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Query: UMLS:C0005940 (bone disease)
7,459 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Data are presented on 97 patients with primary hyperparathyroidism who constitute a representative cohort of the disease seen today. The average calcium (11.1 +/- 0.1 mg/dl; normal 8.7-10.7), phosphorus (2.8 +/- 0.1 mg/dl; normal 2.5-4.5), and parathyroid hormone level by immunoradiometric assay (119 +/- 7 pg/ml; normal 10-65) are typical of the modern presentation of primary hyperparathyroidism. Most patients were asymptomatic in that there was evidence for nephrolithiasis in only 18% and for radiologically evident bone disease in only 1% of patients. Nevertheless, when patients were evaluated with bone densitometry and with histomorphometric analysis of the bone biopsy specimen, evidence for the hyperparathyroid process could be shown in the majority of patients. Selective reduction of cortical bone and preservation of cancellous bone were apparent. Among patients with nephrolithiasis, no particular feature distinguished them from patients without nephrolithiasis. All biochemical data were similar between both stone and non-stone formers. The selective reduction in cortical bone was seen to the same extent among those with stones as among those without stones. The average 1,25-dihydroxyvitamin D level was not increased among those with stones. When the population was divided into groups with elevated or normal 1,25-dihydroxyvitamin D levels, the incidence of nephrolithiasis was unchanged. The results indicate that bone involvement can be demonstrated among most patients with asymptomatic primary hyperparathyroidism and that no pathophysiologic mechanisms are yet apparent to account for nephrolithiasis in primary hyperparathyroidism.
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PMID:Characterization and evaluation of asymptomatic primary hyperparathyroidism. 166 60

Over the last 25 years, the perceived clinical spectrum of primary hyperparathyroidism (HPT) has changed dramatically from a disorder characterized by severe bone and renal disease to one typically manifested by few or mild symptoms and little evidence of organ damage. Reasons for this change in spectrum include changing demographics (primary HPT is primarily a disease of the middle-aged and elderly), diffusion of medical knowledge leading to a higher index of suspicion, and improved clinical laboratory technology (especially inexpensive and accurate determination of serum calcium and parathyroid hormone). In the first 343 cases of primary HPT seen at the Massachusetts General Hospital, 57% had renal stones, 23% had hyperparathyroid bone disease, and less than 1% had no symptoms. By contrast, studies dating from the availability of automated serum calcium measurement found renal stones and hyperparathyroid bone disease in less than 5% of cases, and about half of cases had few or no symptoms. Most patients with primary HPT today have mild, nonspecific symptoms, such as weakness, fatigue, and mental depression, and such signs as arterial hypertension and osteopenia, and detection of their hypercalcemia is generally serendipitous. The mildness and slow progression seen in many cases of primary HPT has resulted in much controversy about appropriate management.
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PMID:Clinical spectrum of primary hyperparathyroidism: evolution with changes in medical practice and technology. 176 71

Primary hyperparathyroidism (HPT) is a common disorder that mainly afflicts elderly women. It can be diagnosed in at least 1% of all postmenopausal females and autopsy studies indicate an even higher frequency. Although the widespread use of automated serum calcium analyses has increased the awareness of HPT, only 10% of all cases seem to be identified. The diagnosis relies on the demonstration of an inappropriately elevated serum concentration of parathyroid hormone (PTH) relative to the serum calcium value, which need not be markedly raised. Measurements of intact PTH with immunometric methods have considerably improved the diagnostic precision but it is still difficult to evaluate patients with only marginal hypercalcemia. Few patients with diagnosed HPT are completely without symptoms. Symptoms commonly encountered are psychiatric and neuromuscular disturbances. Subclinical bone disease might be relevant but there is insufficient information about its importance in otherwise asymptomatic individuals. Various cardiovascular risk factors appear more commonly in patients with HPT and untreated disease is associated with an increased risk of premature death.
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PMID:Primary hyperparathyroidism: epidemiology, diagnosis and clinical picture. 176 33

The authors reviewed the clinical usefulness of routine comprehensive skeletal surveys in monitoring renal osteodystrophy in 66 patients on chronic maintenance hemodialysis. Only fourteen (22%) of the 66 patients had roentgenographic evidence of hyperparathyroid bone disease. There were no significant differences in serum calcium, phosphate, or aluminum levels between patients with and without evidence of phalangeal subperiosteal bone resorption in the hands. However, serum levels of parathyroid hormone (PTH) (both intact and mid-molecule) and alkaline phosphatase values were significantly higher in the group with subperiosteal bone resorption (p less than 0.01 and p less than 0.02, respectively). Serum intact PTH correlated with alkaline phosphatase better than the mid-molecule assay. Neither intact nor mid-molecule PTH values correlated with serum calcium, phosphate, or aluminum. Hand roentgenograms were most sensitive in detecting early changes of hyperparathyroidism; symphysis pubis was the next best. Other skeletal roentgenographic findings were less revealing, and in a subset of 20 patients, roentgenograms correlated poorly with bone histology. During this study the authors found an 8% prevalence of vertebral compression fractures; all in postmenopausal white women.
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PMID:Skeletal surveys in renal osteodystrophy. 176 1

