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

Calcium balance studies and measurement of 25-hydroxyvitamin D3 (25[OH]D3) levels were performed on a vitamin D intoxicated, hypoparathyroid patient before, during, and after successful management of hypercalcemia with oral prednisone therapy. Prednisone effected a dramatic reduction in both mean serum calcium levels and mean 24-hour urinary calcium excretion within four days on two separate occasions. No changes were apparent in fecal calcium excretion. Calcium balance became less negative with prednisone treatment. Levels of 25(OH) D3 during the same period did not change. Decreased calcium mobilization from bone best accounted for the glucocorticoid-mediated amelioration of hypercalcemia.
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PMID:Glucocorticoid effects in vitamin D intoxication. 22 30

Mean plasma 1(alpha),25-dihydroxyvitamin D[1(alpha),25(OH)(2)D] was significantly increased and serum parathyroid hormone was suppressed in three patients with sarcoidosis and hypercalcemia. Prednisone lowered the mean plasma 1(alpha),25(OH)(2)D to normal range and corrected the hypercalcemia. To elucidate the mechanism for the increased sensitivity to vitamin D in this disorder, the effects of orally-administered vitamin D(2) were determined in seven normal subjects, four patients with sarcoidosis and normal calcium metabolism and three patients with sarcoidosis and a history of hypercalcemia who were normocalcemic when studied. Serum and urinary calcium, serum 25-hydroxyvitamin D (25-OHD), plasma 1(alpha),25(OH)(2)D and, in some studies, calcium balance were measured. Vitamin D(2), 250 mug a day for 12 d, produced little, if any, change in mean plasma 1(alpha),25(OH)(2)D and in urinary calcium in the normals and in the patients with normal calcium metabolism. In contrast, vitamin D(2) produced increases in plasma 1(alpha),25(OH)(2)D from concentrations which were within the normal range (20-55 pg/ml) to abnormal values and increased urinary calcium in two patients with abnormal calcium metabolism. In an abbreviated study in the third patient, vitamin D(2), 250 mug a day for 4 d, also increased plasma 1(alpha),25(OH)(2)D abnormally from a normal value. There was a highly significant correlation between plasma 1(alpha),25(OH)(2)D and urinary calcium. Serum 25-OHD and serum calcium remained within the normal range in all subjects and patients. These findings provide evidence that the defect in calcium metabolism in sarcoidosis probably results from impaired regulation of the production and(or) degradation of 1(alpha),25(OH)(2)D. Prednisone may act to correct the abnormal calcium metabolism by reducing circulating 1(alpha),25(OH)(2)D.
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PMID:Evidence that increased circulating 1 alpha, 25-dihydroxyvitamin D is the probable cause for abnormal calcium metabolism in sarcoidosis. 31 11

Fifteen cases of hypervitaminosis D in childhood are reviewed. In all of them, vitamin D was given following medical prescription. In four occasions, excessive dosage of vitamine D impaired the evolution of a previous nephropathy. The clinical, analytical, radiological and histological findings as well as the therapeutical aspects are commented. Hypercalcemia, hypercalciuria, polyuria with hypostenuria, renal failure, bone lesions and nephrocalcinosis are the most prominent features of the picture. Occasionally, arterial hypertension and glycosuria were found. Prednisone, thyrocalcitonine and phosphates were used as therapeutical means. In spite of nephrocalcinosis and renal failure generally present at diagnosis, the clinical course was rather good.
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PMID:[Hypervitaminosis D. Review of fifteen cases]. 44 41

