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

Acute primary hyperparathyroidism is an unusual form of primary hyperparathyroidism characterized by life-threatening hypercalcemia. Forty-three cases reported in the literature since 1974 are reviewed, along with five new cases. The average age of the patients was 55 (27 to 82), with an even distribution between men and women. Marked hypercalcemia (17.5 +/- 2.1 mg/dl) was accompanied by parathyroid hormone levels 20 times normal. Virtually all patients had symptoms. Hyperparathyroid bone disease occurred in 53 percent of patients; even more (69 percent) had nephrolithiasis or nephrocalcinosis. Combined renal and skeletal involvement was seen in 50 percent. Only three deaths were recorded. The pathophysiology of the acute hyperparathyroid state is unknown but appears to consist of uncontrolled parathyroid hormone secretion followed by cycles of hypercalcemia, polyuria, dehydration, reduced renal function, and worsening hypercalcemia. These features of acute primary hyperparathyroidism are compared with the features reported in the literature antedating multichannel screening, and with the features of the common form of primary hyperparathyroidism. Clinical guidelines by which the diagnosis may be suspected are also reviewed.
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PMID:Acute primary hyperparathyroidism. 381 20

In a 26-year-old patient admitted to the emergency ward with acute abdomen, all the symptoms--nausea, vomiting, indeterminate abdominal pain, constipation, renal failure, polyuria and polydipsia--could be explained by calcium intoxication syndrome. Investigation revealed generalized sarcoidosis. Under medical treatment with prednisone all the pathologic findings rapidly regressed. The pathogenesis of hypercalcemia in sarcoidosis, and particularly the disorder of vitamin D metabolism with raised levels of 1,25-dihydroxycholecalciferol, are discussed.
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PMID:[Acute hypercalcemia syndrome in sarcoidosis]. 384 Sep 13

Twelve patients with pheochromocytoma have shown unusual clinical and laboratory presentation. These include three patients with cardiac manifestations (sick sinus syndrome, obstructive cardiomyopathy and ischemic ECG changes). Two patients with gastrointestinal problems (acute abdomen due to ischemic bowel and constipation). One child with sudden blindness and one, non diabetic patient with polyuria. Laboratory findings included four patients with diabetes mellitus, four patients with hypercalcemia two of them with concomitant hyperreninemia and one patient with hypokalemia. Awareness of the illness leads to the discovery of unusual cases and even a most severely sick patient can make a complete recovery.
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PMID:Uncommon presentation of pheochromocytoma: case studies. 390 36

Hypercalcaemia can be caused by many disorders, but is most commonly due to primary hyperparathyroidism in outpatients, and to malignant disease in hospital inpatients. When mild (less than 3 mmol/L) it does not cause symptoms, but can have long term effects such as renal calculi. It is important that the aetiology of the hypercalcaemia be established, as it can reflect serious disease. In most patients the correct diagnosis can be suspected from clinical history and examination, and confirmed by laboratory tests and x-rays. The most difficult diagnostic problem is the patient with negative clinical findings, mild hypercalcaemia and mild renal impairment, when the parathyroid hormone level is normal or slightly elevated. When hypercalcaemia is severe (greater than 3.5 mmol/L), it can cause vomiting, polyuria, dehydration and renal impairment, and is then an important therapeutic problem. Therapy includes treatment of the cause, such as radiotherapy for malignant disease or surgery for primary hyperparathyroidism. In addition, it is usually necessary to treat the hypercalcaemia itself, and the initial step is always rehydration. If the plasma calcium concentration remains high, drug treatment must be added, the most effective and reliable agent being intravenous mithramycin. Aminohydroxypropylidene diphosphonate (APD), though less studied, may be equally useful in this situation. Glucocorticoids are not always effective, and phosphate may cause renal damage, particularly when given intravenously. For long term treatment of malignant hypercalcaemia, oral glucocorticoids and phosphate are often effective, and can be given in combination. When primary hyperparathyroidism cannot be corrected surgically, the hypercalcaemia (and hypercalciuria) are probably best treated with a low calcium diet and cellulose phosphate, a regimen also effective for the hypercalcaemia of sarcoidosis.
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PMID:Hypercalcaemia. What does it signify? 394 Aug 49

A case of malignant pheochromocytoma, with a recurrence 17 years after the initial diagnosis of benign pheochromocytoma, was presented. The autopsy revealed multiple metastases of pheochromocytoma to the bone marrow of the thoracic and lumbar vertebrae. Of particular note is the fact that the patient was associated with paralytic ileus, polyuria and hypercalcemia and that he died of hypercalcemia crisis. Cases like this appear to be very rare.
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PMID:A malignant pheochromocytoma with ileus, polyuria and hypercalcemia: a case of recurrence 17 years after the initial operation. 404 89

