Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical spectrum of MM is variable. Infiltration of bone and bone marrow by malignant plasma cells results in severe osteopenia, lytic lesions, pathological fractures and anaemia. Occasionally, significant numbers of plasma cells circulate in the bloodstream. Hypercalcaemia and Bence Jones proteinuria are the main reasons for renal impairment, but amyloidosis and monoclonal immunoglobulin deposition should also be considered. Neurological impairment is most often due to spinal cord pressure by an extradural plasma cell tumour. In some patients, symptoms and signs of peripheral neuropathy may be present. Amyloidosis complicates the course of a minority of patients with MM and further impairs the performance of affected patients. Circulating monoclonal protein may increase serum viscosity, impair the function of platelets and coagulation factors, and behave as a cryoglobulin. The levels of uninvolved immunoglobulins are usually decreased, rendering patients susceptible to various bacterial infections. One or more of these complications provides a clue for the diagnosis, forms the basis for defining prognosis and must be managed expeditiously and concurrently, with the institution of specific treatment for the myeloma.
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PMID:Complications and supportive therapy of multiple myeloma. 884 76

We describe a case of juvenile systemic granulomatosis in a 22-year-old woman. The rash consisted of purple papules and first appeared at the age of one year. She had persistent symmetrical painless boggy tenosynovitis with minimal roentgenographic changes and chronic granulomatous symptoms. Uveitis resulted in visual impairment. She also had granulomatous changes in her vessels. Renal impairment developed; however, neither renal artery stenosis nor hypercalcemia was found. Clinical features included the development of premature aging with alopecia, which differed from the previously reported progeria syndrome. Poikiloderma may cause a prematurely aged appearance. Our report expands the clinical spectrum of systemic granulomatosis to include the development of premature aging with alopecia.
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PMID:Juvenile systemic granulomatosis manifesting as premature aging syndrome and renal failure. 903 3

Primary hyperparathyroidism was initially regarded as a rare and severe disease. In recent years, introduction of routine screening of serum calcium has contributed to a dramatic increased rate of detection of primary hyperparathyroidism in the population, and asymptomatic forms of this disease are now the rule. Surgery remains the only curative treatment. However a medical follow-up may be justified in asymptomatic patients whose serum calcium levels are only midly elevated and whose renal and bone status are close to normal. The medical follow-up is considered to be safe only with conscientious long-term monitoring. Surgery becomes mandatory if the follow-up shows worsening hypercalcemia, bone deterioration, renal impairment, calcium stone, or increased hypercalciuria.
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PMID:[Primary hyperparathyroidism]. 978 Nov 70

Three patients with extensive, symptomatic tumoral calcinosis (TC) were studied after renal transplantation. Changes in TC-related symptoms, radiological appearances, calcium, phosphate and intact parathyroid hormone concentrations were recorded. All patients noted an immediate reduction in pain and in 2 patients the TC rapidly resolved. Their TC was not palpable by 6 months and radiographs showed near complete resolution at 12 months. Both developed hypercalcemia and in one patient this was associated with polyuria and renal impairment. Bisphosphonates reduced the hypercalcemia but increasing the corticosteroids had no effect. The third patient remained dialysis dependent due to technical problems and rejection but continued on immunosuppression to preserve residual graft function. His TC improved symptomatically but grew radiologically. These cases demonstrate that rapid resolution of TC may occur after successful renal transplantation and that bisphosphonates can ameliorate the associated hypercalcemia. Early symptomatic benefit may occur without graft function and is probably due to the anti-inflammatory action of corticosteroids.
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PMID:Rapid resolution of tumoral calcinosis after renal transplantation. 1087 72

