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

Aluminum intoxication is an increasingly frequent complication of chronic renal failure. Because hypercalcemia, elevated parathyroid hormone levels, and radiologic changes said to be typical of osteitis fibrosa commonly occur with aluminum intoxication, it is frequently confused with hyperparathyroidism. In this report, examples of this dilemma are described. The pathophysiology leading to the confusing clinical picture is discussed, with a suggested approach to the problem.
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PMID:Pseudohyperparathyroidism. Syndrome associated with aluminum intoxication in patients with renal failure. 401 98

A study is reported of the estimation of plasma calcium fractions and the calcium-binding affinity of plasma proteins in a total sample of 59 people, which included 29 normal subjects and 30 patients with either hypercalcaemia or hypocalcaemia. It was demonstrated that when the sample was considered as a whole there was a significant correlation between the total plasma calcium concentration and the ultrafiltrable, ionized, and protein-bound calcium fractions and between the ultrafiltrable and ionized fractions. We have also demonstrated that in patients with either hypercalcaemia or hypocalcaemia, including acidotic uraemics, the calcium-binding affinity of the plasma proteins did not differ significantly from that in normal subjects. A significant correlation was also found between the total plasma calcium concentration and the ultrafiltrable, ionized and protein-bound calcium fractions when the normal subjects and the groups of patients with hypercalcaemia and hypocalcaemia due to chronic renal failure were considered as separate groups. The group of patients with hypercalcaemia included patients both with hyperparathyroidism and with hypercalcaemia due to other causes.
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PMID:Plasma calcium fractions and the protein-binding of calcium in normal subjects and in patients with hypercalcaemia and hypocalcaemia. 513 91

In 16 patients with chronic renal failure and osteomalacia resistant to vitamin-D therapy, aluminium was demonstrated in bone biopsy specimens at the interface between thickened osteoid and calcified bone by means of both X-ray microanalysis and a specific histochemical stain. 14 patients also had hypercalcemia. It is suggested that this is due to the blocking by aluminium of additional calcium uptake into bone coupled with the availability of additional calcium from dialysis fluid and vitamin-D therapy. This study provides more aetiological evidence linking aluminium and the development of osteomalacia in chronic renal failure. Further, if hypercalcaemia develops in such patients it is important that aluminium toxicity be excluded as the cause to prevent unnecessary parathyroidectomy.
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PMID:Hypercalcaemic osteomalacia due to aluminium toxicity. 612 1

Four patients under maintenance dialysis for chronic renal failure were suffering from aluminium toxicity. One showed evidence of encephalopathy, two presented with fractures and one was asymptomatic. Hypercalcaemia was constant, whereas high serum aluminium levels were present in only 2 patients. In all cases, iliac bone biopsy specimens, non-decalcified and stained with Aluminium , were found to contain aluminium deposits along the mineralization fronts, thus confirming the diagnosis of aluminium overload. In addition, biopsies revealed an excess of osteoid tissue with morphological and dynamic signs of osteomalacia (2 cases) or strongly depressed bone formation (2 cases). Histomorphometric bone biopsy appears to be the best mean of diagnosing aluminium intoxication and analyzing its effects on bone remodeling and mineralization. It is also very useful to monitor the treatment.
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PMID:[Aluminum poisoning in renal dialysis patients: bone histology. Value of quantitative bone biopsy]. 623 88

Elucidation of the vitamin D endocrine system and the availability of potent metabolites have led to new approaches to vitamin D therapy. The traditional management of exogenous (sunlight) or endogenous (malabsorption) vitamin D deficiency without evidence of disordered vitamin D metabolism has not changed, since it consists of treatment with vitamin D itself--a therapy which preserves the normal intrinsic mechanisms for regulating the rate of production of 1,25-dihydroxycholecalciferol. 1,25-DHCC and the analogue compound 1 alpha-CC should be reserved for treatment of hypocalcemia consequent on chronic renal failure or hypoparathyroidism, where 1-hydroxylation is lacking or impaired. Hypophosphatemic rickets has been treated with 1-hydroxylated compounds, with promising results; this use of the latter metabolites warrants further investigation. The use of vitamin D metabolites and of pharmacological doses of vitamin D itself must be regarded as substitution of a hormone or hormone precursors. Therefore, careful monitoring of serum and urine calcium is required in every patient receiving these compounds, in order to avoid excessive dosage. Special attention must be paid to patients with sarcoidosis since they often develop hypercalcemia after vitamin D or UV-light exposure, as a result of an intrinsic regulation defect in 1,25-DHCC synthesis.
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PMID:[Therapy with vitamin D and D-metabolites]. 626 26

