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)

In order to assess the correlation between menopause and osteoporosis, both in pathogenetic and therapeutical terms, a study was carried out in four comparable group of patients at Department B of the Institute of Gynaecology and Obstetrics at the University of Turin. Patients were divided as follows: 24 patents affected by evident osteoporosis, 39 patients with the first symptoms of osteoporosis, 27 with hypercalcemia and 33 healthy controls. The following tests were performed in all subjects: serum assay of androstenedione, estrone, 17-beta-estradiol, PTH, calcium, phosphorus, alkaline phosphatase and creatinine. Laboratory tests were repeated monthly in all patients and control subjects. Dual chromatic ray bone densitometry was performed in all patients at the start and end of treatment. With regard to therapy, each group was subdivided into two equal subgroups which were treated with carbocalcitonin or conjugated estrogens. From the findings, it is clear that there is a non-significant difference between serum levels of androstenedione, estrone and estradiol in the three groups examined and control subjects. Although the possibility that the fall in steroid hormones might contribute to bone load cannot be excluded, it is not possible to demonstrate that this is the most important factor in the pathogenesis of osteoporosis given that many women do not develop osteoporotic symptoms after menopause. In addition, in therapeutic terms, all bone density parameters considered in patient osteoporosis improved after therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Comparative analysis of therapeutic effects of carbocalcitonin and and conjugated estrogens in post-menopausal osteoporosis]. 208 96

We treated nineteen haemodialysis patients with secondary hyperparathyroidism with increasing oral doses of 1,25 dihydroxycholecalciferol (calcitriol) over a 12-week period and used low calcium dialysate (1.0 mmol/l) to prevent hypercalcaemia. Nine patients received daily calcitriol and ten received calcitriol thrice weekly, and at the end of the study the mean doses were 2.0 micrograms daily and 2.6 micrograms thrice weekly respectively. The regimen was well tolerated with nine episodes of mild hypercalcaemia, none of which were symptomatic. Mean PTH and alkaline phosphatase concentrations decreased from 62.0 pmol/l (15-125) to 22.0 pmol/l(1-70) (P less than 0.01), and 144 IU/l (48-461) to 123 IU/l (61-346) (P less than 0.05) respectively. Mean serum calcium increased from 2.33 mmol/l (2.05-2.55) to 2.52 mmol/l (2.26-2.67) (P less than 0.01). There were no significant changes in serum phosphate, magnesium, or aluminium concentrations and there were no significant differences in outcome between patients receiving daily therapy compared to those receiving it thrice weekly. A combination of high-dose oral calcitriol and low calcium dialysate can reverse secondary hyperparathyroidism without causing hypercalcaemia and these results suggest a benefit over conventional low-dose calcitriol.
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PMID:Low calcium dialysate and high-dose oral calcitriol in the treatment of secondary hyperparathyroidism in haemodialysis patients. 212 83

We have examined the effects of the diphosphonate, clodronate, in 9 haemodialysis patients with severe hyperparathyroid bone disease. Clodronate (300-600 mg infused after dialysis on 5 consecutive occasions) significantly decreased mean serum calcium, phosphate and hydroxyproline. This was associated with an increase in serum immunoassayable parathyroid hormone and activity of alkaline phosphatase. These changes reversed 2-4 weeks after stopping treatment but were sustained when treatment with oral clodronate (1.6 g daily) was supplemented for 2 weeks. Our findings suggest that intravenous clodronate is capable of inhibiting osteoclast-mediated bone resorption in chronic renal failure. The therapeutic potential of clodronate alone or with vitamin D derivatives merits further evaluation, particularly in patients with severe hyperparathyroidism, when the use of D metabolites alone is precluded by the presence of hypercalcaemia.
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PMID:Effects of clodronate in severe hyperparathyroid bone disease in chronic renal failure. 214 21

