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

Serum osteocalcin (BGP) is an osteoblast product that probably reflects the rate of bone formation. It is a potential marker of skeletal metastases and, to investigate this, BGP was measured by radioimmunoassay in the serum of normal subjects and patients with breast or prostate cancer. Significantly higher levels were found in patients with metastatic bone disease in comparison to both normal subjects (P less than 0.001) and patients with non-metastatic cancer (P less than 0.05 for breast cancer and less than 0.001 for prostate cancer). The range of values was wide. Levels were higher in sclerotic than lytic bone metastases (P less than 0.01) and lower in patients with hypercalcaemia (P less than 0.001). Serial measurements of BGP were made in 53 patients with skeletal metastases from breast cancer receiving systemic therapy. At 1 month BGP rose by greater than 0.5 ng/ml in 15/16 responding patients compared with 7/23 patients with progressive disease (P less than 0.01). Responding patients also showed a rise in the bone isoenzyme of alkaline phosphatase and a paradoxical deterioration in the bone scan appearance, both reflecting a flare in osteoblast activity. The early increase in responding patients was followed by a gradual decrease over subsequent months as the osteoblast reaction induced by systemic therapy subsided. We conclude that BGP measurements reflect a wide variability of bone formation rates in metastatic bone disease. Bone formation was usually increased, particularly when metastases were sclerotic in appearance, but in patients with hypercalcaemia the low BGP levels suggest uncoupling of bone resorption and formation. Serial measurements of BGP may be useful in monitoring response to treatment.
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PMID:Osteocalcin: a potential marker of metastatic bone disease and response to treatment. 326 63

Bone disease is recognized as a major problem in dialysis patients. initially, hyperparathyroidism was thought to be the major cause of bone disease in these patients. However, an aluminum-related bone disease has been identified in dialysis patients receiving exogenous aluminum. Patients with hyperparathyroidism and aluminum toxicity present with similar clinical and laboratory features; therefore, diagnosis of these two bone abnormalities is often difficult. Understanding normal bone development helps to elucidate the distinctions between aluminum and renal osteodystrophy. Patients with either bone syndrome may present with hypercalcemia, elevations in parathyroid hormone levels, bone pain, fractures, and radiographic evidence of subperiosteal resorption. The subtleties of these syndromes must be understood to avoid misdiagnosis. A diagnosis of hyperparathyroidism may lead to a parathyroidectomy, exacerbating the development of aluminum toxicity. Hyperparathyroidism is associated with increased surface osteoid, a high bone formation rate, increased numbers of bone cells, abnormal "twoven" osteoid, and low serum aluminum levels. Aluminum toxicity is associated with a low rate of bone turnover, paucity of bone cells, maintenance of a "laminar" osteoid, and significant aluminum bone deposition. Serum aluminum level measurements are key to the diagnosis of aluminum toxicity. For patients displaying intermediate aluminum values, the deferoxamine (DFO) challenge test is necessary for diagnosis. If noninvasive methods fail to determine a definitive diagnosis, a bone biopsy is required.
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PMID:Aluminum and renal osteodystrophy. 329 91

Radionuclide imaging with Tc-99m diphosphonates is not an effective method for detecting or ruling out most osteoporotic diseases including senile osteoporosis or accelerated postmenopausal osteoporosis, and the slow loss of bone tissue generally remains undetected by this modality. Nonetheless, it frequently surpasses or supplements radiographic findings in evaluating the focal complications of metabolic bone disease, including fractures, microfractures, stress fractures, vertebral compressions, Milkman-Looser zones, aseptic necrosis, and acute infarction. In contrast to its secondary role in osteoporosis, bone imaging is of prime importance in investigating hypercalcemia, because the major cause of this abnormality is skeletal metastatic malignancy. In defective bone mineralization due to hyperparathyroidism or osteomalacia, a general increase in diphosphonate skeletal uptake is detected more frequently than radiographic abnormalities. However, normal skeletal images do not rule out metabolic bone disease. Biochemical testing is more reliable in detecting primary hyperparathyroidism. On the other hand, in renal osteodystrophy, biochemical abnormalities are variable and bone imaging is helpful in assessing the severity of skeletal involvement, but not its etiology. Many methods of quantitating the kinetics of Tc-99m diphosphonates have been explored, such as plasma clearance, bone-to-soft-tissue ratios, 24-hour total body retention and 24-hour urinary excretion. None of these have been widely accepted. The value of bone imaging is established in other systemic diseases, most notably in Paget's disease, hypertrophic pulmonary osteoarthropathy, sickle cell disease, fibrous dysplasia, and sympathetic dystrophy.
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PMID:Radionuclide imaging in metabolic and systemic skeletal diseases. 331 47

