Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0005940 (bone disease)
 7,459 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten patients with renal bone disease have been treated with 1 alpha-hydroxycholecalciferol for periods of 10-18 months. Responses in bone histology, plasma alkaline phosphatase, whole body calcium, spinal calcium content and bone mineral content of the forearm were compared. Improvements in histology of bone were seen in 5 patients. These patients showed greater increases in total body calcium, and the increments in total body calcium correlated significantly with decrements in alkaline phosphatase. Changes in forearm bone mineral content or spinal calcium were less predictable and did not invariably reflect measured changes in whole body calcium. We conclude that total body calcium may provide a useful and early index of response to treatment with 1 alpha-hydroxycholecalciferol. In contrast, skeletal changes noted by regional methods of assessment should not be judged as reflecting changes occurring in the whole skeleton, and may even be misleading.
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PMID:Comparison of whole body and regional assessments of calcium balance in renal osteodystrophy in the response to 1 alpha-hydroxy vitamin D3. 60 Sep 60

Patients with severe symptomatic renal osteodystrophy were treated with either 1,25(OH)2D3 or 1 alpha(OH)D3. In 39 instances, there was either reversal of symptoms and/or a marked fall in plasma alkaline phosphatase. Bone biopsies showed improvement of either osteomalacia or osteitis fibrosa, and serum iPTH often fell. In thirteen patients, no improvement occurred. In seven patients, bone biopsy disclosed osteomalacia, and serum iPTH was normal or only slightly elevated. Thus, there was a defect in mineralisation. apparently unrelated to the lack of 1,25(OH)2D3 and in the absence of evidence of phosphate depletion. The other 'treatment failure' group showed osteitis fibrosa on biopsy and iPTH levels were markedly elevated. They are presumed to have marked secondary hyperparathyroidism. These 'treatment failure' groups had higher pre-treatment levels of serum Ca and Mg than in those showing a favourable response; also, hypercalcaemia developed rapidly during 1,25(OH)2D3 treatment. Thus, 1,25(OH)2D3 is efficacious in treating symptomatic osteodystrophy in many uraemic patients, and in other patients, it may help identify bone disease of other, as yet unknown, pathogenesis.
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PMID:Use of 1,25(OH)2-vitamin D3 to separate 'types' on renal osteodystrophy. 60 Sep 61

(1) The bone histology of 233 non-dialysed and 276 haemodialysed patients with chronic renal failure is reviewed. In non-dialysed patients osteitis fibrosa occurred in 83.7% and osteomalacia in 23.6% of patients. Osteomalacia was not found in the absence of osteitis fibrosa. In haemodialysed patients there was a more variable bone histology, sometimes resembling non-dialysed bone disease, but in general with a greater incidence of osteomalacia, especially with increasing time on dialysis. In some patients there was a predominance of osteomalacia accompanied by no or only mild osteitis fibrosa and the serum alkaline phosphatase was normal. (2) The results of treating twenty-six haemodialysed patients with 1alpha-hydroxyvitamin D3 (1alpha-OHD3) are described. Patients with osteomalacia and minimal or no osteitis fibrosa and a normal serum alkaline phosphatase (Group I) in general failed to respond and it is suggested that 1,25-dihydroxyvitamin D3 deficiency is not the sole factor responsible for the osteomalacia in these patients. In contrast, 1alpha-OHD3 therapy was effective in improving osteitis fibrosa and osteomalacia in some patients with moderate to severe degrees of osteitis fibrosa and osteomalacia (Group IIa) and in improving osteitis fibrosa where this occurred alone (Group IIb).
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PMID:Histopathology of renal osteodystrophy with particular reference to the effects of 1alpha-hydroxyvitamin D3 in patients treated by long-term haemodialysis. 60 22

Thirty-five patients with bone disease and chronic renal failure (twenty-four on maintenance haemodialysis) were treated for 7--39 months with 1alpha-hydroxyvitamin D3, 2--2.5 microgram daily by mouth. Symptoms (bone pain and muscle weakness) and radiographic appearances improved and plasma alkaline phosphatase returned to normal in the majority of patients (87, 76 and 75% respectively). In contrast, histological appearances in bone improved in only 46% twenty-three patients from whom paired biopsies were available, and this change was not greatly different from that seen in a comparable group of untreated patients. Significant correlations were noted in individual patients between the changes in symptoms, X-rays, plasma alkaline phosphatase and immunoreactive parathyroid hormone and these, in turn, were related to histological changes in bone, although these latter changes were often small. It is concluded that 1alpha-hydroxyvitamin D3 is a useful new drug in the treatment of renal bone disease, but that the evaluation of the response depends critically on the method of assessment used.
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PMID:Correlation of clinical, biochemical and skeletal responses to 1alpha-hydroxyvitamin D3 in renal bone disease. 60 24

Twenty-three patients with bone disease and chronic renal failure were treated for periods of 4--28 months with 1alpha-hydroxyvitamin D3 (1alpha-OHD3). Improvements in bone histology were consistently seen in patients with features both of osteitis fibrosa and osteomalacia but were not invariably observed in patients with osteitis fibrosa or osteomalacia alone (37 and 50% improved respectively). Several factors influencing the outcome of treatment were assessed on the basis of histological responses in bone. A low level of plasma calcium before treatment, rather than the dose of 1alpha-OHD3 tolerated, was the major detectable factor which favourably affected the histological outcome. Other factors examined, including initial plasma concentrations of phosphate, immunoreactive parathyroid hormone and alkaline phosphatase, and treatment with haemodialysis or dietary supplements of calcium did not apparently influence the response.
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PMID:Factors influencing the response to 1alpha-hydroxyvitamin D3 in patients with renal bone disease. 60 25

