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

The endogenous overproduction of active vitamin D sterols plays a central causative role in the hypercalcemic/hypercalciuric state associated with granuloma-forming diseases, most notably sarcoidosis, as well as with some human lymphomas. In sarcoidosis, the offending metabolite is most likely 1,25-(OH)2-D and the synthetic source is the disease-activated macrophage. About 50% of hypercalcemic patients with lymphoma harbor frankly elevated or inappropriately high serum 1,25-(OH)2-D concentrations. The source of the hormone in patients with lymphoma is not yet known. The endogenous synthesis of 1,25-(OH)2-D in patients with active sarcoidosis and lymphoma is not subject to regulation by those factors that normally control the production of 1,25-(OH)2-D by the renal 25-OH-D-1-hydroxylase. Treatment and prevention of vitamin D metabolite-mediated hypercalcemia/hypercalciuria consist of pharmacologic inhibition of the abnormal 1-hydroxylation reaction and limitation of substrates for the reaction. The former is best accomplished by the administration of anti-inflammatory concentrations of glucocorticoids and the latter by controlling vitamin D intake and sunlight exposure in susceptible hosts.
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PMID:Vitamin D metabolite-mediated hypercalcemia. 267 72

Severe hypercalcemia is a potentially life-threatening complication of several diseases. Most commonly it is caused by cancers that enhance bone resorption. Impaired renal calcium excretion resulting from a combination of volume contraction and calcium-induced renal injury (nephrocalcinosis) plays a critical role in the genesis and aggravation of hypercalcemia. Treatment of hypercalcemia is based on treating the underlying disease, restoring extracellular volume, correcting electrolyte deficiencies (potassium and magnesium), and reducing bone resorption. Several measures are available to reduce bone resorption, of which the most efficacious are the bisphosphonates and plicamycin (mithramycin). One of these agents in combination with volume expansion can reduce serum calcium concentrations to near normal in most patients within 3 to 6 days. Because of the delayed hypocalcemic action of these agents, they should be administered early. Calcitonin has a more modest hypocalcemic action than the bisphosphonates or plicamycin but has a more rapid effect. Combining calcitonin with plicamycin or a bisphosphonate can enhance the rate of decline of the serum calcium level. Bone resorption also can be reduced by getting patients out of bed to stand or walk. Glucocorticoids may be effective in patients with hypercalcemia associated with high levels of vitamin D, such as sarcoidosis, some lymphomas, or vitamin D intoxication. Patients with mild to moderate hypercalcemia may be asymptomatic. Therapy in these patients should be directed at the primary disease as well as at preventing complications that could raise the level of serum calcium. Efforts should be made to prevent volume contraction and prolonged bed rest. Sedatives and narcotic analgesics, by reducing activity and oral intake, can raise serum calcium levels. In the future it may be possible to predict which patients with cancer are likely to develop accelerated local tumor-mediated or humorally mediated osteolysis. For example, high circulating levels of PTH-like peptides in patients with lung cancer might suggest a greater risk of developing hypercalcemia. These patients could be monitored more closely by periodically measuring urinary calcium. Another prophylactic approach would be to treat patients at risk of developing hypercalcemia with drugs, such as the bisphosphonates, that inhibit bone resorption.
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PMID:Treatment of hypercalcemia. 267 75

Hypercalcaemia is a frequent situation in clinical practice. An earlier detection is facilitated by routine analysis of serum calcium. The clinical manifestations depend on severity and the rate of onset of hypercalcaemia. Paucisymptomatic and asymptomatic presentations are the most frequent. Causes of hypercalcaemia are numerous and the mechanisms are various. PTH and vit. D play a preponderant part. In first of all iatrogenic cause are eliminated (all vit D preparations, thiazide diuretics, milk-alkali syndrome). Among non neoplastic hypercalcaemia primary hyperparathyroidism is the first diagnosis. Nephrolithiasis and asymptomatic forms are the most frequent presentations actually. The biochemical profile is not always typical. Generally the association of echography and tomodensitometry lead to the topographic diagnosis. Parathyroid surgical exploration is often necessary in difficult cases. Secondary, the other rare causes of hypercalcaemia are studied: sarcoidosis and granulomatosis disease, thyrotoxicosis and dome endocrinopathies, immobilisation hypercalcaemia, familial hypocalciuric, hypercalcaemia. All of this causes of hypercalcaemia are potentially reversible.
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PMID:[Non-neoplastic hypercalcemia]. 271 64

Patients presenting with hypercalcaemia caused by the co-existence of sarcoidosis and primary hyperparathyroidism may present a diagnostic problem. Tests for sarcoid activity, together with the cortisone suppression test and an estimation of the immunoreactive parathyroid hormone level are all necessary to differentiate between those conditions.
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PMID:Hypercalcaemia in sarcoidosis co-existing with primary hyperparathyroidism. A case report. 272 21

