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

Pharmacologic doses of triamcinolone hexacetonide were injected intramuscularly or intraarticularly in immature Papio papio baboons. The mandibular condyle served as a model for histologic examinations concerning the effect of glucocorticoid hormone on cartilage and bone. Biochemical examinations of blood and urine indicated the development of distinct hypophosphatemia, hypercalcemia followed by hyperphosphaturia, and hypocalciuria. Serum alkaline phosphatase activity rose during the initial phases of the experiment but decreased considerably after the sixth injection of the hormone. Hyperglycemia and an increase in serum amylase were noticed along with signs of moderate metabolic acidosis. Histologic examinations disclosed signs of severe destruction of cartilage and bone. By the sixth intraarticular injection, definite fibrillation was noted in the articular cartilage, followed by complete disappearance of cartilage. The subchondral bone appeared to be adversely affected by the hormone as it lost its typical lamellar organization and attained the characteristics of woven bone. The condyle showed clear signs of fibro-osseous transformation, with fibrosis as the dominant structural feature. The preceding biochemical and morphologic findings are indicative of parathyroid hyperactivity.
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PMID:Mechanisms involved in mandibular condylopathy secondary to intraarticular injections of glucocorticoids. 41 94

The effect of local and systemic calcium administration was tested on the pancreas of cat and guinea pig. After 3 h of local calcium infusion (0.6 mmol/kg x h) via the splenic artery of the cat hemorrhagic pancreatitis could be shown. Control animals treated with potassium (1.1 mmol/kg x h) or 0.9% NaCl alone showed no morphological change in the pancreas. Intravenous administration of calcium (0.6 mmol/kg x h) led to a 1.8-fold increase in serum ionized calcium levels in the cat and a 1.6-fold increase in levels in the guinea pig. The cat showed necrosis of acinar and ductal cells throughout the gland at 12 h. In the guinea pig, acinar cell vacuolisation and cell necrosis started at 3 h, and at 9 h degeneration of entire acini, hydropic swelling and degeneration of ductal cells, and perivascular leukocytic infiltration was present. In both species, a significant increase in the number of intraductal precipitates and a significant increase in urinary amylase output was present in calcium treated animals. The findings suggest that hypercalcemia has a deleterious effect on the pancreas that causes acinar and ductal cell necrosis and eventually pancreatitis.
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PMID:Acute hypercalcemia induces acinar cell necrosis and intraductal protein precipitates in the pancreas of cats and guinea pigs. 198 43

In this problem-oriented review of abnormalities associated with cancer, we have emphasized distinctive diagnostic points related to pathogenesis for each condition and outlined how the approach to management is determined by pathogenesis. For abnormalities of the complete blood count, it is important to distinguish between abnormalities directly related to marrow malignancy and abnormalities associated with extramarrow malignancy. Hemopoietic tumors consist of developmentally deficient blood cells produced by a clonal population of malignant stem cells. Tumors infiltrating marrow cause overcrowding in the limited marrow microenviroment. Extramarrow malignancies cause blood abnormalities, but the potential for normal marrow function is present. Abnormalities of blood cells secondary to therapy are usually clearly identified by consideration of clinical history. The initial differential diagnosis for hypercalcemia is malignancy. An aggressive diagnostic approach may be needed to identify the neoplasm, and therapy should incorporate measures to prevent renal failure. Hypoproteinemia and hyperproteinemia may be caused by neoplasia. Monoclonal gammopathies should be identified and may be associated with hyperviscosity syndrome. Hypoglycemia in the adult animal is most frequently caused by insulin-secreting tumors, but it has also been associated with hepatic and other tumors. Increased blood urea nitrogen, creatinine, lipase, amylase, and liver enzyme activities may also be caused by malignancy. Inadequate urine concentrating ability may be caused by hypercalcemia or malignancy-associated renal insufficiency. Hematuria in older animals is suggestive of urinary tract neoplasia. Exfoliated tumor cells may be identified in the urine sediment of these patients.
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PMID:Laboratory abnormalities in patients with cancer. 219 37

