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)

Over a 25-year period, two carcinomas of the parathyroid were observed in 67 cases of primary hyperparathyroidism. The most important signs and symptoms were bone disease, palpable neck metastases, renal stones, and hypercalceamia with high blood levels of parathyroid hormone. Histology revealed that in principle parathyroid carcinoma can be distinguished from adenoma by a trabecular pattern and thick fibrous bands. The presence of cellular atypia and variation or mitotic figures (regressive polymorphia) was not a useful criteria for carcinoma. Local recurrence occurred in both cases.
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PMID:[Parathyroid neoplasm associated with hyperparathyroidism]. 68 29

76 kidney transplant recipients who were up to 4 years post transplant, were studied to assess the incidence of secondary hyperparathyroidism. All patients had good renal function with a mean serum creatinine of 1.4 mg/100 ml. Secondary hyperparathyroidism, as evidenced by increased serum parathyroid hormone levels, was present in 53 of the 76 patients (66%) and radiologic bone disease in 26 of the 76 patients (34%), while hypercalcemia (serum calcium greater than 11.0 mg/100 ml) occurred in only 6 patients (8.5%). The incidence of secondary hyperparathyroidism decreased slightly with time following transplantation, but the degree of secondary hyperparathyroidism as indicated by the levels of serum parathyroid hormone at various times following renal transplantation was essentially similar. The causes for the persistence of this condition are not totally known, but it was found that its incidence was related to the duration of dialysis prior to transplantation.
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PMID:Secondary hyperparathyroidism in human kidney transplant recipients. 78 18

Two children who were receiving maintenance hemodialysis were treated with 1 to 4 microng/day of 1 alpha-hydroxyvitamin D3 for 500 to 700 days, respectively. Sequential parathyroid hormone levels and radiologic evaluations showed considerable improvement in one patient. The second patient initially responded with healing of the bone disease. Subsequent deterioration may be related either to medical noncomplicance and/or interference by diphenylhydantoin in the subsequent hepatic 25-hydroxylation of 1 alpha-OH-D3.
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PMID:Effectiveness of 1 alpha-hydroxyvitamin D3 in children with renal osteodystrophy associated with hemodialysis. 85 43

Chondrocalcinosis is known to be common in hyperparathyroidism. In order to discover the effect of parathyroidectomy on chondrocalcinosis and to investigate this association further, we studied two groups of patients. In one group were 41 postparathyroidectomy patients, and in the other 100 admissions to the acute geriatric unit. The total incidence of chondrocalcinosis in the parathyroidectomy group was 32%, and in the elderly control group 11%. There was little or no osteoarthrosis in these patients. It was found that chondrocalcinosis occurred in the normal population from the age of 75 and in the hyperparathyroid group from the age of 45. In both groups the incidence rose steadily with age. In the hyperparathyroid group alone, preoperative serum calcium levels were no different in those without chondrocalcinosis, suggesting that hypercalcaemia alone is not a sufficient stimulus for chondrocalcinosis. Those with chondrocalcinosis had higher mean preoperative alkaline phosphatase levels, nearly twice as much radiological bone disease, and were older. Parathyroidectomy had no effect on attacks of pseudogout or on preexisting cartilage calcification. A connection with high levels of circulating parathyroid hormone is suggested, and a link with physical age-related changes in cartilage postulated.
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PMID:Chondrocalcinosis in primary hyperparathyroidism. Influence of age, metabolic bone disease, and parathyroidectomy. 85 41

Although anemia has not been widely appreciated as a complication of primary hyperparathyroidism, 5.1% of the individuals with this disorder seen at the Massachusetts General Hospital since 1962 had a normochromic, normocytic anemia that could not be related to blood loss,a deficiency state, or uremia. The anemic group had more advanced bone disease and higher levels of serum calcium, alkaline phosphatase, and parathyroid hormone than the nonanemic group. Results of bone marrow biopsies performed in five patients showed variable degrees of myelofibrosis. However, none of the patients had hepatosplenomegaly, a myelophthisic peripheral blood smear, leukopenia, or thrombocytopenia. Removal of the abnormal parathyroid glands led to improvement or correction of the anemia.
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PMID:Anemia in primary hyperparathyroidism. 85 57