A group of 25 patients with chronic terminal renal failure, treated regularly by haemodialysis, was examined. Activity of the bone serum alkaline phosphatase isoenzyme was significantly elevated in 12 patients with signs of bone disease, either isolated or combined with liver damage, even when total alkaline phosphatase activity was within normal limits. The intensity and incidence of raised bone isoenzyme activity increased with the duration of dialysis therapy. Elevated activity of liver alkaline phosphatase isoenzyme correlated with the other laboratory and clinical signs of liver involvement in 16 patients. Activity of the intestinal isoenzyme was elevated in over half the patients, unrelated to liver or bone damage, and was in an inverse correlation to the total serum calcium level. The evaluation of total serum alkaline phosphatase activity had no diagnostic value.
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PMID:The source and clinical significance of serum alkaline phosphatases in patients treated by chronic dialysis. 61 70

Osteomalacia may be a contributory factor in some patients in the development of fractures of the femoral neck and complicate the subsequent management. The level of serum alkaline phosphatase is often valuable in the diagnosis of metabolic bone disease but rises after any uncomplicated fracture, and since such a rise may limit the diagnostic usefulness of this measurement in detecting osteomalacia its extent was assessed in 106 patients. In the majority serum levels were normal on admission, rising after seven to nine days to reach a maximum within a month after fracture. Elevated levels on admission were found in patients with osteomalacia, liver damage or where there had been a delay of several weeks between injury and admission. In a small number of patients normal levels on admission subsequently reached very high values, usually in association with comminution or instability of the fracture. Elevated levels persisted for six to twelve weeks after fracture, the major influence upon the level at this time being the maximum value achieved rather than the presence of osteomalacia. If patients are to be screened for osteomalacia, the alkaline phosphatase must be measured within the first week after a fracture to avoid the distorting influences of the fracture itself.
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PMID:Changes in serum alkaline phosphatase after femoral fractures. 62 81

The alkaline phosphatase isoenzymes in 105 patients with stage D carcinoma of the prostate who entered the National Prostatic Cancer Study were analyzed and these values were correlated to clinical response. Only patients with at least 3 measurements of alkaline phosphatase were evaluated. In 91% of patients with metastatic bone disease, bone alkaline phosphatase was elevated. Those patients with higher pre-treatment levels of alkaline phosphatase generally showed a poorer response to therapy. The results of alkaline phosphatase isoenzyme estimation indicate that these biological markers may be used in the evaluation of patients with metastatic prostatic cancer to predict and monitor their response to chemotherapy. The evaluation of bone and liver alkaline phosphatase isoenzymes in earlier stages also may be valuable.
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PMID:Clinical significance of serum alkaline phosphatase isoenzyme levels in advanced prostatic carcinoma. 63 86

Urinary glycosaminoglycan excretion was studied in 24 cases of disseminated neoplasm, 12 of which had unequivocal evidence of skeletal involvement. Urinary hydroxyproline, cetylpyridinium chloride (CPC)-precipitable uronic acid, and CPC-precipitable hexosamine were expressed as a ratio to urinary creatinine. Glycosaminoglycans contained in urine concentrated x 1000 by vacuum-dialysis were separated by electrophoresis on cellulose acetate and stained with alcian blue. Of the 12 cases with clear evidence of skeletal involvement, eight (66%) showed elevation of serum alkaline phosphatase, five (42%) showed elevation of urinary hydroxyproline, and three (25%) showed elevation of urinary uronic acid. It is concluded that urinary uronic acid is not a sensitive index of skeletal involvement in disseminated neoplasm. The most striking feature of the study was the identification of a well-defined fraction indist inguishable from hyaluronic acid in seven (58%) of the cases with evidence of skeletal involvement. Hyaluronic acid is not normally identifiable in adult human urine. The hyaluronic acid excretors showed more consistent biochemical evidence of bone disease (elevation of serum alkaline phosphatase and urinary hydroxyproline) than the non-excretors. The possibility that the urinary hyaluronic acid is derived from degradation of skeletal hyaluronic acid is discussed. An alternative explanation is that the hyaluronic acid is derived from neoplastic cells as part of a reversion of glycosaminoglycan synthesis to a more ;fetal' state, a glycosaminoglycan counterpart of the production of oncofetal antigens by neoplastic cells.
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PMID:Urinary excretion of glycosaminoglycans in disseminated neoplasm. 64 71

The effectiveness of 1alpha-hydroxycholecalciferol [1alpha-OH)D3] in healing uremic bone disease was investigated in 10 uremic patients on maintenance dialysis. Seven patients received 1alpha-(OH)D3, 2 microgram/day, for six months, and three patients served as a control group. Bone density was determined from X-rays of the second phalanx of the second digit. The apparent intestinal calcium absorption improved on treatment with 1alpha-(OH)D3, serum calcium levels and bone density significantly increased, and a significant decrease in serum alkaline phosphatase activity was observed. In one patient, reversal of uremic myopathy occurred after 17 days of 1alpha-(OH)D3 therapy.
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PMID:1alpha-hydroxycholecalciferol: a promising therapeutic approach for renal osteodystrophy. 68 Nov 63


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