Total amylase activity in serum and urine is formed by pancreatic (P) and salivary (S) isoenzymes. The evaluation of isoamylases provides better information on enzyme changes during the disease than total activities alone. The resolution of pancreatic from extrapancreatic origin of hyperamylasemia may be clinically important. The experience obtained from the analysis of isoamylases in more than 1500 patients with different clinical diagnoses we compare with a contemporary knowledge of disturbances in amylase activities. We developed a method separating quantitatively both isoamylases on the mini-columns of ion-exchanger which we used in routine clinical investigation. In the first section we selected the findings on physiology and biochemistry of isoamylases. We described for the first time a significant decrease of P-isoamylase activity in serum during the intravenous infusions of hypertonic glucose, amino acids and during acute hypercalcaemia. We suggested that hypertonic glucose, amino acids and calcium may regulate directly or indirectly the amylase flux from acinar cells in the pancreas across basolateral membrane into blood. This endocrine secretion of amylase may be important in different clinical conditions in which changes of neurohumoral and/or hormonal regulation are developed. The isoamylase activities in patients with different diagnosis are analyzed in the clinical section. The results may be correctly evaluated only in connection with the pathogenesis of isoamylase changes. Disorders of the organs producing amylase (i.e. pancreas or salivary glands) may induce changes of isoamylases depending on their functional status. A progressive loss of amylase producing cells may be accompanied by a decrease of enzyme activity in serum as was described in chronic pancreatitis with exocrine insufficiency. However, the amylase activity in serum is significantly influenced by clearance mechanisms, too. Disorders of the liver or kidneys are accompanied predominantly with hyperamylasemia caused by the disturbed clearance mechanisms. The amylase activity in serum is a consequence of the result between input and output of the enzyme within the blood stream. Some humoral and hormonal regulations are able to modulate both processes in vivo. We suppose that pathogenetic standpoint has the main role for correct interpretation of isoamylase activities. The pathogenesis of hyperamylasemia is therefore discussed in single chapters. In conclusion, the isoamylase activities in serum and urine are influenced beside genetic background by many factors in health and disease which may be respected during the evaluation of the results.
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PMID:Clinical significance of amylase isoenzyme determination. 244 82

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 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

The mechanism for acute hypercalcaemia increasing pancreatic enzyme secretion is unknown. To determine if raised extracellular calcium concentrations can directly stimulate pancreatic enzyme output, we measured discharges of pulse labelled protein and chymotrypsin from isolated cat pancreatic lobules in the presence of normal and raised calcium concentrations. Incubation in 5.0 mmol/l calcium increased discharges of pulse labelled protein (four fold), chymotrypsin (2.5 fold) and amylase (2.2 fold), compared with control experiments with 2.5 mmol/l calcium (p less than 0.001). This effect was similar to the maximal effect of carbachol or caerulein. Compared with 5.0 mmol/l calcium, incubation at the higher calcium concentration of 10.0 mmol/l induced similar discharges of chymotrypsin and amylase, whereas the increase in discharge of pulse labelled protein was smaller (p less than 0.01). The effects of raised calcium were not altered by atropine. Incubation in a high calcium medium did not impair pancreatic acinar response to subsequent stimulation with carbachol, but incubation in hypothermia abolished the effects of high calcium concentrations, suggesting that increased enzyme discharge is caused by stimulation of secretion not to cell damage. These data are consistent with a direct stimulatory effect of raised extracellular calcium concentrations on pancreatic acinar cell function.
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PMID:In vitro stimulation of pancreatic enzyme discharge by calcium. 367 49

While pancreatitis may provide the clue to the diagnosis of hyperparathyroidism preoperatively, the occurrence of pancreatitis following parathyroidectomy is not generally recognized. In this study preoperative and postoperative serum amylase estimations, together with a clinical assessment, were performed on 86 patients undergoing neck exploration for hyperparathyroidism. It was found that postoperative hyperamylasaemia occurred in 35% of the total group, while clinically significant pancreatitis was found in 9% of cases. Pancreatitis was significantly more common when thyroidectomy was performed at the time of parathyroidectomy, occurring in 23% of this group of patients, and may be due to the blunted C-cell response of calcitonin secretion to the induced hypercalcaemia associated with operative manipulation. Careful attention should be paid to postoperative abdominal symptoms, for they may indicate pancreatitis.
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PMID:Pancreatitis following parathyroid surgery. 617 21

The numerous physiological and nutritional factors which influence the concentration of serum calcium are considered. The causes of hypercalcaemia and hypocalcaemia are briefly discussed, with particular reference to the clinical symptoms and pathology. The effect of the acid-base status on the serum-ionized calcium level is stressed. The causes of changes in the serum concentrations of phosphorus and magnesium are briefly reviewed, along with the abnormalities of lactate, pyruvate, and hydrogen ion concentrations. The kidney function tests, blood urea nitrogen, serum creatinine, and the renal clearance tests are discussed, with emphasis placed on correlating their results with the findings from repeated urinalyses. The important physiologic influences and pathological processes which result in changes in the concentrations of these parameters are delineated. The causes of increases in the serum enzymes, alkaline phosphatase, alanine transaminase, asparate transaminase, lactic dehydrogenase, sorbitol dehydrogenase, glutamic dehydrogenase, gamma glutamyl transpeptidase, creatinine phosphokinase, amylase and lipase are discussed. The changes in serum bilirubin concentration and its components are fully described, with emphasis placed on the correlation of the findings with urinalysis data and the complexities resulting from the numerous pathologic conditions causing jaundice. These conditions are listed for each of the domestic animals. The other liver function tests, bromosulphthalein dye retention or excretion, serum uric acid and blood ammonia concentration are briefly considered. All the tests described are very useful, and frequently essential, in aiding the veterinary practitioner to arrive at a diagnosis and prognosis, but they never replace clinical acumen.
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PMID:Correlation of changes in blood chemistry with pathological changes in the animal's body: II Electrolytes, kidney function tests, serum enzymes, and liver function tests. 727 79


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