1. In a prospective study of 160 Asian outpatients, plasma calcium, phosphate, alkaline phosphatase, 25-hydroxyvitamin D and parathyroid hormone were compared with a clinical score to determine which measurements singly or in combination were most useful in the detection of osteomalacia. 2. Bone biopsies were performed in 45 of 48 patients considered to be at risk of osteomalacia. Of the 39 quantifiable bone biopsies, nine showed unequivocal osteomalacia, 13 were judged to be borderline and 17 biopsies were normal. 3. The clinical score was highly sensitive, identifying eight of nine patients with osteomalacia, but not specific, six of 17 normal patients having an abnormal score. 4. Plasma parathyroid hormone was the best single biochemical test for identifying osteomalacia. By using a discriminant function based on parathyroid hormone and alkaline phosphatase, it was possible to classify 96% cases correctly; a discriminant function utilizing calcium, phosphate and alkaline phosphatase was successful in 85% of cases. It was not possible to discriminate between histological groups on the basis of plasma 25-hydroxy-vitamin D values. 5. We confirm that the clinical score is a useful and inexpensive screening test for osteomalacia in British Asians. In those patients with an abnormal score we suggest that parathyroid hormone and alkaline phosphatase are measured. Where both parathyroid hormone and alkaline phosphatase are high, in the absence of hypercalcaemia, histological osteomalacia is extremely likely.
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PMID:Detection of osteomalacia in British Asians: a comparison of clinical score with biochemical measurements. 216 Mar 56

Treatment with 1,25-(OH)2D3 (calcitriol) was compared with placebo in a double-blind, randomized, parallel clinical trial of 24 months' duration. Subjects were white women with postmenopausal osteoporosis. The study was completed by 15 patients who received placebo and 12 patients who received calcitriol. Positive slopes were observed in the active treatment group for total body calcium, bone mineral content of the radius, bone mineral density of the lumbar spine, and radiographic absorptiometry of the middle phalanges. In contrast, negative slopes were observed for the bone mineral measurements in the placebo group. Measurement of urinary hydroxyproline and of serum alkaline phosphatase and osteocalcin suggested that the mechanism of action of 1,25-(OH)2D3 involved reduction of bone resorption. Hypercalciuria occurred regularly and preceded hypercalcemia by about 2 weeks. A decline in creatinine clearance was observed in two patients, one of whom had nephrolithiasis on sonography. Calcitriol is effective in preventing bone loss, but must be used with caution.
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PMID:Role of calcitriol in the treatment of postmenopausal osteoporosis. 218 76

A 10-year-old boy with leukaemia-associated hypercalcaemia was treated with aminohydroxypropylidene biphosphonate (AHPrBP previously APD) in a total dosage of 60 mg over 5 days, when the condition failed to respond to rehydration and frusemide and no sustained effect was produced by haemodialysis with a calcium (Ca)-free dialysate. Bone films showed no lytic lesions, and AHPrBP, which is a potent inhibitor of osteoclast-mediated bone resorption was well tolerated and induced a rapid and sustained fall in plasma Ca (from 3.42 to 2.07 mM in 5 days). Plasma magnesium and alkaline phosphatase remained normal. The results could have been affected by other drugs [vincristine, cyclophosphamide, zorubicin (Rubidazone) L-asparaginase and prednisone] which were simultaneously administered. However, the observation that: (1) the response curve of plasma Ca was similar to that reported when AHPrBP was used alone, (2) there was complete inhibition of urinary Ca excretion and (3) hypocalcaemia occurred suggests that AHPrBP was the major cause of the reduction in plasma Ca. AHPrBP should be considered a potential therapy for hypercalcaemia in childhood malignancy.
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PMID:Leukaemia-associated hypercalcaemia in a 10-year-old boy: effectiveness of aminohydroxypropylidene biphosphonate. 224 18

We evaluated the serum osteocalcin and alkaline phosphatase levels and the urinary hydroxyproline excretion in patients with blastic, lithic or mixed metastases, humoral malignant hypercalcemia (HMH) and myeloma. In patients with metastasis of any type osteocalcin did not reach a significant increase although in blastic metastases an increase approaching signification was observed. However, the sensitivities of alkaline phosphatase or hydroxyproline were much higher. In HMH hydroxyproline increased to levels similar to those found in primary hyperparathyroidism. By contrast, although osteocalcin had a significant increase, its values were much lower than in parathyroid disease. The changes in alkaline phosphatase were nonevaluable. In myeloma none of the three markers changed. The major conclusion of the present study is that osteocalcin has little practical usefulness for the investigation of neoplastic patients.
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PMID:[Bone turnover markers in tumor pathology with bone involvement]. 235 62

