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

The increasing detection of asymptomatic hypercalcaemic patients by biochemical screening has led to an increase in the number of patients referred for neck exploration. Familial Hypocalciuric Hypercalcaemia (FHH) has emerged as an important condition to distinguish from primary hyperparathyroidism as a cause of hypercalcaemia. Patients with FHH are usually asymptomatic, have similar biochemical findings to primary hyperparathyroidism, but fail to respond to parathyroid surgery. We have studied 15 members of a large kindred with FHH. The initial diagnosis was made in the propositus after a failed neck exploration for presumed primary hyperparathyroidism. Of the 7 affected members, 2 had recurrent acute pancreatitis and 2 had incidental malignant disease with no evidence of bony involvement. Measurement of the calcium: creatinine clearance ratio provides a good method of identifying hypercalcaemic patients who might have FHH. A ratio of less than 0.013 is an indication to screen first-degree relatives before considering neck exploration.
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PMID:The importance of distinguishing familial hypocalciuric hypercalcaemia from asymptomatic primary hyperparathyroidism prior to neck exploration. 235 Aug 91

The incidence and possible etiologic factors of acute pancreatitis and hyperamylasemia were statistically evaluated in renal transplant recipients. Two hundred twenty-four patients were randomized in a prospective trial of cyclosporine and antilymphoblast azathioprine immunosuppressive regimens. They had a median follow-up of 20 months. Pancreatitis developed in 8 patients and hyperamyl asemia developed in 20 patients. There were no statistical relationships between the incidences of pancreatitis and hyperamylasemia and the immunosuppressive drugs or viral infections. However, pancreatitis developed in 11 percent of the transplant patients with repeatedly elevated serum calcium levels (37 patients, p less than 0.01) and hyperamylasemia developed in 19 percent (p less than 0.025). Other etiologic factors, such as gallstones, alcoholism, and corticosteroids, played a minor role in this patient population. These results suggest that hypercalcemia is a major etiologic factor for pancreatitis in renal transplant recipients.
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PMID:Hypercalcemia associated with pancreatitis and hyperamylasemia in renal transplant recipients. Data from the Minnesota randomized trial of cyclosporine versus antilymphoblast azathioprine. 244 14

We investigated the effects of hypercalcemia on pancreatic duct permeability and pancreatitis in cats. Acute hypercalcemia was maintained by an infusion of calcium gluconate; controls received saline solution. Chronic hypercalcemia was maintained by diet and by vitamin D and dihydrotachysterol injections. Portal venous blood was analyzed for large dextran molecules that had been perfused through the pancreatic duct. In a separate group of hypercalcemic animals, we perfused the duct with activated pancreatic enzymes to induce acute pancreatitis. After 24 hours of hypercalcemia, dextrans were detected in the portal venous blood of 6 of 11 hypercalcemic and none of the 6 control animals (p less than 0.05). After 12 hours of hypercalcemia, dextrans were detected in all 7 hypercalcemic and 1 of 7 control animals (p less than 0.001). The degree of pancreatic inflammation was greater in the 12-hour animals than in the controls (p less than 0.001). After 14 days of hypercalcemia, however, there were no differences in dextran permeability or pancreatitis in experimental or control animals. Our results indicate that acute hypercalcemia increases the permeability of the pancreatic duct to molecules the size of pancreatic enzymes. This could be important in the pathogenesis of acute pancreatitis associated with hypercalcemic states.
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PMID:Acute hypercalcemia, pancreatic duct permeability, and pancreatitis in cats. 245 25

A 66-year-old patient had been admitted four times for recurrent episodes of acute pancreatitis. At each time, elevated serum calcium levels, between 13.5-14.5 mg/dl, were found. Surgical drainage of necrotic pancreatic tissue had to be done on one occasion. Extensive investigations failed to disclose any conventional hypercalcemic disease. At his latest admission, the serum calcium level was 13.4 mg/dl, and the serum amylase level was 440 IU/L (N, less than 85). This time, the serum 25-OH vitamin D levels were investigated using radioimmunology and proved to be raised to 330 micrograms/L (normal, 16-74 micrograms/L). Specific questioning of the patient revealed that he had been taking regularly excessive quantities of vitamin supplements as a self medication. After stopping vitamin intake, his serum amylase levels returned to normal, and he had no more episodes of pancreatitis. This case illustrates vitamin D intoxication as a cause of recurrent pancreatitis. Measuring serum 25-OH vitamin D levels is advocated in pancreatitis associated with hypercalcemia of unclear origin.
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PMID:Recurrent pancreatitis secondary to hypercalcemia following vitamin D poisoning. 247 70

