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

Although corticosteroids are effective in the treatment of hypercalciuria and hypercalcemia in chronic sarcoidosis, complications of their long-term use frequently limit therapy. We studied the efficacy of chloroquine in two patients with sarcoidosis who were unable to tolerate the dosage of corticosteroids required to control hypercalciuria and prevent the formation of renal stones. Over a three-year period, each patient received a 6-month and a 10-month course of oral chloroquine phosphate (500 mg per day) while continuing to receive corticosteroids at a fixed dose. Chloroquine therapy was associated with a significant reduction in levels of serum 1,25-dihydroxyvitamin D (1,25(OH)2D) and urinary calcium. We observed a direct correlation between serum 1,25-(OH)2D levels and 24-hour urinary calcium excretion, supporting the hypothesis that excessive serum 1,25-(OH)2D is responsible for the hypercalciuria in sarcoidosis. Serum levels of 25-hydroxyvitamin D (25-(OH)D) did not change with therapy, suggesting that chloroquine may act by inhibiting the conversion of 25-(OH)D to 1,25-(OH)2D. Current dosage guidelines and ophthalmologic-surveillance techniques, which allow chloroquine to be administered with little risk of retinopathy, should permit an expanded role for this agent in the treatment of the calcium abnormalities of sarcoidosis.
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PMID:The effects of chloroquine on serum 1,25-dihydroxyvitamin D and calcium metabolism in sarcoidosis. 375

We report a case of sarcoid hypercalcaemia treated with the bisphosphonate, APD [(3-amino-1-hydroxypropylidene)-1,1-bisphosphonate]. Investigations showed that the hypercalcaemia was associated with a high plasma 1,25 dihydroxy vitamin D concentration. A low dietary intake of calcium partially corrected the hypercalcaemia but APD rapidly normalized plasma calcium without reducing the elevated 1,25 dihydroxy vitamin D concentration. The case demonstrates that hypercalcaemia in sarcoidosis results from the effects of 1,25 dihydroxy vitamin D on bone as well as on calcium absorption and that prolonged suppression of the effect on bone occurs with APD treatment.
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PMID:Hypercalcaemia due to sarcoidosis corrects with bisphosphonate treatment. 377 26

About 80 percent of sarcoidosis cases are benign and do not require treatment, but 20 percent will have chronic unremitting disease for which therapy is essential. It is important that the physician identify this group and begin therapy promptly. If the disease is active, treat. If it is inactive, do not treat. Activity depends upon three major tests: serum angiotensin converting enzyme, gallium 67 scan, and bronchoalveolar lavage. The other consideration is involvement of vital organ systems; ie, active ocular disease, progressive pulmonary involvement as evidenced by increasing symptoms, impaired and deteriorating pulmonary function, or radiographic changes; hypercalcemia or hypercalciuria; central nervous system involvement; disfiguring cutaneous lesions; and myocardial sarcoidosis. Following a therapeutic decision to treat, adrenocorticoids are the drugs of choice. Methylprednisolone, prednisone, and cortisol are listed in order of benefit. Alternate day and/or low-dose steroids are increasing in popularity. Chloroquine phosphate is beneficial for skin lesions, while oxyphenbutazone has been found to be at least as effective as prednisone. Immunosuppressives may be used also. Chlorambucil and azathioprine have shown variable results. Cyclosporine (Cyclosporin A) shows promise and is now undergoing therapeutic trials.
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PMID:When should sarcoidosis be treated? 378 58

Large lung bullae are a rare manifestation of pulmonary sarcoidosis. Of three patients with this complication, all had pulmonary infiltrates at presentation and two had bilateral hilar adenopathy. Hypercalcaemia developed during the course of the illness in all three patients. In each case the bullae had developed within four years of the diagnosis of sarcoidosis. In one woman a bulla resolved almost completely after it had become infected.
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PMID:Large lung bullae in sarcoidosis. 378 10

This is a first report of primary hyperparathyroidism (HPT) masquerading as a destructive fibrous sphenoid sinus "Brown tumor" associated with progressive blindness and hypercalcemia. Diagnosis of a Brown tumor was delayed despite serial computerized tomography of the head and repeated transnasal and transethmoid sphenoid biopsies demonstrating diffuse fibrosis. Only detection and medical evaluation of hypercalcemia, demonstrating elevation of both serum calcium and C-terminal parathyroid hormone with an elevated chloride/phosphate ratio, prompted neck exploration, thus confirming a solitary left superior parathyroid adenoma. Postoperative normocalcemia occurred synchronously with the return of light perception and the arrest of sphenoid sinus and parasellar erosion. Although maxillary Brown tumors of secondary HPT have been reported, this is the first report of osteitis fibrosa of the sphenoid sinus. Differential diagnosis of an erosive sphenoid lesion with cranial nerve dysfunction, exclusive of inflammatory or vascular disease, should include sarcoidosis, primary and metastatic sphenoid carcinoma, fibrous dysplasia, giant cell reparative granuloma, midline lethal granuloma, chordoma, and chondrosarcoma. Furthermore, the bony destructive lesions with concomitant hypercalcemia of sarcoidosis and HPT are distinguishable by radiographic and laboratory analyses and by the Dent corticosteroid suppression test. Hypercalcemia of primary HPT is associated with elevated serum C-terminal parathormone, osteitis fibrosa, a negative Dent test, and a chloride/phosphate ratio greater than 33 in 94% of primary HPT patients. Hypercalcemia of sarcoidosis is associated with a normal or decreased C-terminal parathormone assay and a positive Dent test, as well as elevated serum immunoglobulins and erythrocyte sedimentation rate, and a positive angiotensin-converting enzyme assay.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sphenoid sinus brown tumor, hypercalcemia, and blindness: an unusual presentation of primary hyperparathyroidism. 379 83