Hypercalcemia has been infrequently associated with Hodgkin's disease. When seen, most cases have been attributable to skeletal invasion by disease. Herein is described a 40-year-old man with a 15-year history of Hodgkin's disease. Each of four disease recurrences was heralded by hypercalcemia occurring in the absence of bone disease or elevation of parathyroid hormone levels. Marked elevations of 1,25-dihydroxyvitamin D levels were observed that paralleled his disease course and response to therapy. The repetitive association of hypercalcemia with an elevation of 1,25-dihydroxyvitamin D in this case provides further evidence of lymphoma-associated production of this vitamin.
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PMID:Recurrent hypercalcemia and elevated 1,25-dihydroxyvitamin D levels in Hodgkin's disease. 333 20

In 61 hemodialysis patients undergoing subtotal parathyroidectomy, there was a good correlation between the preoperative serum immunoreactive parathyroid hormone value (iPTH) and the weight of parathyroid tissue removed surgically (p less than or equal to 0.001). Postoperatively, iPTH decreased rapidly from an initial mean (+/- SD) of 2,928 +/- 1,600 muleq/ml and remained at 365 +/- 296 muleq/ml at last follow-up of patients still undergoing hemodialysis (normal, less than 50 muleq/ml). Of six patients who had recurrent hyperparathyroidism (10 percent of total), three required a second subtotal parathyroidectomy. Aluminum-related osteomalacia eventually developed in six patients with bone biopsy-proven hyperparathyroidism before parathyroidectomy. Nine patients with severe fracturing bone disease and hypercalcemia preoperatively but without clear evidence of hyperparathyroidism did not show a favorable response to subtotal parathyroidectomy (high mortality within 28 months, persistence of hypercalcemia, and symptomatic bone disease). Thus, subtotal parathyroidectomy can benefit patients with clearly established severe progressive hyperparathyroidism not responsive to medical therapy but is contraindicated in patients with low iPTH values and no bone biopsy evidence of severe hyperparathyroidism.
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PMID:Results of subtotal parathyroidectomy in hemodialysis patients. 333 31

The treatment of hypercalcemia of malignancy is troublesome. Personal experience with breast cancer associated hypercalcemia is presented. Eight patients were hydrated with intravenous administration of saline solution containing high doses of salmon calcitonin and subsequently six were treated with antiblastic polychemotherapy. Calcium level fell to normal in all patients. Hypercalcemia, with or without evidence of metastatic bone disease, may be caused by the production of humoral substance by tumoral tissue. In our experience the first therapeutic stage is the infusion of saline solution containing high doses of calcitonin, while the elective treatment is antiblastic polychemotherapy which, acting on tumour growth, may inhibit the release of humoral mediators of hypercalcemia causing a slower but stable reduction in serum calcium level.
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PMID:[Update on paraneoplastic hypercalcemia. Our experience in the treatment of hypercalcemic states of patients with advanced breast carcinoma]. 340 54

Over a period of 42 years, 581 patients with presumed hyperparathyroidism underwent an initial cervical exploration. Abnormal parathyroid glands were removed from 495 patients (85.2%). There was a greater probability of operative success in women, patients over 50 years of age, and patients with hypercalcemia, hypertension, or nonspecific abdominal pain. There was no association of operative outcome with some of the "classic" manifestations of hyperparathyroidism--peptic ulcer disease, neuropsychiatric symptoms, pancreatitis, bone disease, or urolithiasis. The probability of surgical success improved with time, increasing from 56 per cent in the 1950s to 97 per cent in the present decade. This improvement appears to be related to greater operative experience, since all four parathyroid glands were more likely to be found with increased experience, and there was a strong correlation between finding four parathyroids and achieving persistent normocalcemia. The most common causes of operative failure were inaccurate calcium assays (the patient was not truly hypercalcemic), an inappropriate diagnosis ("normocalcemic hyperparathyroidism"), and surgical inexperience. These three factors accounted for at least three fourths of all negative explorations. More accurate diagnostic studies, and careful exploration by an experienced surgeon should maximize the probability of a successful operation for primary hyperparathyroidism.
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PMID:Causes of the failed cervical exploration for primary hyperparathyroidism. 341 98