Ten clinical episodes of acute pancreatitis (AP) occurred in six patients (mean age 10 years, range 3-15 years) with chronic renal failure (CRF) during a 9-year period (1977-1986). The underlying cause of CRF was vesicoureteral reflux (2); urethral valves (1); ureterohydronephrosis (1); nephronopthisis (1) and a haemolytic uraemic syndrome which occurred 12 years before (1). In all patients a diagnosis of AP was established both on clinical grounds and with a serum amylase level of greater than 600 IU/l. In 3 patients laparotomy was performed because of suspected appendicitis. All patients required exclusive parenteral feeding (mean duration 25 days) and 2 patients had a partial pancreatectomy. No patient developed pancreatic pseudocysts, 2 patients experienced one relapse (3 and 21 months later) and 1 patient had two relapses and died. Mean duration of follow up was 3 years (range 1-10 years). Possible aetiological factors were: choledochal cyst (1); parotitis without a rise in mumps antibodies (1); familial dyslipidaemia but without AP in other family members (1), and aluminium intoxication with hypercalcaemia and convulsive encephalopathy treated with valproic acid in 1 patient. Severe hyperparathyroidism with radiological signs was absent in all patients. Transplantation had been performed either before AP in 2 patients (1 and 3 years before AP) or had followed AP in 1 patient (7 years after) without occurrence or relapse of AP.
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PMID:Acute pancreatitis in six non-transplanted uraemic children. A co-operative study from the French Society of Paediatric Nephrology. 248 54

A patient with hypercalcemia and newly diagnosed multiple myeloma developed acute pancreatitis. Other etiologic factors for pancreatitis were excluded. Hypercalcemia secondary to hyperparathyroidism is associated with acute pancreatitis. In English literature, only one other case has been published where the hypercalcemia of multiple myeloma may have caused pancreatitis. Pancreatitis should be considered in patients with hypercalcemia and multiple myeloma who develop nausea/vomiting, and abdominal pain.
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PMID:Acute pancreatitis in a case of multiple myeloma with hypercalcemia. 248 50

A 55-year-old man who had liver metastasis after undergoing surgery for renal cancer was hospitalized immediately on May 4, 1987 with complaints of general malaise, epigastric pain, nausea and vomiting. Because of abnormally high levels of blood calcium 15.6 mg/dl and serum amylase 2,069 IU/l, the case was diagnosed as hypercalcemic crisis and acute pancreatitis. Following recovery from the critical stage with administration of elcatonin and FOY, therapy for cancer initiated. We report the clinical course of this patient and discuss about hypercalcemia and acute pancreatitis as cases of oncologic emergency.
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PMID:[A case of renal cancer complicated with acute hypercalcemia and acute pancreatitis]. 251 63

Hypercalcemia occurred in a patient with leiomyosarcoma when multiple lung metastases developed. Despite normal plasma parathyroid hormone (PTH) levels and low 1,25-dihydroxyvitamin D, this hypercalcemic patient had a marked hypercalciuria and phosphaturia associated with an increased excretion of nephrogenous cyclic AMP (NcAMP). Administration of cisplatin ameliorated both the hypercalcemia and hypercalciuria without any reduction in tumor size of NcAMP excretion. Terminally, acute pancreatitis occurred producing a profound hypocalcemia. In the extract of tumor tissue obtained post mortem, bioactivity stimulating the generation of cyclic AMP in osteogenic cells was demonstrated along with the immunoreactive PTH-related protein (PTH-rP). the first report of a solid non-epithelial malignancy producing PTH-rP and associated with humoral hypercalcemia of malignancy. The hypercalcemia in this case caused acute pancreatitis, which led to a profound hypocalcemia.
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PMID:A case of leiomyosarcoma associated with humoral hypercalcemia of malignancy: demonstration of biological and immunological activities of parathyroid hormone-related protein in the tumor extract. 255 69

Medical emergencies due to severe hypercalcaemia and hypocalcaemia are relatively rare in clinical practice. 89 cases of hypercalcaemia were seen during 1975-1987 and 16 presented as medical emergencies; renal colic (7) acute renal failure (3), spontaneous fractures (3), acute pancreatitis (1), cardiac arrhythmia (1) and acute hypercalcaemic crisis resulting in death (1). 81 cases of severe hypocalcaemia were seen during the same period. 22 presented initially as epileptic seizures with one ending fatally due to status epilepticus. The other emergencies were severe laryngeal stridor and inability to speak (7), papilloedema (3) and acute behavioural disorder (4). A few illustrative cases have been briefly described.
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PMID:Medical emergencies associated with disorders of calcium homeostasis. 229 66

A 12-year-old girl was admitted to our hospital with signs of an acute abdomen with paralytic ileus. The previous and family history were without abnormalities. Abdominal pain and vomiting had started two days earlier. On palpation the swollen abdomen was painful and there was an increased tension in the left upper part. The clinical diagnosis of acute pancreatitis was confirmed by an increased serum level of lipase (4480 U/l). Clinical chemical investigations further revealed a permanent hypercalcemia in the range of 6.4 to 8.3 mval/l. This, together with concomitantly reduced levels of serum phosphate and a threefold increased level of parathyroid hormone (343 pg/ml, upper limit of reference = 100 pg/ml) were consistent with a hyperparathyroidism. In fact, sonography of the cervical organs revealed a solitary adenoma of the parathyroid glands. After surgery serum levels of calcium returned to normal. Hypercalcemia as a consequence of primary hyperparathyroidism has to be included in the differential diagnosis of acute pancreatitis in childhood.
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PMID:[Acute pancreatitis as an initial manifestation of hypercalcemia in primary hyperparathyroidism in childhood]. 265 77


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