive dialysate cultures were found in five patients, in most cases with skin flora. No direct correlation with the pancreatitis could be established. Mortality was 58%. Continuation of CAPD or transfer to haemodialysis had no apparent effect on the outcome, but the best prognosis was found in patients with a persistently clear dialysate.
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PMID:Acute pancreatitis during CAPD in The Netherlands. 815 8

Hyperparathyroidism is a rare cause of pancreatic inflammatory disease. Appropriate treatment of coexistent hyperparathyroidism and pancreatitis, especially when complicated by pseudocyst formation, is unsettled. We describe two patients with primary hyperparathyroidism who developed pancreatitis associated with multiple pseudocysts. The largest cyst in each patient was 9 and 5 cm, respectively. After correction of hyperparathyroidism and normalization of serum calcium levels by removal of a parathyroid adenoma, the pseudocysts resolved in both patients, as documented with computed tomography. We conclude that uncomplicated pancreatic pseudocysts in patients with primary hyperparathyroidism can be treated expectantly. Surgical correction of hyperparathyroidism and normalization of serum calcium levels should precede pancreatic intervention when possible, since pseudocyst resolution is likely and the risks of postoperative hypercalcemia are avoided.
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PMID:Pancreatic pseudocyst resolution after parathyroidectomy for hyperparathyroidism. 820 42

In a population of 716 patients with end-stage renal disease (ESRD), 46 patients (6.4%) were identified as having pancreatitis. Pancreatitis was significantly more common in those with alcohol abuse, systemic lupus erythematosus (SLE), and polycystic kidney disease. It was not significantly associated with hyperlipidemia, biliary tract disease, or hypercalcemia. Acute pancreatitis occurring before the patient developed ESRD was mainly alcohol-related and did not appear to be a significant risk factor for future episodes of pancreatitis during dialysis. Chronic calcific pancreatitis diagnosed before ESRD was almost invariably due to alcohol abuse, and tended to be a marker for recurrent acute exacerbation after development of ESRD, whether alcohol consumption continued or not. Pancreatitis occurring for the first time after ESRD in patients on dialysis was generally benign, and was usually accompanied by an uneventful recovery and few recurrent episodes. However, a significant elevation of the calcium x phosphate product was observed in these patients, occurring in about half the patients without any known precipitating factor. After kidney transplantation, the development of pancreatitis was associated with higher morbidity and mortality. Chronic calcific pancreatitis diagnosed after ESRD occurred only in patients with SLE; reported here for the first time, it may be a manifestation of long-standing disease, chronic steroid therapy, or both.
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PMID:Pancreatitis in patients with end-stage renal disease. 830 63

The association of hypercalcemia and acute pancreatitis had been experimentally reproduced in cats by local infusions of the divalent cation calcium whereas the monovalent cation potassium did not induce any pancreatic pathology. The purpose of the present study was therefore to investigate the role of further divalent cations in order to determine the relevance of ion valency for pancreatitis induction. Anesthetized male SIV-rats received divalent cations, of which a role in the pancreas had already been reported in the literature, through retrograde infusions into the splenic artery at a dose of 0.6 mmol/kgh for 3 hours and at a flow of 0.5-1.0 ml/h. The pancreas was then removed for morphologic studies. In the animals treated with calcium and manganese, pancreas showed a hemorrhagic necrosis of the acinar lobuli with leucocytic infiltrates. The barium treated animals spontaneously died after 49 +/- 15 minutes and revealed acute pancreatitis in the perfused, but not in the residual pancreas. Zinc at the initial dose induced an immediate heparin-refractory blood-clotting with subsequent ischemic necrosis whereas a lower dosis (0.002 mmol/kgh) led to an acute pancreatitis as seen after calcium. The magnesium treated animals and the controls did not reveal any pathology. We conclude that some divalent cations may induce an acute pancreatitis, but that the induction is not dependent on the cation valency.
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PMID:[Acute pancreatitis after local infusion of divalent cations]. 837 61


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