Sixty-eight patients with mild primary hyperparathyroidism were studied for a mean period of 4.5 years (median 3.3). Seven of these patients presented with renal colic while the rest had no symptoms. There was no significant deterioration in mean serum creatinine, total calcium or ionized calcium concentrations during this period. No patient had progressive renal stone or parathyroid bone disease. Hypertension was defined as a systolic or diastolic blood pressure greater than one standard deviation from the age-sex mean, or if hypotensive drugs were required. Thirty-nine per cent were hypertensive at presentation and 42 per cent became hypertensive later. Four patients died from causes unrelated to hypercalcaemia and three required parathyroidectomy when serum calcium concentration rose above 3.0 mmol/l. Patients over 55 with mild asymptomatic primary hyperparathyroidism may be managed conservatively for several years without significant renal impairment, progressive stone disease, parathyroid bone disease or worsening hypercalcaemia. We suggest that observation in these patients could be restricted to six-monthly checks of physical state, blood pressure and serum biochemistry, particularly concentration of calcium creatinine and alkaline phosphatase.
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PMID:The conservative management of primary hyperparathyroidism. 345 52

Between 1978 and 1984, 19 patients at Royal Perth Hospital (RPH) underwent parathyroidectomy for secondary (renal) hyperparathyroidism. This represented 6.0% of the overall dialysis population treated at RPH during this period of time. The mean duration of pre-operative dialysis for these 19 patients was 48 months, compared with a mean duration of 30 months for the overall dialysis population. The principal indications for parathyroidectomy were symptomatic hyperparathyroid bone disease (10), hypercalcaemia (six), progressive lower limb ischaemia (two) and painful peri-articular calcification (one). The complications of chronic renal failure that were most consistently improved by parathyroidectomy were the clinical, radiological and biochemical manifestations of hyperparathyroid bone disease and hypercalcaemia. Features such as pruritus, soft tissue calcification, vessel wall calcification and peripheral ischaemia responded less predictably. Hyperparathyroid bone disease and hypercalcaemia remain the principal indications for parathyroidectomy in chronic renal failure. Profound postoperative hypocalcaemia was the major early postoperative management problem (seven patients) and was closely linked with the severity of pre-operative hyperparathyroid bone disease. It was also seen more frequently in those patients undergoing total parathyroidectomy with immediate autotransplantation of parathyroid tissue (TP-A), than in those in whom residual parathyroid tissue was left in situ (subtotal parathyroidectomy or STP). Recurrent hyperparathyroidism (four patients) was the major late postoperative complication, but was more frequently the result of a supernumerary or previously overlooked fourth parathyroid gland (three), than due to hyperplasia of residual parathyroid tissue (one). STP and TP-A were equally effective in controlling or reversing renal hyperparathyroidism, but the former was associated with a lower incidence of postoperative management problems and should be the preferred operation in this group of patients.
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PMID:Parathyroidectomy in chronic renal failure. 345 32

Eight patients with childhood acute lymphoblastic leukemia (ALL) and hypercalcemia, osteopenia, or vertebral compression fractures seen at our institution during the last 12 years were evaluated for biochemical evidence of bone disease. Five patients were hypercalcemic, three had abnormal phosphorous levels, and four had elevated alkaline phosphatase values. Parathyroid hormone (PTH) was measured by a polyvalent radioimmunoassay in five patients and these levels were abnormally high in three patients. Four of these five patients also had PTH measured by a midregion-specific radioimmunoassay. One patient had a high PTH value. Two patients had low levels and one patient had a normal PTH level. Although these studies suggest diverse biochemical mechanisms may be contributing to the bone changes and hypercalcemia seen in childhood ALL, ectopic PTH production as well as ectopically produced fragments of PTH may have a role in mediating bone resorption and hypercalcemia.
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PMID:The spectrum of metabolic bone disease in lymphoblastic leukemia. 346 23


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