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

Five adult patients with chronic renal failure and associated renal osteodystrophy have been treated for 6 months with 1-alpha-hydroxycholecalciferol (1 alpha-OH-D3), a synthetic vitamin D analogue. All 5 patients had severe metabolic bone changes as estimated by bone scintigraphy. Three patients were hypocalcemic, 4 had elevated serum alkaline phosphatases, 5 had elevated serum immunoreactive parathyroid hormone (i-PTH) concentration and 3 had bone pains. During treatment serum calcium increased in all patients (mean 11.4%) and 3 originally hypocalcemic patients became normocalcemic. Serum alkaline phosphatases decreased (mean 27.3%) and became normal in 4 patients, who initially had elevated values. A pronounced decline in the serum concentration of i-PTH (mean 53%) was seen in all patients and 1 patient obtained normal i-PTH levels after 4 months of treatment. The intestinal calcium absorption, which was low initially, even when calcium intake was considered, rose almost threefold (mean 273%) and reached normal values in all cases. The bone mineral content increased in all patients, but the changes were small (mean 4.9%) and insignificant. Finally, bone pain disappeared in 2 patients and improved in 1 of 3 patients exhibiting this symptom. A linear correlation (r = 0.48, p less than 0.001) was found between the dose of 1 alpha-OH-D3 and serum calcium. But in spite of this and the frequent control, all patients developed one episode of hypercalcemia. This disappeared within 48 hours after discontinuing the drug. It is concluded that treatment with 1 alpha-OH-D3 appears to be of therapeutic value in metabolic bone disease associated with chronic renal failure, but frequent control of blood biochemistry seems mandatory.
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PMID:L-alpha-hydroxycholecalciferol treatment of adults with chronic renal failure. 96 64

The introduction of synthetically produced calcitriol in the early 1970s was an important contribution to the prevention and treatment of renal bone disease. However, despite the efficacy and the availability of oral calcitriol many dialysis patients continued to develop secondary hyperparathyroidism (Norris, 1991). Effective treatment was often impossible in patients with osteitis fibrosa because even low oral doses of calcitriol could cause hypercalcemia (Andress, Norris, Coburn, Slatopolsky, & Sherrad, 1989). From 1981 to the present, numerous studies have been conducted that have demonstrated intravenous calcitriol as being more effective and having several advantages over the oral route of administration, particularly in patients with poor compliance and those with a tendency to develop hypercalcemia.
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PMID:Calcitriol injection for the management of renal osteodystrophy. 129 20

Renal bone disease is an important cause of morbidity in patients on dialysis. The prevalence of renal bone disease, especially aluminium related bone disease, has not been studied in the Singapore dialysis population. As such, we studied 45 haemodialysis patients for renal bone disease using biochemical and radiological parameters. Selected patients underwent a renal biopsy. There were 29 males and 16 females, mean (+/- SEM) age, 44.6 +/- 13.4 years. The duration of haemodialysis ranged from two months to ten years, mean 18.5 months. 75.4% of patients had hyperphosphatasemia, 24.4% had hypocalcemia and two patients had hypercalcemia. There was a wide range in the serum parathyroid hormone levels and 55.4% of patients had serum parathyroid hormone levels > 1000 pmol/L. Patients with symptoms and radiological abnormalities had significantly higher serum parathyroid hormone and alkaline phosphatase levels than those without (P < 0.005). The desferrioxamine infusion test was positive, with an increment in serum aluminium (DL) > 100 mg/L in five patients. Skeletal survey was positive for renal bone disease in 24.4% of patients. There was a significant correlation between the serum parathyroid hormone level, DA1 and the duration of dialysis (r = 0.752, p < 0.001 and r = 0.837, p < 0.001 respectively). There was no correlation between serum parathyroid hormone, calcium, phosphate levels and DA1. The serum haemoglobin concentration and ferritin levels did not show a correlation with DA1. Bone biopsy revealed hyperparathyroid bone disease in two patients, aluminium-related bone disease in one patient and mixed uraemic osteodystrophy in one patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal bone disease in patients on haemodialysis: biochemical and radiological assessment. 129 14

Bisphosphonates appear to provide an attractive, novel approach in the management of patients with uremic bone disease. Only limited studies are available. Based on the understanding of the pathogenesis of renal bone disease, three major indications for the use of bisphosphonates in patients with uremic bone disease emerge: 1. Hypercalcemia related to increased release of calcium from bone. 2. Excessive elevation of bone turnover related to increased parathyroid hormone effects. 3. Extraosseous calcifications due to high calcium phosphorus product. Moreover, further studies may reveal how the combination between bisphosphonates and 1,25 vitamin D therapy might affect uremic bone. Details on doses, mode of administration (continuously vs. intermittently) and optimal duration of therapy should be tested in an animal model of uremic bone disease.
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PMID:The possible use of bisphosphonates in the treatment of renal osteodystrophy. 129 13

