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)

Aluminum-containing phosphate (Al-binders) employed to control serum phosphorus in patients with chronic renal failure can be associated with the development of aluminum toxicity. To obviate the need for Al-binders, we examined the effectiveness of CaCO3 as a phosphate binder in 31 hemodialysis and 8 CAPD patients followed for 2 months while receiving Al-binders, and then, for 3-14 months while receiving CaCO3 (5.8 +/- 0.4 g/day). Monthly serum phosphorus averaged 5.4 +/- 0.2 mg/dl with Al-binders and 5.1 +/- 0.3 to 5.7 +/- 0.4 mg/dl with CaCO3 (p = NS). There were 25.2 episodes of hyperphosphatemia (serum phosphorus greater than 6.5 mg/dl) per 100 treatment months with Al-binders and 19.2 episodes/100 treatment months with CaCO3 (p = NS). Plasma aluminum levels, 105 +/- 21 micrograms/l during ingestion of Al-binders, fell to 34 +/- 11 micrograms/l after 8 months of therapy with CaCO3 (p less than 0.01). Monthly serum Ca averaged 9.5 +/- 0.1 mg/dl during Al administration and was 8.9 +/- 0.8 to 10.0 +/- 0.2 mg/dl with CaCO3 (p = NS). Thirty-four episodes of hypercalcemia (serum Ca greater than 11.0 mg/dl) occurred in 14 patients ingesting CaCO3, but hypercalcemia did not occur with ingestion of Al-binders. Al-related bone disease was found on bone biopsy in 11 of 13 patients who developed hypercalcemia, compared to only 5 of the 11 biopsied patients who remained normocalcemic (p less than 0.01 by chi 2 analysis). Other side effects included diarrhea in 1 patient and constipation in 3 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Use of calcium carbonate as a phosphate binder in dialysis patients. 380 29

Quantitative bone histology, biochemistry and height velocities were studied in 18 children suffering from chronic renal failure. Eight received calcitriol, 7 ergocalciferol and 3, though alloted to a treatment group, failed to comply with therapy. A histochemical stain for aluminum showed heavy deposition at the calcification front in 3 patients; 2, in the calcitriol group had severe osteomalacia which worsened during treatment, and 1 in the ergocalciferol group had osteomalacia which did not improve. One had never undergone hemodialysis. Bone histology improved markedly in the remaining 12 patients, whichever vitamin D preparation was used; it was unchanged in 3 non-compliant children. Plasma calcium levels rose while parathyroid hormone and alkaline phosphatase levels fell following both treatments, and were unchanged in non-compliant children. Hypercalcemia occurred more frequently following calcitriol therapy (11 episodes) than following ergocalciferol therapy (3 episodes). Height velocities, studied in 11 children, increased in 5 (3 on ergocalciferol and 2 on calcitriol) and were unchanged in 6 (1 on ergocalciferol, 5 on calcitriol). Improved bone histology did not correlate with increase in height velocity. As ergocalciferol and calcitriol had similar therapeutic effects and as side-effects were more common with calcitriol, it is concluded that calcitriol provides no advantage over ergocalciferol in the treatment of renal bone disease in children.
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PMID:Treatment of childhood renal osteodystrophy with calcitriol or ergocalciferol. 387 85

In patients with severe chronic renal failure (SCRF), especially in those undergoing chronic dialysis, aluminium may accumulate in the body. The aluminium is derived from the dialysate and/or from orally-administered, aluminium-containing phosphate binders. Accumulation preferentially occurs in the bone causing aluminium-induced osteomalacia. The physiopathological mechanisms of the disease still have to be elucidated. It has been suggested that aluminium accumulates at the osteoid/calcified-bone boundary (OCBB) inhibiting the influx of calcium there, and also that aluminium directly suppresses the secretion of parathyroid hormone (PTH). A third factor inducing the mineralization defect may be the presence of aluminium within the mitochondria of the osteoblast. In accordance with these hypotheses, hypercalcemia and relatively low iPTH levels are frequently found in aluminium-induced osteomalacia. Histologic methods are essential for demonstrating the actual existence of aluminium-induced osteomalacia. A large bone biopsy is desirable. When the biopsy is not decalcified and embedded in plastic, excellent histologic pictures are obtained wherein mineralized and non-mineralized bone (i.e. osteoid) can be distinguished clearly. Furthermore, the un-decalcified sections can be stained for aluminium, iron or both, and they are suitable for evaluation of the bone marrow status. Several features, like irregularly distributed osteoid with variable thickness, a relatively low number of cubic osteoblasts, and the absence of marrow fibrosis, are suggestive of aluminium-induced osteomalacia. However, the latter can only be proven by histochemical methods, e.g. by the aluminon staining. The treatment of aluminium-induced osteomalacia is quite different from that of other types of renal bone disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aluminium-induced osteomalacia in severe chronic renal failure (SCRF). 391 58