From 1974 to 1987, 450 children with non-Hodgkins' lymphoma (NHL) were seen at the Institut Gustave Roussy (IGR); 14 children had malignant lymphoma of bone (MLB). Eleven of the 14 were newly diagnosed, whereas three presented in relapse. Nine patients presented with multifocal bone involvement. The median age of these eight girls and six boys was 9.5 years (range 1.25-15 years). Bone pain was present in all patients as the initial symptom. Evaluation included physical examination, routine serum chemistries, complete blood count, chest roentgenography, skeletal survey, radionuclide bone scan, lumbar puncture, bone marrow aspiration, and intravenous pyelography, and/or abdominal ultrasonography. Hypercalcemia was found in six patients. Biopsy was performed in 12 patients, revealing high-grade lymphoblastic lymphomas in all. In two patients diagnosis was made on cytological examination of bone marrow aspirate. Immunophenotyping in four cases, demonstrated non-B, non-T cell origin in three and pre-B cell origin in one. Three patients were treated prior to 1982 with Cyclophosphamide/Oncovin/Prednisone/ADriamycin (COPAD) and seven patients, seen after 1982, were treated with a modified LSA2L2 protocol (LMT). None of the previously untreated patients received radiotherapy. All patients treated with COPAD have died, whereas four out of seven treated with LMT are alive with a median follow up of 51 months (range 36-82 months). One child treated on a pilot study died. One of the three children seen at relapse is disease-free with a follow-up of 98 months after high-dose chemotherapy followed by autologous bone marrow transplantation (ABMT). Five out of six patients presenting with hypercalcemia have died. Results with LMT are encouraging and together with published results suggest that sufficiently intensive chemotherapy can result in complete remission and cure in MLB. Radiotherapy does not seem to be necessary, avoiding possible serious long-term effects. Hypercalcemia is a bad prognostic feature.
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PMID:Childhood malignant lymphoma of bone. 199 Feb 54

We describe a patient who initially formed calcium-containing renal stones owing to gouty diathesis and hypocitraturia. On therapy with 300 mg. allopurinol and 60 mEq. potassium citrate daily serum uric acid decreased from 9.2 to 5.8 mg. per dl., urinary pH increased from less than 5.5 to 6.6 and urinary citrate increased from 223 to 1,005 mg. per day. Four months later while still on this medical regimen, the patient presented with hypercalcemia (13.4 mg. per dl.), high serum 1,25-dihydroxyvitamin D (65 pg. per ml.) and hypercalciuria (598 mg. per day), which subsequently were found to result from sarcoidosis. Prednisone therapy normalized the disturbances in calcium metabolism. During 33 months of combined treatment with 7.5 to 10 mg. prednisone a day, allopurinol and potassium citrate, the patient was free of stones and he had normal urinary calcium, pH and citrate. However, a calcium stone formed 1 month after discontinuation of prednisone therapy, although treatment with allopurinol and potassium citrate was continued. The patient had marked hypercalciuria of 447 to 465 mg. per day, despite normal urinary pH, citrate and uric acid. This case represents calcium stone formation in a patient with 2 separate etiologies for stone disease, that is gouty diathesis and sarcoidosis. Therapeutic regimens directed at the correction of both metabolic disturbances were required to control renal stone formation.
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PMID:Gouty diathesis and sarcoidosis in patient with recurrent calcium nephrolithiasis. 337 3

It is generally agreed that the kidneys are the only site of 1-hydroxylation of vitamin D and that the abnormal calcium metabolism in sarcoidosis is caused by increased production of 1,25-dihydroxyvitamin D (1,25-[OH]2D). We describe a patient with sarcoidosis with hypercalcemic nephropathy and end-stage renal disease undergoing long-term maintenance hemodialysis who was initially seen with hypercalcemia and elevated serum levels of 1,25-(OH)2D. Prednisone administration resulted in decreased serum calcium and 1,25-(OH)2D levels. These results confirm the recent evidence for extrarenal production of 1,25-(OH)2D in sarcoidosis and illustrate the importance of altered vitamin D metabolism in the development of hypercalcemia in sarcoidosis.
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PMID:Elevated 1,25-dihydroxyvitamin D levels: occurrence with sarcoidosis with end-stage renal disease. 689 30

In order to study the response of patients with multiple myeloma of the bones (MM) to various anti-cancer drugs (Melphalan M, Cyclophosphamide Cy, Nitrosourea NU, Vincristine V, Adriamycine A and Prednisone P), 70 MM received the following treatment : 1) Induction therapy : a) M and P or b) M and Cy and P ; 2) Levelling with partial or complete response : V Cy P (in case a) or V M Cy P (in case b) ; 3) Relapse : A and NU. The following results were obtained : 1) Only 42.6% of patients respond to induction therapy ; 2) Fewer than 10% of patients showing a response reach a second levelling with Vincristine ; 3) 50% of those not showing a response reach a levelling between --20 and --50 and have prolonged survival ; 4) Only 20% of non responders are improved by Cy P or A and NU. The median actuarial survival is 42 months. Among the responders two poor prognosis factors must be underlined : hypercalcemia and the speed of response.
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PMID:[Value of successive chemotherapy in multiple myeloma of bone. Prospective study over 4 years]. 736 Oct 63