We report the case of a 33-year-old woman who was operated on with the diagnosis of primary hyperparathyroidism (PHP) in 1986. She had bone disease and slight hypercalcemia. Two parathyroid glands were removed with a lack of clinical improvement. Subsequently, the serum calcium levels were normal with occasional slight increases. Depressed phosphorus values and elevated alkaline phosphatases and PTH levels were also present, associated with severe bone involvement and muscular weakness. A second cervical exploration performed in 1989 disclosed only a normal parathyroid gland, which was not removed. In 1990, a thoracic CT scan showed the presence of a 1 cm mediastinal nodule close to the great vessels. A thoracotomy was performed to remove this nodule, which proved to be a parathyroid adenoma. After surgery, the patient presented with a "hungry bone" syndrome, characterized by very low levels of calcium, phosphorus and magnesium, which required enteral and parenteral calcium and magnesium supplements, plus dihydroxyvitamin D. The association of normocalcemia and intermittent hypercalcemia with severe bone disease is very rare, as is the presence of a mediastinal adenoma. This could explain the difficulty in the diagnosis in this case.
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PMID:[Primary hyperparathyroidism caused by a mediastinal adenoma with intermittent hypercalcemia and severe bone disease]. 134 71

In order to prevent aluminum toxicity induced by the association of aluminum phosphate binder with 1 alpha(OH) vitamin D3 derivatives and the use of deferoxamine with its own hazards to diagnose and treat this toxicity, we have shown in 1982 that it was possible to replace the iatrogenic association of aluminum phosphate binder with 1 alpha OH vitamin D derivatives by oral calcium carbonate taken with the meals in order to bind phosphate and correct the negative calcium balance. This led to the disappearance of the crippling aluminic osteomalacia and adynamic bone diseases in our center. The effectiveness of CaCO3 without 1 alpha(OH)D3 derivatives in the control of hyperparathyroidism in dialysis patients has been proven by the appearance in four patients of our dialysis population of an histological idiopathic adynamic bone disease associated with relative hypoparathyroidism, and by the finding that more than 50% of our dialysis population treated by this sole treatment have plasma concentration of intact PTH below twice the upper limit of normal (that is, the threshold above which only significant histological osteitis fibrosa is observed). Besides the compliance problem, the limit of CaCO3 is the occurrence of hypercalcemia which occurs in about 8% of the measurements. Since calcium acetate binds twice as much phosphate for the same dose of elemental calcium as CaCO3, its use has been recommended. However, clinical experience has shown that in spite of the fact that half the dose of calcium element given as acetate does actually control predialysis plasma phosphate as well as CaCO3, the incidence of hypercalcemia is not decreased, probably because calcium availability at the alkaline pH of the intestine is much greater with Ca acetate. When hypercalcemia is frequent (and not explained by autonomized hyperparathyroidism, adynamic bone disease, overtreatment with vitamin D, granulomatosis or neoplasia) it is necessary either to decrease the dose of calcium and complete the necessary binding of phosphate by adding small doses of Mg(OH)2 or Mg carbonate, provided the dialysate Mg is decreased to 0.2 to 0.35 mmol/liter to prevent hypermagnesemia or to decrease the dialysate calcium (DCa) concentration. The decrease of DCa can be made either just when hypercalcemia occurs or on a systemic basis according to the amount of CaCO3 used and to the necessity of associating 1 alpha(OH) vitamin D3 derivatives.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use of alkaline calcium salts as phosphate binder in uremic patients. 140 82

Renal osteodystrophy presents with a spectrum of histologic abnormalities. A new entity characterized by a marked decrease in bone turnover without osteoid accumulation, that is, adynamic bone disease, has recently emerged. This new form was thought to be primarily related to aluminum accumulation. Since aluminum-containing phosphate binders have been widely replaced by calcium salts, adynamic bone disease would be expected to disappear over time. However, not only is adynamic bone disease observed in the absence of aluminum intoxication, its incidence does not seem to have decreased. We conducted a retrospective study in 1,803 patients on chronic maintenance dialysis who were biopsied during the last 10 years and assessed the incidence of adynamic bone disease over time in an effort to elucidate the factors associated with its occurrence. Adynamic bone disease was first seen in 1984 in the laboratory. Its incidence increased gradually over the years and, in 1991, still affected approximately 20% of the patients. The primary factors associated with the occurrence of adynamic bone disease include: (a) aluminum accumulation which is currently found in 60% of the patients on chronic maintenance dialysis undergoing biopsies, (b) increasing age of the patients on dialysis, (c) diabetes, and, possibly, (d) chronic ambulatory peritoneal dialysis. The clinical relevance of adynamic bone disease deserves further study. At present, this entity is associated with a tendency towards hypercalcemia, aging of bone due to stunted bone remodeling, a condition which might be associated with impaired repair of physiologic microdamages, and accumulation of microfractures leading to mechanical incompetence and ultimately to higher risk of fractures.
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PMID:Risk of adynamic bone disease in dialyzed patients. 140 83