The physiopathology of metabolic bone disease described during long term total parenteral nutrition is poorly understood. We therefore prospectively assessed bone status of seven adult patients [mean age, 42 +/- 16 (SD) yr] treated with cyclic total parenteral nutrition for a period of 7 +/- 2 (SD) months. All patients had hypercalciuria (381 +/- 96 mg/day) associated with negative calcium balance in six of seven patients (-49 +/- 120 mg/day). A correlation was found (r = +0.74, P less than 0.01) between protein intake and calciuria. Two patients developed slight transient hypercalcemia. Serum magnesium and phosphate levels remained within the normal range. A high aluminum load due to the added phosphate solution (253 +/- 84 micrograms/day) was associated with increased serum aluminum levels (52 +/- 38 micrograms/liter). Normal serum levels of 25 hydroxyvitamin D (12 +/- 7 ng/ml) and low normal 1,25 dihydroxyvitamin D levels (21 +/- 8 pg/ml) were found. Serum PTH was normal in five and increased in two of the seven patients. However, in these two patients skeletal unresponsiveness to the action of PTH was found. A new histomorphometric picture of bone was observed; it consisted of a markedly reduced bone formation with subnormal osteoclastic activity leading to a low trabecular bone volume. No osteomalacia was found. The aluminum load may have played a role in these bone defects. The hypercalciuria with negative calcium balance was attributed to the cyclic amino-acid delivery during TPN.
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PMID:Multifactorial low remodeling bone disease during cyclic total parenteral nutrition. 391 65

Ten dialysis-treated patients with hypercalcemia (11.5 +/- 0.3 mg/dl, mean +/- SE) due to renal osteodystrophy were compared with 30 control dialysis-treated patients who were not hypercalcemic (9.5 +/- 0.1 mg/dl). The hypercalcemic patients were more disabled than the control patients. Fifty percent of the hypercalcemic patients and 37 percent of the control patients had a mineralization defect (p greater than 0.6). In the control group, intact parathyroid hormone level was significantly higher in patients with osteitis fibrosa than in those with osteomalacia (247 +/- 39 pg/ml versus 60 +/- 20 pg/ml, respectively, p less than 0.005) whereas in the hypercalcemic patients, parathyroid hormone measurements did not discriminate between these two types of bone disease. Osteomalacia was more severe and bone aluminum staining was stronger in the hypercalcemic patients than in the control patients (2.02 +/- 0.47 versus 0.35 +/- 0.11 mm/mm2 tissue area, p less than 0.001). The mean serum calcium level fell from 11.2 +/- 0.2 mg/dl to 10.5 +/- 0.3 mg/dl (p less than 0.01) in eight hypercalcemic patients treated with 24,25-dihydroxyvitamin D. It is concluded that hypercalcemia in patients undergoing dialysis is associated with an increase in bone aluminum level, and with more severe osteomalacia. Intact parathyroid hormone levels are useful for predicting bone histomorphometric parameters but only when hypercalcemia is not present. The drug, 24,25-dihydroxyvitamin D, was effective in lowering the serum calcium level.
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PMID:Spontaneous hypercalcemia in patients undergoing dialysis. Etiologic and therapeutic considerations. 396 41

From 1948 to 1983, 28 patients with parathyroid carcinoma underwent treatment and analysis at the Massachusetts General Hospital. This represents about 2 percent of the 1,200 patients with hyperparathyroidism managed during the period. Patient ages ranged from 18 to 72 years (mean 45 years) with equal numbers of both sexes (14 women and 14 men). There are several hallmarks that are clues to an increased index of suspicion preoperatively. Nine of the patients (32 percent) presented with palpable neck masses. Eleven patients (39 percent) had a serum calcium level greater than 14 mg/100 ml. Significant elevations of the parathyroid hormone level were noted with values two to three times normal. The incidence and severity of metabolic complications were prominent. These complications included renal stones in 18 patients (64 percent), bone disease in 14 patients (50 percent), peptic ulcer disease in 5 patients (18 percent), parathyroid crisis in 4 patients (14 percent), and pancreatitis in 2 patients (7 percent). Eleven of the patients underwent previous surgical therapy at other institutions, and 17 patients had their initial operation at our institution. Cervical parathyroid carcinomas that ranged from 1.5 to 27 g and 1.5 to 6 cm were excised. The characteristic appearance was a gray-white, stone hard parathyroid mass with invasion of adjacent tissue. The outcome was favorable for 16 surviving patients, with 14 (50 percent) showing no evidence of recurrence 2 to 17 years postoperatively and 2 alive with persistent disease 3 years after operation. Twelve patients died. Of these, eight had unsuccessful initial operative intervention with capsular rupture and dissemination of cancer, one had advanced disease with mediastinal extension which was unresectable, and three died from unrelated causes. Recurrences became apparent within 6 months to 3 years after operation and unfortunately denoted incurable disease. The mean survival time after operation in patients with recurrent disease was 7.6 years, ranging from 1 to 22 years. Carcinoma of the parathyroid gland is a rare entity. Although it is difficult to diagnose preoperatively, there should be an increased index of suspicion in those hyperparathyroid patients with palpable neck masses, profound hypercalcemia (greater than 14 mg/100 ml), marked increase in the parathyroid hormone level to greater than twice normal, and significant metabolic complications. The initial operation must be aggressive yet meticulous with en bloc resection of the parathyroid tumor and all adjacent invaded tissues, avoiding capsular violation or tumor spillage.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Natural history of parathyroid carcinoma. Diagnosis, treatment, and results. 398 91

