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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Case records from 21 dogs with hypercalcemia and hyperparathyroidism were evaluated. The dogs were greater than or equal to 7 years old, and 6 were Keeshonds. The most common clinical signs were polydipsia/polyuria, listlessness, and muscle weakness. The serum calcium concentrations were 12.1 to 19.6 mg/dl. Serum phosphorus concentrations were low in 5 dogs, within the reference range in 13 dogs, and high in 3 dogs that also had high concentrations of BUN. Twenty dogs had a parathyroid adenoma, and 1 had a parathyroid carcinoma. Nineteen dogs had their parathyroid tumor surgically removed. Within 5 days of tumor removal, 11 of the 19 dogs became hypocalcemic and the remaining 8, normocalcemic. Nine of the 11 hypocalcemic dogs developed clinical signs. Iatrogenic hypercalcemia was induced in 7 of 16 dogs treated orally with calcium carbonate plus vitamin D. Only 1 of 19 dogs that had their parathyroid tumor excised died in hypocalcemic tetany. Two additional dogs died within 2 weeks of surgery, one because of pancreatitis, the other due to renal failure. Eight dogs died 9 to 37 months after surgery of unrelated problems. Eight dogs were alive for at least 7 to 28 months after surgery.
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PMID:Primary hyperparathyroidism in dogs: 21 cases (1976-1986). 365 3

Side effects of carbamazepine (CBZ), valproate (VPA) and clonazepam (CZP) are rare during long-term use but rather common and usually transient during the early phases of treatment. The usual side effects of CBZ are drowsiness, dizziness, and diplopia, which are dose dependent in long-term use, but CBZ does not seem to cause cognitive disturbances, as do phenobarbital and phenytoin. Other reactions to CBZ may include leukopenia, hyponatremia, disturbances of vitamin D metabolism and fortunately rarely, agranulocytosis and hepatitis. Use of VPA can lead to gastrointestinal discomfort, weight gain, hair loss, tremor and sedation, but these side effects are rather uncommon, mild, and transient during VPA monotherapy. Potentially hazardous reactions such as hepatitis and pancreatitis have occurred in a few patients on VPA, generally with multidrug therapy. Some of the side effects are dose related. They infrequently lead to withdrawal of VPA. Side effects limited to initiation of CZP therapy include drowsiness, ataxia, and behavioral changes; they are usually transient but can lead to dose reduction or even withdrawal of the drug. Except for development of tolerance, CZP seems to be practically free of long-term side effects.
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PMID:Side effects of carbamazepine, valproate and clonazepam during long-term treatment of epilepsy. 642 98

A 22-year-old woman with chronic calcific pancreatitis had dramatic relief of pain after pancreaticojejunostomy. Four years later, she presented with steatorrhea with osteomalacia and secondary hyperparathyroidism, a rare occurrence in chronic pancreatitis. She improved with pancreatic enzyme supplementation and calcium and vitamin D therapy.
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PMID:Chronic calcific pancreatitis associated with osteomalacia and secondary hyperparathyroidism. 891 80

We report a 12-year-old boy receiving long-term peritoneal dialysis who developed marked hypercalcemia and pancreatitis. Hypercalcemia was successfully treated by conducting dialysis with non-calcium-containing dialysate fluid. Factors predisposing to the development of hypercalcemia included the presence of adynamic bone disease and the use of vitamin D and calcium carbonate therapy. This case is presented to emphasize potential complications that can be associated with the adynamic bone lesion in patients on peritoneal dialysis.
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PMID:Hypercalcemia and pancreatitis in a child with adynamic bone disease. 909 Jun 72