Seventeen undialysed adult patients with chronic renal failure took part in a controlled study of the effects of 1,25(OH)2D3 and D3. After a 6-month observation period the patients were allocated at random to two groups for 6 months of treatment with either 1,25(OH)2D3 (mean dose 0.5 microgram daily) or D3 (dose 100 microgram daily). The treatment was then discontinued and the patients were studied for a further 3 months. In the 1,25(OH)2D3 group the mean serum concentration of 1,25(OH)2D rose significantly during treatment, whereas serum concentratins of 25OHD and 24,25(OH)2D remained unchanged. In the D3 group there was a highly significant increase in serum concentrations of 25OHD and 24,25(OH)2D, whereas serum 1,25(OH)2D remained unchanged. There was a significant fall in serum iPTH in both treatment groups. This fall was unrelated to serum calcium in the D3 group unlike the findings in the 1,25(OH)2D3 group. The data support previous experimental evidence that serum iPTH can be suppressed by 24,25(OH)2D3 and suggest that this analogue may be of clinical importance in the treatment of chronic renal failure without inducing hypercalcaemia.
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PMID:A possible direct effect of 24,25-dihydroxycholecalciferol on the parathyroid gland in patients with chronic renal failure. 627 28

Experimental chronic renal failure (CRF) in rats gave rise to azotemia, hyperphosphatemia, reduction in the proportion of the diaphyses, decrease in them of calcium, phosphorus and hydroxyproline, and to the lowering of the calcium content in the epiphyses. Administration to the animals of 0.025 microgram of 1,25-dioxycholecalciferol (1,25(OH)2D3) a day did not make the indicators under consideration return to normal. At the same time 1,25(OH)2D3 enhanced the degree of hyperphosphatemia and demineralization of the epiphyses, provoked moderate hypercalcemia and dramatically enhanced calcinosis in the aorta and in the remainder of the kidney. Administration of 24,25-dioxycholecalciferol (24,25(OH)2D3) in a dose of 0.25 microgram made the majority of the indicators return to normal, increasing the proportion of the diaphyses and the content in them of calcium and phosphorus, reducing the blood phosphorus content and the degree of azotemia. Furthermore, 24,25(OH)2D3 raised the collagen content in the diaphyses and epiphyses. A higher dose of 24,25(OH)2D3 (1.25 microgram) did not appear more effective. In none the doses applied, 24,25(OH)2D3 produced hypercalcemia or calcinosis. Combination of 1,25(OH)2D3 in a dose of 0,025 microgram and 24,25(OH)2D3 in a dose of 1,25 microgram slightly reduced the hypercalcemic, hyperphosphatemic and calcinosis-inducing effects of 1,25(OH)2D3, completely prevented osteoporotic alterations in the diaphyses, but enhanced the demineralization in the epiphyses, which may point to the advisability of reducing the doses of these metabolites on combined use. The data obtained indicate that 24,25(OH)2D3 is a more effective and safer agent for correcting the disturbances of the phosphorus-calcium metabolism and osseous lesions in CRF than 1,25(OH)2D3.
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PMID:[Effect of 24,25-dioxycholecalciferol on calcium-phosphorus metabolism and bone tissue in rats with experimental renal failure]. 633 22

Intense diffuse uptake of Tc-99m-labeled methylene diphosphonate was seen in both lungs of a patient submitted to surgery for a primary parathyroid adenoma. Five scans performed over the 3 yr following the operation showed persistence of lung uptake despite restoration of normal blood calcium concentration. Mild chronic renal failure caused by the hypercalcemia also persisted postoperatively. The present case confirms that pulmonary uptake of bone tracer can occur asymptomatically when both hypercalcemia and renal failure are present. Lung uptake of a bone tracer probably reflects tissue deposition of hydroxyapatite rather than of amorphous structures. Correction of the hypercalcemia failed to resolve the abnormal scan pictures.
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PMID:Pulmonary uptake of Tc-99m-Labeled methylene diphosphonate in a patient with a parathyroid adenoma. 645 36

Over a period of six months all reports in the South Tees Health District of serum calcium levels greater than 2.70 mmol/l were extracted and patient records examined to establish the associated diseases and patterns of management. A total of 235 reports were evaluated, and after exclusion of doubtful cases 196 patients were included in the study. No cause had been identified in 57 (29%). Many of these were elderly females in whom hypercalcaemia may have been due to primary hyperparathyroidism, but parathyroid hormone levels had not been measured. Of those in whom a diagnosis had been made, 62 (45%) were associated with malignancy and 50 (36%) with chronic renal failure. 72% of cases of hypercalcaemia reported to general practitioners and 13% of those reported to hospital doctors were not investigated further. Despite the inclusion of serum calcium estimation on routine biochemical profiles, many cases of hypercalcaemia are being ignored or not investigated further. The study emphasizes the need for a reliable screening test for primary hyperparathyroidism.
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PMID:Hypercalcaemia in Cleveland: a hospital-based survey. 648 55

A 49-year-old woman at recent climacterium was admitted to our hospital for a dyspeptic-type symptomatology, weight loss, bone pain, moderate polyuric-polydipsic syndrome and in a marked astheno-depressive state. Paraclinical explorations revealed constant hypercalcemia with hypophosphoremia, calciuria, chronic renal failure in the polyuric phase with retention of nitric bases. X-ray films showed diffuse osteoporosis, right nephrocalcinosis and diffuse calcifications of the galactophorous ducts in both breasts. Computerized tomography revealed and surgery confirmed the presence of tumoral tissues on the anterior aspect of the trachea. Histopathologic examination revealed a parathyroid adenoma.
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PMID:Primary hyperparathyroidism associated with galactophorous ducts calcification. 649 88


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