A patient is described with malignancy, hypercalcaemia and radiological evidence of severe parathyroid bone disease but undetectable concentrations of circulating immunoreactive PTH. Autopsy showed the tumour to be a metastatic bronchial carcinoid with no evidence of primary parathyroid disease. Extracts of the tumour had no PTH immunoreactivity but had high concentrations of a substance with identical activity to PTH in a cytochemical bioassay. The biological activity of the extract was not inhibited by PTH antibodies but was inhibited by an antagonist to PTH bioactivity.
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PMID:Parathyroid hormone-like bioactivity in a patient with severe osteitis fibrosa cystica due to malignancy: renotropic actions of a tumour extract as assessed by cytochemical bioassay. 403 33

In a group of 32 patients with terminal renal failure the initial hypocalcaemia was corrected after two months' adequate maintenance haemodialysis. In seven patients hypercalcaemia occurred with a peak incidence after about six months' treatment. In six of these patients hypercalcaemia was transient and the plasma calcium became normal with haemodialysis alone. In one patient the hypercalcaemia was persistent and the plasma calcium reverted to normal only after subtotal parathyroidectomy. This patient had no radiological bone disease, a normal alkaline phosphatase, and no metastatic calcification of the soft tissues.It is concluded that in some patients with terminal renal failure treated with maintenance haemodialysis autonomy of the parathyroids becomes evident in the absence of bone disease or a raised plasma alkaline phosphatase, and that subsequently with continued dialysis there is a spontaneous involution towards normal parathyroid function.
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PMID:Transient and persistent hypercalcaemia in patients treated by maintenance haemodialysis. 568 Oct 49

The relation between serum calcium and the extent of metastatic bone disease as judged by radionuclide bone scan was examined in a consecutive series of 195 patients with malignant disease. Of 87 patients with hypercalcaemia, 40% had no evidence of skeletal metastatic bone disease and serum calcium values. Of 160 patients judged to have bone-scan evidence of metastatic skeletal involvement, only 32.5% were significantly hypercalcaemic. Further, a negative correlation was found between the extent of metastatic bone disease and serum calcium value. The development of hypercalcaemia in malignancy is not directly related to the presence or extent of metastatic bone disease. It is suggested that the development of hypercalcaemia may depend on an alternative mechanism, such as the production of a humoral substance by tumour tissue, having its effect on calcium metabolism at sites or organs distant from local areas of tumor involvement.
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PMID:Hypercalcaemia and metastatic bone disease: is there a causal link? 612 53

Clodronate disodium (dichloromethylene diphosphonate), a specific inhibitor of bone resorption, was given by mouth (1.0-3.2 g daily) to nine patients with primary hyperparathyroidism for two to 32 weeks so that its clinical and metabolic effects could be evaluated. Bone resorption decreased in all patients as judged by a fall in the fasting urinary calcium to creatinine and hydroxyproline to creatinine ratios. Serum calcium concentration was increased in all patients before treatment and fell in response to treatment to values near the upper end of the normal range. Hypercalcaemia and hypercalciuria recurred when treatment was stopped. In three patients treated for longer than 19 weeks clodronate failed to sustain the reduction in serum calcium concentration but the concentration remained below pretreatment values. These results suggest that clodronate may be of use in the medical management of primary hyperparathyroidism, particularly in patients in whom suppression of bone disease is desirable before surgery or in whom surgery is contraindicated.
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PMID:Drug treatment of primary hyperparathyroidism: use of clodronate disodium. 621 61


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