A 17-year-old patient with a small paratesticular embryonic sarcoma presented with symptoms of renal failure, polyuria and widespread bone metastases. Investigation revealed hypercalcaemia and uraemia without any evidence of hyperparathyroidism. The hypercalcaemia responded over a period of weeks to administration of mithramycin with initial improvement in the symptoms and metabolic derangements. Control was lost with the necrosis of intra-abdominal tumour deposits and haemorrhagic polypoid deposits in the alimentary tract. The value and hazards of mithramycin are well demonstrated by these rare complications of this type of tumour.
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PMID:Mithramycin treatment of hypercalcaemia and renal failure in a patient with paratesticular embryonic sarcoma. 425 8

Renal impairment in sarcoidosis is usually due to hypercalcaemia and nephrocalcinosis but can also be caused by granulomatous nephritis or interstitial nephritis without sarcoid granulomata. A variety of types of glomerulonephritis have also been described in sarcoidosis but these rarely cause impaired renal function. Renal failure as an isolated manifestation of sarcoidosis is uncommon. A 66-year-old woman presented with a 1-year history of lethargy, polyuria and nocturia. Clinical examination was unremarkable and she had impaired renal function (urea 18 mmol/l (108 mg%) and creatinine 380 mumol/l (4.3 mg%)). As her kidneys were normal in size, she underwent renal biopsy, which revealed granulomatous interstitial nephritis. Reevaluation showed no other evidence of sarcoidosis and she had impaired urinary acidification and concentrating capacities. Therapy with corticosteroids produced a marked improvement in symptoms and renal function. This case confirms the view that granulomatous sarcoid nephritis is steroid sensitive and that full recovery can be expected provided interstitial fibrosis and scarring do not occur.
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PMID:Reversible renal failure due to isolated renal sarcoidosis. 646 14

Primary hyperparathyroidism was diagnosed in two German shepherd pups from a litter of four females. Clinical signs were apparent by two weeks of age and included stunted growth, muscular weakness, and polydipsia/polyuria. Radiography revealed diffuse reduction in bone density. Both pups had marked hypercalcemia, hypophosphatemia, increased plasma immunoreactive parathyroid hormone concentrations and increased fractional clearance of inorganic phosphate in the urine. Intravenous infusion of one affected pup with calcium gluconate failed to suppress the plasma concentration of immunoreactive parathyroid hormone, suggesting autonomous secretion of parathyroid hormone. Necropsy of the other pup at eight weeks of age revealed diffuse hyperplasia of parathyroid chief cells, nodular hyperplasia of thyroid C-cells, skeletal alterations consistent with fibrous osteodystrophy, hypercalcemic nephropathy, and extensive mineralization of the lungs and gastric mucosa. The dam and sire were half sibs. One male pup from a previous litter of six had developed similar clinical signs and radiographic lesions, suggesting autosomal recessive inheritance. This is the first report of hereditary primary hyperparathyroidism in domestic animals, a disease which may be analogous to hereditary neonatal primary hyperparathyroidism in children.
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PMID:Primary hyperparathyroidism in German shepherd dogs: a disorder of probable genetic origin. 646 98

Direct measurement of plasma AVP and indirect assessment of antidiuretic activity during standard dehydration tests were made in 21 polyuric and polydipsic patients to establish the efficacy of each method in determining the cause of polyuria. Patients with acquired nephrogenic diabetes insipidus (e.g. diabetes mellitus, renal failure, hypercalcaemia) were excluded from the study. Cranial diabetes insipidus was diagnosed by plasma AVP responses to osmotic stimulation during infusion of hypertonic 5% saline which were subnormal in 13 patients, 4 of whom had undetectable plasma AVP and 3 who had reduced but osmoregulated AVP release. Standard water deprivation tests confirmed cranial diabetes insipidus in all but 2 patients who were diagnosed as partial nephrogenic diabetes insipidus. The remaining 8 patients had normal, osmoregulated AVP secretion; the cause of their polyuria was determined by their renal response to desmopressin. Two patients had nephrogenic diabetes insipidus and 6 had primary polydipsia. The majority of polyuric patients could be accurately diagnosed by carefully performed dehydration tests. We suggest that direct measurements of plasma AVP during osmotic stimulation are only necessary to distinguish mild forms of cranial from nephrogenic diabetes, or to define precisely the characteristics of AVP secretion.
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PMID:A comparison of diagnostic methods to differentiate diabetes insipidus from primary polyuria: a review of 21 patients. 665 43

A number of advances which took place during the last decade have increased our understanding of the physiology and pathophysiology of urinary concentrating defects. The development of a highly sensitive radioimmunoassay for plasma vasopressin concentration has shed new light on vasopressin control mechanisms. The cellular action of vasopressin in biological membranes has been studied by various techniques. The role of adenylate cyclase, cyclic adenosine monophosphate (cAMP), microtubules, and microfilaments, in the response of vasopressin-sensitive membranes is now partially understood. New models of countercurrent multiplication systems, in which urea plays a prominent role, offer a better explanation of certain experimental facts. Such advances had permitted a better understanding of clinical conditions characterized by concentrating defects, including hyperkalemia, hypercalcemia, parenchymal renal disease, obstructive renal disease, and polyuria induced by certain drugs.
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PMID:Pathophysiology of renal concentrating defects. 679 72


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