MC-903 is a novel vitamin D analogue which has been shown to promote epidermal cell differentiation but is 100 times less active than 1,25 dihydroxyvitamin D3 (1,25(OH)2D) in causing hypercalcemia. In order to determine the activity of this compound on bone cells, we have compared the effects of MC-903 and 1,25 dihydroxyvitamin D3 (1,25(OH)2D) on parameters of cell proliferation and differentiation in cultured normal human osteoblastic cells derived by migration from trabecular bone fragments. Dose response curves showed that MC-903 was 10 to 100 times less effective than 1,25(OH)2D in stimulating the synthesis of the osteoblast specific protein osteocalcin by human bone cells depending on the basal osteocalcin production. In cells showing high basal osteocalcin synthesis, 1,25(OH)2D (10(-8) M) was 2- to 3-fold more potent than MC-903 (10(-8) M) in inducing osteocalcin from 48 to 96 h of treatment. The greater activity of 1,25(OH)2D over MC-903 was observed in human bone cell cultures with elevated basal osteocalcin levels, indicating that the response to 1,25(OH)2D but not to MC-903 was amplified in cells with the higher osteoblastic characteristics. The effects of MC-903 and 1,25(OH)2D on alkaline phosphatase activity were not markedly different. Transforming Growth Factor-beta (TGF beta) (0.5 ng/mL, 48 h) was found to completely suppress the osteocalcin synthesis induced by 1,25(OH)2D (10(-8) and 10(-9) M), whereas the MC-903-induced osteocalcin synthesis was not affected, suggesting a negative interaction between TGF beta and 1,25(OH)2D but not MC-903 on osteocalcin synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative effects of a novel vitamin D analogue MC-903 and 1,25-dihydroxyvitamin D3 on alkaline phosphatase activity, osteocalcin and DNA synthesis by human osteoblastic cells in culture. 239 Mar 75

X-Ray signs of hyperparathyroid osteodystrophy (HPOT) have been singled out in analysis of roentgenograms of 86 patients. Hypercalcemia has been detected in 76 +/- 5% of patients presenting an x-ray picture of HPOT, hypophosphatemia has been diagnosed in 66 +/- 5%, hypercalciuria in 72 +/- 6%, and increased alkaline phosphatase activity in 67 +/- 7%. Studies of the P-Ca metabolism should be carried out repeatedly over the course of hyperparathyrosis. Combined analysis of laboratory and x-ray findings will help improve the diagnosis and differential diagnosis of HPOT.
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PMID:[A comparative study of laboratory and x-ray data in the diagnosis of hyperparathyroid osteodystrophy]. 247 66

Hypophosphatasia is a hereditary disease characterized by congenital deficiency of tissue alkaline phosphatase. One of its dental features is the shedding of teeth. We have experienced a case which was referred to our clinic with the chief complaints of loss and shedding of lower deciduous central incisors and was diagnosed to be highly suspected of hypophosphatasia as a result of hematological examination at the pediatric clinic. As a result of close systemic and dental examination and further study of changes in the course for two and a half years, the following findings were obtained: 1. Low serum alkaline phosphatase level and hypercalcemia were the systemic findings of the disease. 2. There was no delayed ossification in terms of carpal bone age. 3. X-ray cephalography revealed no particular cephalic abnormality, except the lack of development of frontalis and mandibular. 4. Dental findings comprised marked resorption of upper alveolar bone in the front teeth area and pronounced instability of front deciduous teeth. 5. As for changes in oral symptoms, extraction of A because of pronounced instability was followed by spontaneous shedding of A. About one year later, A was extracted because of marked instability. At the time of this writing, A was slightly instable without any abnormality in the other teeth. 6. Pathohistological study of the extracted teeth disclosed only a little resorption of cement of root apex and dysgonic periodontium without any marked tissue changes.
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PMID:[Dental study of hypophosphatasic child]. 248 52


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