The hallmark of acute hypocalcemia (ionized calcium <0.75 mmol/l) is tetany, which is characterized by neuromuscular irritability. The symptoms may be mild with circumoral numbness, paresthesias of hands and feet, and muscular cramps or severe with laryngospasm, focal or generalized tonic muscle cramps, or seizures. Myocardial dysfunction and prolongation of QT interval also may occur. Most often, acute hypocalcemia occurs after thyroid or parathyroid surgery. Rarer cases are intravascular binding of ionized calcium by phosphate, citrate, or drugs such as foscarnet or bisphosphonates. The most appropriate treatment is intravenous calcium, in the form of 100-200 mg of elemental calcium. Thereafter, the therapy depends on the underlying disease. In most cases vitamin D has to be added to calcium substitution. In cases of hypomagnesemia, magnesium and not calcium has to be substituted. It has not yet been proven in clinical trials whether substitution of magnesium and/or calcium influences the clinical outcome in patients with severe sepsis or pancreatitis who show both hypomagnesemia and hypocalcemia.
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PMID:[Tetany]. 1468 85

Chronic pancreatitis is a longlasting inflammatory disease manifested clinically in the advanced stage by malabsorption syndrome. Its manifestations include also changes in the calcium metabolism and the occurrence of osteoporosis and osteomalacia or their combination. The objective of the study was to assess the vitamin D3 blood concentration in patients with chronic pancreatitis. The group comprised 15 patients (8 men and 7 women), median age 45.0 years. The authors found a significantly reduced serum concentration of vitamin D3 (p < 0.01) in patients with chronic pancreatitis. They assume that vitamin D deficiency is one of the decisive causes of bone complications in prolonged pancreatitis. Supplementation with vitamin D or its metabolites is then a necessary part of preventive and therapeutic provisions.
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PMID:[Vitamin D deficiency as one of the causes of bone changes in chronic pancreatitis]. 1564 Dec 50

The authors describe a 9-year-old girl with precursor-B acute lymphoblastic leukemia (ALL) who presented with dehydration and severe hypercalcemia. She had received oral vitamin D and calcium supplementation for 4 days, the last dose 48 hours prior to admission, and required pediatric intensive care unit (PICU) hospitalization for management of the hypercalcemia and safe initiation of induction chemotherapy. Her clinical course was complicated by pancreatitis, disseminated intravascular coagulation, pleural effusion, and focal seizures. Although the exact mechanism of hypercalcemia was not elucidated, it was likely related to the underlying ALL, without dismissing the prior vitamin D and calcium supplementation as a possible contributing factor. The hypercalcemia resolved with specific antileukemic therapy along with supportive care and administration of calcitonin. Hypercalcemia is an uncommon metabolic abnormality in children with ALL, but it can be life-threatening. Children with ALL should be referred to tertiary-care institutions with PICU and subspecialty support because serious metabolic and other complications can occur before or after the administration of chemotherapy.
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PMID:Life-threatening hypercalcemia complicated by pancreatitis in a child with acute lymphoblastic leukemia. 1589 68

There is a high prevalence of protein-energy malnutrition (PEM) in chronic dialysis patients. Causes of PEM include the catabolic effects of hemodialysis treatments, acidemia associated with end-stage renal disease, common comorbid conditions, and uremia-induced anorexia. Morbidity and mortality increase with PEM. Before considering parenteral nutrition (PN) as a nutrition intervention in a maintenance dialysis patient, all other efforts to promote optimal nutrition need to be exhausted. The first step is careful evaluation of protein-energy status, followed by intensive nutrition counseling. If necessary, this is followed by oral nutrition supplementation, appetite stimulation, enteral tube feedings, and finally PN. Short-term parenteral nutrition (PN) became a crucial component of the management of a 38-year-old hemodialysis (HD) patient who endured serious complications after kidney transplant rejection. A profound and prolonged malnourished state followed her treatment for necrotizing pancreatitis. She had developed persistent hypercalcemia believed secondary to tertiary hyperparathyroidism (HPT) and immobilization. Later, she developed hungry bone syndrome (HBS) after parathyroidectomy (PTX). She also developed refeeding syndrome after initiation of PN. The patient's persistent, poorly understood hypercalcemia did not resolve even after PTX and removal of all other sources of vitamin D and calcium from her feedings, medications, and dialysis bath. The close communication of the inpatient and outpatient dialysis multidisciplinary teams became a key component to the successful outcome in this complex patient.
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PMID:The use of parenteral nutrition in a severely malnourished hemodialysis patient with hypercalcemia. 1620 98


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