Renal impairment is a common complication of multiple myeloma occuring in 50% of patients at some stage in their disease. Pathogenesis is multifactorial. Nephrotoxic manifestations of monoclonal immunoglobulin overexpression include the 'myeloma kidney', light chain deposition disease, AL amyloid, plasma cell infiltration and glomerulonephritis. Other factors, such as hypercalcaemia, hyperuricaemia, infection, hyperviscocity and nephrotoxic drugs can precipitate or exacerbate acute and chronic renal failure. Aggressive treatment has dramatically improved outcome in patients who present with acute or acute-on-chronic renal failure. Dialysis has become an accepted treatment acutely and in end stage renal disease due to myeloma. Conventional therapy with melphalan and prednisolone is still advocated for elderly patients. However, renal failure is not a contraindication to aggressive cytoreduction, stem cell collection, double hemibody radiotherapy and autologous transplantation in those otherwise fit to tolerate these procedures. Prognosis is primarily determined by the response of the myeloma clone to chemotherapy. Outcome in chemosensitive patients approaches that of patients with equivalent disease stage without renal dysfunction.
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PMID:Renal failure and multiple myeloma: pathogenesis and treatment of renal failure and management of underlying myeloma. 1041 44

The methods for preventing hyperparathyroid bone disease, the major variety of renal osteodystrophy, from developing in patients with renal impairment are reviewed. With far-advanced chronic renal failure (creatinine clearance [CCr] < 15 to 20 ml/min), when many of these patients are seen by nephrologists, the use of diets very low in protein, and hence also very low in phosphorus content, combined with calcium-containing phosphate binders, have been shown to lower serum intact PTH levels and improve the osseous pathology. However, the degree of dietary restriction required to achieve success may be quite difficult to follow by most patients encountered in clinical practice. In less-advanced renal insufficiency (CCr, 25 to 60 ml/min), the active vitamin D sterols calcitriol or alfacalcidol [1 alpha-hydroxyvitamin D3] have been shown to ameliorate the skeletal lesions of renal osteodystrophy. The results of six double-blind, placebo-controlled studies and five major open-labeled studies with calcitriol or alfacalcidol are reviewed. Skeletal biopsies were improved and sometimes normalized by using calcitriol or alfacalcidol in daily doses of 0.25 to 0.5 microgram/d, and the incidence of hypercalcemia was quite low with these doses. When the dosage was increased in one study, there was a higher incidence of hypercalcemia. Improved bone mineral density of the spine and hip was reported after 1 yr in calcitriol-treated patients compared with results in the placebo group. Another report documented more favorable intact PTH suppression with intermittent dosing of 2.0 micrograms given either once or three times weekly compared with daily dosing (0.5 microgram/d); there was no rise of serum Ca over the 3-mo trial with any protcol. Other data support the greater likelihood of having normal bone if treatment is initiated when CCr exceeds 25 ml/min. There was no risk of more rapid progression of renal insufficiency in any of the studies reviewed, which include 242 patients who were given an active vitamin D sterol. One trial that used a calcitriol dose of 0.5 microgram/d noted a fall in CCr and a rise in serum creatinine, but true GFR (inulin clearance) did not change. A calcitriol-induced reduction of tubular creatinine secretion is suggested. The risk of inducing low bone turnover (adynamic bone) seems to be quite low with 10.4% of alfacalcidol-treated patients versus 6.5% of placebo developing this "lesion" after 2 yr. Despite the lack of Food and Drug Administration approval for use of these sterols in the predialysis state, evidence is compelling that: there are benefits in retarding the development or progression of metabolic bone disease; there is minimal risk, providing that low doses are used; and there is close monitoring of serum Ca, P, and creatinine. The optimal benefits may be obtained if this treatment is started early in the course of renal insufficiency (CCr in the range of 25 to 60 ml/min).
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PMID:Prevention of metabolic bone disease in the pre-end-stage renal disease setting. 1144 72

