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

A case of acute pancreatitis associated with primary hyperparathyroidism is reported. There was none of usual causes of pancreatitis, which did not recur following the removal of a parathyroid adenoma. There are over one hundred of cases of acute or chronic pancreatitis associated with hyperparathyroidism in the literature, suggesting a causal relationship between the two entities. The pancreatic disease has been attributed either to the hypercalcemia or to the excess of circulating parathyroid hormone. However, some authors have recently questioned any link between these two diseases.
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PMID:[Acute pancreatitis associated with primary hyperparathyroidism]. 175 Oct 69

Hypercalcemia has been associated with acute pancreatitis clinically and in the experimental animal. We studied the pancreatic ultrastructure in acute experimental hypercalcemia. Anesthetized cats (Pentobarbital, 0.55 mg/kg) received Ca++ (Calcium-Gluconate: 0.6 mmol/kgh; n = 4), K+ (KCl: 1.1 mmol/kgh; n = 4) or NaCl (0.9%; n = 4) locally through retrograde infusion into the splenic artery. Biopsies for electron microscopy (EM) were taken at three hours. Eight cats received intravenous Ca++ (0.6 mmol/kgh, 0.3 mmol/kgh after three hours) or NaCl (0.9%) for 12 hours. Biopsies were collected in two animals in three-hour intervals, and in all animals at twelve hours. After local calcium infusion necrotizing pancreatitis was seen macroscopically in the body of the pancreas. Biopsies for EM showed acinar cell necrosis, hydrops of nuclei and mitochondria and needle-like precipitates in the cytoplasma in the center of calcium perfusion. Biopsies taken from the peripheral region of the macroscopically altered tissue revealed desorganisation of the acinar polarisation and the endoplasmic reticulum, with zymogen granules appearing in the basolateral cell-portion. After intravenous calcium administration no macroscopical changes were seen. In EM acinar cells showed dilatation and proliferation of the golgi apparatus and increased number of condensing vacuoles indicating stimulation. Again, disorganisation of acinar cell polarisation was present. Control animals treated with K+ or NaCl showed normal pancreatic ultrastructure. The morphological changes after calcium infusion indicate direct damage to the acinar cell. Our results suggest that hypercalcemia induced pancreatitis could originate in the acinar cell.
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PMID:[Electron microscopy of the exocrine pancreas in experimental acute hypercalcemia]. 186 39

Metolazone-induced acute pancreatitis and hypercalcemia are described in a 58-year-old woman with severe congestive cardiac failure. Her symptoms and laboratory abnormalities rapidly resolved upon discontinuation of metolazone. Both clinical and laboratory findings make other etiologies for the patient's pancreatitis extremely unlikely. The pathophysiology of thiazide-related hypercalcemia and pancreatitis is reviewed. To our knowledge, neither hypercalcemia nor the combination of acute pancreatitis with hypercalcemia has been reported previously in association with metolazone therapy, and the association of pancreatitis and metolazone has been noted previously only once.
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PMID:Case report: metolazone-associated hypercalcemia and acute pancreatitis. 192 34

Familial hypocalciuric hypercalcemia (FHH) or familial benign hypercalcemia is an autosomal dominant inherited disorder of calcium metabolism. It is characterized by lifelong asymptomatic hypercalcemia associated with a relative hypocalciuria and a tendency to hypermagnesemia. The biochemical features of this disorder are difficult to distinguish from mild primary hyperparathyroidism. Several patients have therefore been operated upon for hyperparathyroidism with no effect on calcium levels. The most important diagnostic criterion of FHH in a single individual is the demonstration of asymptomatic hypercalcemia in other family members including children. The pathophysiology of the disorder is unknown. A genetic defect of cellular calcium transport leading to a disturbed regulation of extracellular calcium by parathyroid glands and kidneys has been suggested. The hypercalcemia in this disorder is asymptomatic, usually without complications and does not require treatment. Partial parathyroidectomy has no effect on the hypercalcemia. However, it is important to diagnose this condition in order to avoid unnecessary neck explorations. Two complications have been described in some families: pancreatitis and neonatal primary hyperparathyroidism. The recommended management of these complications is total parathyroidectomy.
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PMID:[Familial hypercalciuric hypercalcemia]. 203 54

Chronic "idiopathic" pancreatitis (CP) in a 7 year-old-boy, whose father has suffered from CP, and whose former grandfather had suffered from pains possibly of pancreatic origin, led us suspect a hereditary etiology. An analysis, extended in a control fashion to the relatives of the healthy spouse of the affected grandfather, surprisingly revealed 2 more proven and 3 more suspected CP, giving the overall number of 8 affected members in this 35-member 3 generation kindred and revealed a maternal heredity instead of paternal heredity (which was first thought to be apparent). We therefore recommend that in a family suspected to suffer from hereditary CP (HCP), a screening should be extended to cover even the unaffected spouse's family--the present extended study revealed for 23 new members them to belong in an affected family. Without an extensive screening advises for family planning, alcohol consumption etc. can not be given. Plain abdominal X-ray accompanied with epigastric ultrasonographic are suitable for screening, which might be extended to every individual in smaller families, but may be safely restricted to the members ever suffered from epigastric pains in the case of a huge family. Pancreatic duct anomalies, hyperlipidaemia, hypercalcaemia, aminoaciduria or hyperimmunoglobulinaemia, all of which have been seen to accompany HCP, were not present in this family. Neither was any linkage found between the penetrance of HCP and ABO/Rh blood groups or HLA haplotypes.
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PMID:Screening a family for hereditary chronic pancreatitis. 226 97

The majority (about 75%) of patients who suffer from acute pancreatitis do so as a consequence of gallstones or alcohol abuse. The other 25% of patients often present difficult diagnostic problems. Over several years the author has accumulated a series of patients with remedial causes of pancreatitis. They include a group of congenital conditions such as pancreas divisum, choledochal cysts and congenital abnormalities of the pancreatic ductal system. Patients who have had pancreatitis and who have an intact gallbladder often have stones that are difficult to identify. Repeated attacks of pancreatitis in the absence of any other apparent cause justifies cholecystectomy, which will often identify the cause so that recurrence can be prevented. A group of nonanatomic causes are also known. They include hyperlipidemia, drugs and toxins, certain systemic illnesses such as systemic lupus erythematosus, pregnancy, hypercalcemia, hereditary causes and occasionally cancer. In his lecture the author reviews the various etiologies of acute pancreatitis and describes an algorithm that can be used when the diagnosis is difficult.
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PMID:Recurrent acute pancreatitis--rarely idiopathic: 1989 Du Pont lecture. 226 8

A case of a patient with pancreatitis and familial hypocalciuric hypercalcaemia is presented and the literature linking FHH and pancreatitis is reviewed. The case for a causal link between the two conditions is not proven and seems unlikely. In view of this we strongly challenge the recommendation of total parathyroidectomy in such cases.
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PMID:Familial hypocalciuric hypercalcaemia and pancreatitis: no causal link proven. 228 90

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


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