Forty-two patients with sarcoidosis were studied with special attention to renal disease and disturbance of calcium metabolism. Abnormal calcium metabolism was found in 19 patients and prednisone corrected hypercalcaemia in those affected within two weeks, except in one patient who had concomitant primary hyperparathyroidism. Renal failure was found in 19 patients, 15 of whom had hypercalcaemia. Prednisone had a beneficial effect on kidney function within four weeks in all patients except in one with co-existing glomerulonephritis. Arterial hypertension was found in six patients, proteinuria in six, and calcinosis in six. Among 14 patients who underwent renal biopsy, granulomas were found in five. In only one of these was granulomatosis extensive bringing out renal failure and death within two years after temporary remission with prednisone. Co-existent non-sarcoid diseases affecting the kidneys or calcium metabolism occurred in ten out of 23 patients with sarcoidosis and kidney disease/calcium abnormality. In most cases these conditions contributed more to the prognosis than did sarcoidosis. From the present series and review of the literature it appears that young males within the first two years of diagnosis are at the greatest risk of hypercalcaemia or kidney disease.
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PMID:Renal manifestations and abnormal calcium metabolism in sarcoidosis. 746 60

Angiotropic large B cell lymphoma (angiotropic LCL) or intravascular large cell lymphoma (IVLCL) was diagnosed by liver and bone marrow biopsies and immunohistochemical studies in a 52 year old Caucasian male. IVLCL is a very rare disease characterized by widespread intravascular proliferation of lymphoma cells. Although it most commonly affects the central nervous system or skin and occasionally bone marrow, angiotropic LCL may be present without evidence of localized disease, as seen initially in our patient. To date, only a few cases of intravascular malignant lymphomatosis associated with parathyroid hormone related protein (PTH-rP) induced humoral hypercalcemia have been published. Our extraordinary case was diagnosed mainly by liver biopsy. The neoplastic lymphoid cells stained diffusely and strongly positive with CD-20 (Pan B) and were negative for CD-3 (Pan T) immunostain. The most significant, initial clinical finding was severe, unexplained hypercalcemia (until 18.6 mg/dl). Plasma PTH-rP showed a ten-fold increase at 8 pmol/L (normal value less than 0.8 pmol/L). Very unusual cytogenic abnormalities were found. The patient received the massive third generation combination chemotherapy comprising of Methotrexate, Doxorubicine, Cyclophosphamide, Vincristine, Prednisone and Bleomycin and developed, complete although temporary, clinical, humoral and cytogenetic remission.
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PMID:[Malignant humoral hypercalcemia associated with angiotropic large B cell lymphoma]. 1130 43

Although hypercalcemia has long been recognized as a complication of sarcoidosis, the incidence of hypercalcemia (> or = 11 mg/dl) in Japan is probably less than 5%. 1 alpha, 25(OH)2D3 is the main cause for hypercalcemia in sarcoidosis and overproduced by sarcoid granulomata. Gamma-interferon produced by activated lymphocytes and macrophages plays a major role in the synthesis of 1 alpha, 25(OH)2D3. PTH release is down regulated by high serum concentration of 1 alpha, 25(OH)2D3. Parathyroid hormone related protein may also contribute to the hypercalcemia of sarcoidosis. Treatment of hypercalcemia and hypercalciuria consists of a low calcium diet, adequate hydration, minimization of exposure to sunlight and reducing overproduction of 1 alpha, 25(OH)2D3. Prednisone, 15 to 25 mg/day, is the drug of choice to reduce the overproduction of 1 alpha, 25(OH)2D3.
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PMID:[Hypercalcemia in sarcoidosis]. 1223 75


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