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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

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

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

A 44 year old Japanese woman with adult T-cell leukaemia (ATL) was admitted to Kyushu University hospital to receive a course of alpha-interferon treatment. She experienced a sudden onset of hypercalcaemia and epigastric pain associated with an increase in the level of pancreatic enzymes. Her serum parathyroid hormone related protein level was above normal although her high sensitive PTH level was within the normal range. Ultrasonography and computed tomography (CT) of the abdomen showed enlargement of the pancreas with indistinct margins and massive accumulation of extrapancreatic fluid. Cullen's sign was observed. A few days after the onset of acute pancreatitis, the serum amylase level increased to 3400 IU/L, and the serum calcium level fell to 4.2 mg/dL from 13.3 mg/dl. Her fasting blood glucose level increased to 242 mg/dL. Although the first episode of pancreatitis appeared to respond to treatment, she experienced a second episode of pancreatitis accompanied by an elevation of the serum calcium level. These findings suggest that acute pancreatitis was caused by hypercalcaemia associated with ATL.
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PMID:Acute pancreatitis induced by hypercalcaemia associated with adult T-cell leukaemia: a case report. 867 68

We present a case of severe acute pancreatitis in a 14-year-old boy that may have been caused by hyperparathyroidism. The clue to finding the parathyroid adenoma was the hypercalcaemia. Although the patient did have acute pancreatitis, no therapy had been effective until the discovery of the parathyroid adenoma. After the excision of the parathyroid adenoma, the function of the pancreas and serum calcium returned to normal. This result suggests a certain cause and effect relationship between hyperparathyroidism and acute pancreatitis.
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PMID:Severe acute pancreatitis as a first symptom of primary hyperparathyroid adenoma: a case report. 876 89

Malignant hypercalcemia is seldom the cause of an acute pancreatitis; this complication is more frequent when hypercalcemia is due to hyperparathyroidism. We present a case of acute pancreatitis triggered by a malignant hypercalcemia as the first sign of the neoplastic process. Solid tumors with bone extension can produce hypercalcemia and may be the origin of hypercalcemic pancreatitis.
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PMID:[Pancreatitis caused by hypercalcemia of malignant origin]. 896 82

Several adverse effects have been reported to occur after clinical application of all-trans retinoic acid (RA) in acute promyelocytic leukemia (APL). Except for severe side effects including retinoic acid syndrome, the mechanism of action of RA on adverse effects remains unclear. Here we describe some rare adverse effects and their management. We reviewed the English literature, and we added our cases of endocrine and metabolic adverse effects, such as hypercalcemia, male infertility, bone marrow necrosis, fibrosis and acute pancreatitis. We also described our cases of thromboembolic events, RA-dependent growth of pathologic cells including Sweet's syndrome, erythema nodosum, hyperhistaminemia, granulomatous proliferation, and mild cases of pulmonary complications. In addition, we reviewed the efficacy of RA administration for other types of leukemia or myelodysplastic syndrome. RA and chemotherapeutic agents might induce complete remission, but we obtained a response in only one case of M2 in the third relapse. During RA administration the patient should be monitored for these adverse effects, and early diagnosis and appropriate treatment are important.
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PMID:Rare but important adverse effects of all-trans retinoic acid in acute promyelocytic leukemia and their management. 922 Jun 56


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