We recently encountered two patients with coexistent hyperparathyrodism and sarcoidosis presenting with hypercalcaemia. The association between hypercalcaemic primary hyperparathyroidism and sarcoidosis is reviewed.
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PMID:Co-existing hyperparathyroidism and sarcoidosis presenting with hypercalcaemia--a diagnostic challenge. 279 75

We have previously reported serum elevations of the soluble form of the interleukin-2 receptor (IL-2R), a marker of T-cell activation, in sarcoidosis. In the present study, an enzyme-linked immunosorbent assay for soluble IL-2R was employed to compare sera from normal controls with those from patients with active sarcoidosis or idiopathic pulmonary fibrosis (IPF). Sera from patients with active sarcoidosis and parenchymal lung disease (radiographic Stages II or III) had geometric mean values for soluble IL-2R of 1975 units/ml compared to 640 units/ml for normal controls (p less than 0.001, Student's t-test). By contrast, soluble IL-2R levels were lower (989 units/ml, p less than 0.05 compared to normals) in patients with active sarcoidosis but no radiographic evidence for parenchymal disease (Stages 0 or I). Soluble IL-2R levels were not elevated in patients with inactive sarcoidosis. Three of the 4 sarcoidosis patients with the highest levels of soluble IL-2R also manifested hypercalcemia. While levels of soluble IL-2R were elevated for the group of patients with IPF (1171 units/ml, p less than 0.05 compared to normals), the striking elevations of soluble IL-2R noted in active sarcoidosis were not seen and there was greater overlap with normal values. We conclude that marked serum elevations of soluble IL-2R are more suggestive of active pulmonary sarcoidosis than IPF.
Sarcoidosis 1987 Sep
PMID:Elevated serum levels of soluble interleukin-2 receptors in active pulmonary sarcoidosis: relative specificity and association with hypercalcemia. 282 1

A 54 year-old woman presented with an asymmetrical polyneuropathy, with in addition signs of hepatitis and hypercalcemia. The diagnosis of sarcoidosis was made by hepatic and neuromuscular biopsies. Electrophysiological studies showed an asymmetrical clear neurogenic involvement with an axonal pattern. Ultrastructural study of the nerve showed sarcoid granulomas in epineurium, perineurium and endoneurium, with images of Wallerian degeneration. No features of primary demyelination were found. Granulomas were also present in muscle and liver. Possible etiological mechanisms are discussed: compression of nerve or vessels, or immune angiitis.
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PMID:[Peripheral neuropathies disclosing sarcoidosis]. 284 3

Sarcoidosis of the kidneys and liver without radiologically demonstrable lung involvement in a 44-year-old woman was shown to be the cause of a hypercalcaemia syndrome. The hypercalcaemia was presumably due to an increased production of 1,25-(OH)2-vitamin D3 which--like the increased angiotensin converting enzyme--is produced in the epithelioid and giant cells. Corticoid treatment normalized serum calcium and ACE levels and improved renal function. These observations demonstrate that measurement of ACE and 1,25-(OH)2-vitamin D3 levels is helpful in the differential diagnosis of hypercalcaemia, in view of the possibility of sarcoidosis, and should be among the diagnostic tests.
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PMID:[Angiotensin-converting enzyme and 1,25-dihydroxyvitamin D3 in hypercalcemia of unknown origin]. 284 36

A patient with pulmonary sarcoidosis and symptomatic hypercalcemia had elevated serum 1,25-dihydroxyvitamin D and angiotensin-converting enzyme levels, with evidence of deterioration of renal function. Pulmonary function tests were normal and there were no other findings to warrant immediate steroid use. She was treated with cellulose sodium phosphate, in an effort to control the hypercalcemia. Serum calcium declined to normal values within 4 weeks and was associated with symptomatic improvement and normalization of BUN and creatinine, indicating perhaps a direct relationship between serum calcium and renal function in this setting. These observations suggest that the hypercalcemia of sarcoidosis may be successfully treated with cellulose sodium phosphate presumably by reducing intestinal calcium absorption, but further clinical trials will be necessary to establish its effectiveness in the long term.
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PMID:Hypercalcemia of sarcoidosis treated with cellulose sodium phosphate. 285 38

Mean plasma calcitriol was significantly increased in a patient with sarcoidosis and hypercalcemia without elevation of PTH. Recent studies provided evidence for an extrarenal production of calcitriol. To investigate this possibility, the conversion of calcidiol by a sarcoid lymph node homogenate was studied. After 2-hour incubation, a product was present in the incubation, which comigrated with synthetic calcitriol on two high performance liquid chromatography systems, was detected by ultraviolet absorption spectrometry and was bound with high affinity by the chick intestinal receptor for calcitriol. These results provide further evidence for an extrarenal synthesis of calcitriol, contributing to the excessive amounts of this metabolite found in the plasma of patients with sarcoidosis.
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PMID:[Extrarenal synthesis of calcitriol in sarcoidosis]. 295 Apr 28


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