We report the case of a 38 year-old man admitted for the treatment of a neuroendocrine carcinoma of the lung with multiple bone metastases. At the diagnosis, the serum biochemistry revealed an evidence of malignant hypercalcemia with acute renal impairment. At this point, a Tc 99-m MDP bone scan was performed and showed intense uptake throughout the gastric walls. The patient underwent a repeat bone scan after normalization of biochemistry; no more abnormal uptake was noted in the stomach. Hypercalcemia is an abnormality of the calcium metabolism frequently associated with malignant condition. Metastatic calcification results from increased accumulation of the calcium-phosphate salts in different tissues related to a local physiological alcalinity. Usually reversible, metastatic calcifications appear as various extraskeletal uptake at Tc 99-m MDP bone scan.
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PMID:[Metastatic gastric calcifications and bronchial neuroendocrine tumor]. 1192 91

Hypercalcemia is a potential dosage-related adverse effect of 13-cis-retinoic acid in patients with neuroblastoma. Severe hypercalcemia requiring dosage reduction has been reported in children receiving 13-cis-retinoic acid 200 mg/m2/day and in those with concurrent renal impairment receiving 160 mg/m2/day. A 12-year-old girl without renal dysfunction, diagnosed with neuroblastoma, developed severe hypercalcemia requiring several hospitalizations while receiving 13-cis-retinoic acid 160 mg/m2/day. Her hypercalcemia resolved with hydration, diuretic therapy, and temporary discontinuation of 13-cis-retinoic acid. Despite a 50% dosage reduction to 80 mg/m2/day, severe hypercalcemia recurred with the next treatment cycle. Further treatment with 13-cis-retinoic acid was made tolerable by shortening the duration of the remaining cycles. Serum calcium levels should be monitored in patients with neuroblastoma who receive 13-cis-retinoic acid.
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PMID:Hypercalcemia induced by 13-cis-retinoic acid in a patient with neuroblastoma. 1201 65

The combination of hypercalcaemia, hypercalciuria, and nephrocalcinosis with and without renal impairment is rare in paediatric clinical practice. However, this constellation of findings has been reported in three children with trisomy 21, but the absence of detailed nutritional data has failed to clarify the underlying pathogenesis. This report describes a 4 year old girl with trisomy 21 who was found coincidentally to have hypercalcaemia, hypercalciuria, nephrocalcinosis, and renal impairment in the absence of metabolic alkalosis, following a prolonged period of excessive calcium intake.
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PMID:Hypercalcaemia in association with trisomy 21 (Down's syndrome). 1210 Dec 6

Multiple myeloma is frequently associated with renal dysfunction. In addition, it has been shown that the presence of renal failure indicates a higher tumor burden and consequently more aggressive disease. Patients who are diagnosed with renal insufficiency should be aggressively treated because reversal of renal insufficiency results in survival outcomes similar to patients who have normal renal function at diagnosis. However, the presence of renal impairment could add significantly to the morbidity of these patients and make it difficult to tolerate aggressive treatment regimens. Therefore, the treatment approach to this group of patients should include a thorough understanding of the feasibility and outcomes of the various antimyeloma treatments that are available, including newer options such as thalidomide. We recommend the following sequence of treatment in newly diagnosed patients with multiple myeloma with renal insufficiency (creatinine > 2 mg/dL): correction of hypercalcemia with full-dose bisphosphonates in patients with hypercalcemia, induction therapy that may be initiated before correction of hypercalcemia with bolus VAD (vincristine 2 mg, doxorubicin 40 mg/m(2), dexamethasone 40 mg on days 1-4, 9-12, and 17-20), and stem cell collection (cyclophosphamide 2.5-3 g/m(2)) with high-dose melphalan (140-150 mg/m(2)) with autologous stem cell transplant. Dialysis support should be considered whenever necessary for all newly diagnosed patients if renal function does not improve with aggressive initial therapy. For patients who develop renal insufficiency later in the course of the disease, therapeutic options need to be tailored to the patient's treatment history, disease status, and performance status.
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PMID:Management of renal dysfunction in multiple myeloma. 1271 1


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