During pregnancy, calcium is continuously transferred directly from the maternal intestine to the fetal bone, a transfer that is mainly induced by the interrelated actions of the calcium-regulating hormones parathyroid hormone (PTH), 1,25-dihydroxyvitamin D (1,25(OH)2D) and calcitonin. It has recently been demonstrated in animals that PTH-related protein (PTHrP) is the fetal equivalent of PTH. Human PTHrP, originally described as a product of a human lung cancer cell line and implicated in the pathogenesis of humoral hypercalcemia of malignancy, is a protein with 141 amino acids, and it has biochemical actions similar to PTH. It is believed that fetal PTHrP is mainly derived from the placenta during early gestation and from the fetal parathyroid glands during further development and that this protein has the role of maintaining the maternal-fetal calcium gradient either alone or in concert with 1,25(OH)2D. With birth, the placental supply of calcium ceases abruptly, stimulating the increase of PTH and 1,25(OH)2D, which are the main regulators of postnatal calcium metabolism. Alterations in the placental calcium (and phosphate) gradient may be caused by maternal hypo- or hypercalcemia and placental insufficiency and may be followed by transient disorders of calcium metabolism in the newborn. Due to abrupt cessation of the calcium and phosphate supply after delivery at a time when mineral demands are the highest, preterm infants are especially prone to hypocalcemia and osteopathy. If bone disease of prematurity is to be prevented, the amounts of calcium and phosphate must be adequate, as demonstrated by laboratory tests, the most important being calcium and phosphate in urine and alkaline phosphatase activity in serum.
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PMID:[Perinatal calcium metabolism. Physiology and pathophysiology]. 143 20

Calcium carbonate (CaCO3) is an effective phosphate (PO4) binder in uremics, and its use reduces aluminum (AI) intake. By maintaining high serum Ca2+ levels, it decreases serum parathyroid hormone (PTH) levels. Hypercalcemia, however, often limits the dosage. To evaluate the effects of a low Ca2+ peritoneal dialysis solution (PDS; 1.25 mmol/L) on calcium metabolism, the following were studied in continuous ambulatory peritoneal dialysis (CAPD) patients with hypercalcemia (six with high PTH levels, and high turnover bone disease [Group 1], and six with low PTH levels, and low turnover bone disease [Group 2] documented by bone biopsies): 1) serum Ca2+ and PO4 levels; 2) serum PTH levels; 3) serum AI levels; and 4) bone morphology. The follow-up was 12 months. In both groups, within the third month, there was a decrease in serum Ca2+. In Group 2, serum PTH increased, reaching the norm, and in Group 1 it further increased, exceeding the norm. Because in both groups serum Ca2+ was normal, it was possible to give oral CaCO3 (10.5 +/- 2.5 g/day) to control PO4 levels while stopping AI gels. This did not induce any increase in serum Ca2+, whereas serum AI fell significantly. In Group 1, to avoid a further rise of serum PTH, the low Ca2+ PDS was supplemented with calcitriol (mean 3.5 +/- 0.5 microgram/day); this was followed by a reduction in serum PTH with no increase in serum Ca2+ or PO4.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Low calcium peritoneal dialysis solution. Effects on calcium metabolism and bone disease in CAPD patients. 145 29

Parathyroid carcinoma accounts for 0.5 to 5% of all cases of hyperparathyroidism. We reviewed the clinical, surgical, and pathologic features observed in all patients with parathyroid carcinoma evaluated at the Mayo Clinic from 1920 through 1991. Forty-three patients (22 women, 21 men; mean age, 54 yrs, range 29-72) were identified, including 2 with familial hyperparathyroidism. Information on initial presentation was available in 40 patients: 15 (38%) presented with polydipsia or polyuria, 11 (27%) with myalgias or arthralgias, 7 (17%) with weight loss, and 4 (10%) with nephrolithiasis; 3 patients (7%) were asymptomatic at presentation. Of 31 patients in whom the initial neck examination was recorded, 14 (45%) had a palpable neck mass. The mean serum calcium and serum phosphorus levels were 14.6 mg/dl and 2.3 mg/dl, respectively. Parathyroid hormone levels were elevated in 21 of 21 patients (mean elevation, 10.2 times upper limit of normal). Complications included nephrolithiasis in 14 of 25 patients (56%), bone disease in 20 of 22 patients (91%) and both in 8 of 15 patients (53%). All patients underwent primary surgical resection of parathyroid carcinoma. Twenty-six of 43 patients (60%) required a second operation with 18 patients requiring multiple re-explorations. At the second operation, residual tumor was found in the neck (68%), mediastinum (16%), or both (12%). Six patients received radiation therapy to the neck (5 patients) or bones (1 patient) for recurrent or metastatic disease. Of these, 1 patient appeared cured of parathyroid carcinoma by radiation therapy 11 years after documented tumor invasion of his trachea. Repeated excision of tumor recurrences was an effective means of controlling hypercalcemia in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parathyroid carcinoma: clinical and pathologic features in 43 patients. 151 93


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