Calcium metabolism was studied prospectively in 12 patients with amyotrophic lateral sclerosis. Two patients showed mild hypocalcemia, malabsorption of calcium, and elevated plasma parathyroid hormone concentrations. Serum 25-hydroxyvitamin D was decreased in one and low-normal in the second. These two patients and a third showed aminoaciduria on thin layer chromatography. Calcium metabolism was apparently restored to normal by dihydrotachysterol, a vitamin D analog, but no improvement in neurologic function resulted. Bone radiographs taken in search of metabolic bone disease showed a significant increase in the incidence of congenital vertebral anomalies in the ALS patients (50% versus 8%). The relationship of the abnormalities in calcium metabolism and in vertebral structure to the etiology of motor neuron disease is not known.
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PMID:Calcium metabolism in amyotrophic lateral sclerosis. 86 4

The effects of small oral doses (1-2 microgram/day) of 1alpha-hydroxycholecalciferol, given for 1 to 2 years, have been examined in four nondialysed adolescents with chronic renal failure and bone disease. Treatment increased calcium retention and plasma calcium, and decreased plasma levels of alkaline phosphatase, hydroxyproline, and immunoreactive parathyroid hormone. X-ray abnormalities of bone regressed, and 2 patients underwent successful surgical correction of knock-knees; bone histology in these 2 was normal at the time of operation. 2 patients developed hypercalcaemia which promptly reversed when 1alpha-hydroxycholecalciferol was withdrawn. In one patient treatment was initially successful, but later there was biochemical, radiographic, and histological evidence of relapse. Long-term treatment of such patients with 1alpha-hydroxycholecalciferol may be effective and facilitate the surgical correction of deformities, but this is not invariable. Toxic effects are similar to those of vitamin D itself, but are more readily reversible.
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PMID:Renal osteodystrophy in nondialysed adolescents. Long-term treatment with 1alpha-hydroxycholecalciferol. 87 33

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

Plasma biochemistry, bone radiology and morphometry were studied in a group of 20 patients receiving maintenance hemodialysis. The aim was to determine if increasing the dialysate calcium concentration would decrease plasma parathyroid hormone and improve the radiologic appearances of bone in patients without producing serious side effects. Dialysate calcium concentration was increased stepwise from 4.5 to 6.0 and then to 7.0 mg/100 ml. Mean predialysis plasma calcium concentration increased from 9.4 to 9.7 and then to 10.0 mg/100 ml and mean predialysis phosphate concentration increased from 5.3 to 5.6 mg/100 ml. Parathyroid hormone concentration was elevated in all patients but the mean concentration did not change significantly although in seven patients a decrease occurred. Six patients had radiologic signs of renal bone disease, two patients showed improvement and three patients developed bone disease during the study. The patients with radiologic bone disease had the highest parathyroid hormone concentrations and the majority were female. Morphometric bone measurements showed that bone loss during the study occurred mainly in the male patients. Soft tissue calcification continued to appear during the study. Although the response to some patients to an increased dialysate calcium concentration was favorable, it was impossible to predict which types of patient would benefit from the use of a dialysate calcium concentration of 7.0 mg/100 ml.
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PMID:Effect of dialysate calcium concentration on bone disease in patients on hemodialysis. 97 45

Pseudohypoparathyroidism (PsH) is a genetic disease characterized by hypocalcemia, hyperphosphatemia, and metabolic unresponsiveness to parathyroid hormone (PTH). The administration of PTH elicits neither a significant rise in serum calcium (calcemic response) nor a decrease in the renal tubule reabsorption of phosphorus (phosphaturic response). The diminished phosphaturic response is due to an inability of PTH to generate cyclic AMP in renal tubule cells. We investigated the question of whether hypocalcemia and deficient calcemic response to PTH are due to a similar cyclic AMP defect in bone or to an acquired vitamin D deficiency. Four patients were studied. The active form of vitamin D (1,25-dihydroxycholecalciferol) was measured in 3 and was low. Treatment with vitamin D2 restored the serum calcium and the calcemic response to PTH to normal without changing the impaired renal response. Bone biopsy was performed in 2 patients and showed morphologic evidence of increased osteoclastic activity and osteomalacia. The data indicate that the hypocalcemia and bone disease in PsH are due to active vitamin D deficiency, possibly resulting from the genetic renal lesion.
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PMID:1,25-Dihydroxycholecalciferol deficiency: the probable cause of hypocalcemia and metabolic bone disease in pseudohypoparathyroidism. 108 95


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