Renal impairment in sarcoidosis is unusual: cases with granulomatous interstitial nephritis (GIN) and without associated glomerular disease, nephrocalcinosis and hypercalcemia have rarely been described. We report 2 such cases, one of whom is the first patient documented as surviving following presentation in dialysis dependent renal failure. Review of the literature revealed a further 20 patients. Of the 22 patients, including our own, 3 failed to respond to treatment, all dying in acute renal failure. Relapse occurred in 4, in association with rapid reduction or early cessation of treatment. No relapse was reported later than 9 months after starting treatment with corticosteroid. The majority of patients (15/19) who responded to treatment had residual renal impairment after up to 30 months of steroid treatment.
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PMID:Renal impairment in sarcoidosis: granulomatous nephritis as an isolated cause (two case reports and review of the literature). 380 88

A 42-year-old man had a 4 year history of sarcoidosis stage II (lung). In biopsied specimens of the antrum we found epithelioid granulomas caused by gastric involvement in sarcoidosis. Coincidentally we found a gastric ulcer which was later the source of gastric bleeding. The granulomas were located around this ulcer and also under intact mucosa. Therefore, in our opinion it was not the case that granulomatous gastritis caused the ulceration in a direct way. We saw a connection between hypercalcemia--often found in patients with sarcoidosis, as in our patient--and the gastric ulcer. Therapy was thus aimed at lowering the blood calcium concentration. Steroids were avoided at this time. The ulceration healed, although granulomatous gastritis continued.
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PMID:[Granulomatous gastritis of the antrum in generalized sarcoidosis]. 380 61

Sarcoidosis is frequently attended by hypercalciuria and sometimes by hypercalcaemia. The type of hypercalciuria and its relationships with disease extension and activity have rarely been investigated. In order to clarify these issues we undertook an investigation by a calcium absorption test in 39 patients with untreated thoracic sarcoidosis, and tried to establish correlations with vitamin D3 metabolism and some features of the disease. We found three types of responses. Group I (n = 12) with a normal test had normal 1,25-(OH)2D3 and rare extrathoracic localisations. Group II (n = 14) with absorptive hypercalciuria had higher serum calcium; 1,25-(OH)2D3 (p less than 0.001) and the free 1,25-(OH)2D3 index (p less than 0.05) were raised. Sarcoidosis was more often inflammatory, developing and disseminated. Group III (n = 13) had resorptive hypercalciuria, and hypercalcaemia was frequent. 1,25-(OH)2D3 (p less than 0.01) and the free 1,25-(OH)2D3 index (p less than 0.05) were raised but to the same degree as in Group II. Sarcoidosis was more disseminated and developing than in Groups I and II. In the 39 patients, iPTH and nephrogenous cAMP were low. Post-calcium load urinary calcium/creatinine (Ca/Cr) and 1,25-(OH)2D3 were correlated (p less than 0.05). Extrathoracic extension was associated with higher fasting urinary Ca/Cr (p less than 0.001), and development with higher post-load urinary Ca/Cr (p less than 0.001). Thus, absorptive hypercalciuria is related to the development of sarcoidosis and can be explained by high free 1,25-(OH)2D3, while resorptive hypercalciuria seems to be linked with disease extension. In such a case, the mechanism of osteolysis is not solely accounted for by high 1,25(OH)2 vitamin D3 serum levels, and we postulate that some other factor is at work, related to the extent of the granulomatous process.
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PMID:Resorptive versus absorptive hypercalciuria in sarcoidosis: correlations with 25-hydroxy vitamin D3 and 1,25-dihydroxy vitamin D3 and parameters of disease activity. 383 15

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

We have studied a hypercalcemic patient with sarcoidosis and advanced renal failure. Bone biopsy and urinary cAMP excretion indicated suppression of parathyroid function. 1,25(OH)2D levels were moderately elevated and dropped to low normal levels during prednisolone treatment. Discontinuation of prednisolone treatment caused deterioration of renal function and hypercalcemia, 1,25(OH)2D serum levels being within the normal range. Our data demonstrate the rapid speed at which prednisolone causes a drop in serum 1,25(OH)2D level. Since hypercalcemia was observed both during periods of hypercalciuria and normal serum 1,25(OH)2D levels, increased sensitivity to active vitamin D seems likely. There was no significant correlation between 25(OH)D, 24,25(OH)2D or 25,26(OH)2D. Furthermore there was no correlation between any of these three metabolites and either 1,25(OH)2D or serum calcium.
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PMID:Rapid effect of prednisolone on serum 1,25-dihydroxycholecalciferol levels in hypercalcemic sarcoidosis. 384 60


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