During the study of parathyroid function in 19 hemodialysis patients with low turnover aluminum bone disease, it was observed that serum parathyroid hormone (PTH) levels were higher during the induction of hypocalcemia than during the recovery from hypocalcemia. This type of PTH response has been termed hysteresis. Hypocalcemia was induced during hemodialysis with a calcium-free dialysate. When the total serum calcium level decreased to 7 mg/dL, the dialysate calcium concentration was changed to 3.5 mEq/L and the dialysis session was completed. One week later, hypercalcemia was induced during hemodialysis with a high-calcium dialysate. The mean basal PTH level was 132 +/- 37 pg/mL (normal, 10 to 65 pg/mL; immunoradiometric (IRMA), Nichols Institute, San Juan Capistrano, CA) and increased to a maximal PTH level of 387 +/- 91 pg/mL during hypocalcemia. For the same ionized calcium concentration, the PTH level was higher during the induction of hypocalcemia than during the recovery from hypocalcemia. Conversely, for the same ionized calcium concentration, the PTH level was greater when hypercalcemia was induced from the nadir of hypocalcemia than when hypercalcemia was induced from basal serum calcium. The set point of calcium (defined as the serum calcium concentration required to reduce maximal PTH by 50%) was greater during the induction of hypocalcemia than during the recovery from hypocalcemia (4.44 +/- 0.10 versus 4.25 +/- 0.09 mg/dL; P = 0.03). The mean basal ionized calcium concentration and the mean ionized calcium concentration at the intersection of the two PTH-calcium curves were the same (4.61 +/- 0.13 versus 4.61 +/- 0.12 mg/dL).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hysteresis of the parathyroid hormone response to hypocalcemia in hemodialysis patients with low turnover aluminum bone disease. 177 94

Twelve patients with serologically and histologically defined symptomatic primary biliary cirrhosis were randomized to receive either oral cyclosporin A or vehicle placebo. The cyclosporin A-treated group had improvement in serum alkaline phosphatase and gamma-glutamyltransferase, suggesting a moderating effect on the course of the liver disease. However, other indices of the liver disease, including liver biopsies, did not show significant improvement. The purpose of this study was to examine the effect of the cyclosporin A treatment on serum indicators of bone and mineral metabolism in these patients, as in its later stages, primary biliary cirrhosis is associated with significant osteopenic bone disease. There were no significant changes in serum calcium, phosphate, magnesium, or vitamin D metabolites between the two groups. However, after one year of treatment, mean serum parathyroid hormone level was significantly lower in the cyclosporin A treatment group, and serum osteocalcin rose significantly. There were no significant changes in any parameter of mineral metabolism in the placebo group. The changes in parathyroid hormone and osteocalcin following cyclosporin A therapy suggest a reduction in the secondary hyperparathyroidism commonly seen with primary biliary cirrhosis and also an increase in bone formation, respectively. This study therefore provides preliminary evidence that cyclosporin A therapy seems to have a mild beneficial effect on the abnormalities of mineral metabolism seen with this disorder.
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PMID:Parameters of calcium metabolism during a pilot study of cyclosporin A in patients with symptomatic primary biliary cirrhosis. 178 26

Gastric exclusion has been introduced as a surgical treatment for morbid obesity. We describe two women who had undergone gastric bypass for obesity with metabolic bone disease and secondary hyperparathyroidism. In one patient transiliac bone biopsy after double tetracycline labelling demonstrated histologic evidence of hyperparathyroidism with osteitis fibrosa cystica. Six additional women who had undergone gastric exclusion were evaluated. Serum phosphorus, calcium, and creatinine were normal in all but one patient who had hypocalcemia. Serum immunoreactive parathyroid hormone was elevated in seven of eight patients and urinary calcium was less than or equal to 2 mmol/d (80 mg/24 h) in 6 patients. Lumbar spine bone mineral density was 86 +/- 7 (mean +/- SE) per cent of predicted and femoral neck bone mineral density was 89 +/- 6 per cent of predicted. Women who have had gastric exclusion for obesity may develop secondary hyperparathyroidism which could result in loss of bone mass.
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PMID:Secondary hyperparathyroidism and osteopenia in women following gastric exclusion surgery for obesity. 179 Apr 6

Renal osteodystrophy is a metabolic bone disease resulted from chronic renal failure. The long-standing alterations in a mineral metabolism generated by renal failure have a profound effect on the skeleton and induce severe systemic metabolic bone disease. Iliac crest biopsies of 194 patients of chronic renal failure were taken and among them 10 cases were examined for Calcium(Ca), phosphorus (p), parathyroid hormone (PTH), 1,25(OH)2D3 and aluminium (Al). The histological bone changes are characterized by development of osteitis fibrosa, increase of bone resorption and the number of osteoclast, increase of osteoid volume (osteoblastic osteoid and acellular osteoid), active remodelling of bone and aluminum deposition in the bone. According to histological appearance, advanced renal bone disease could be subdivided into three groups namely: Secondary hyperparathyroid bone disease (high turnover uremic osteodystrophy), osteomalacia (low turnover uremic osteodystrophy) and mixed uremic osteodystrophy consisting of mild to moderate hyperparathyroid bone disease and defective mineralization. Aluminum-related bone changes might be obtained in various extent in all these groups. Although this classification does not fully represent all the separated entities, and there is also transformation from one form to another, it seems no less significant as a reference for clinical considerations.
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PMID:[Pathological analysis of renal osteodystrophy in 194 cases]. 181 63

Prevention of bone disease associated with impairment of the renal function is desirable. Attempts at such prevention inevitably also embrace prevention of the extraosseous consequences of autonomous hyperparathyroidism, such as the effects of hypercalcaemia, need for parathyroid surgery, and, perhaps, toxic effects of the parathyroid hormone. Strategies for prevention in early, moderate, and end-stage renal failure are reviewed and discussed with particular reference to dietary phosphorus restriction, use of gut phosphorus binders, control of acidosis, calcium supplementation, use of oral and intravenous calcitriol, and use of synthetic analogues of 1,25-dihydroxyvitamin D3. The onset of severe renal osteodystrophy can be delayed. Early attempts at prevention are logical, but we do not know whether these will reduce the need for parathyroid surgery or will make patients feel better or live longer. The costs of prophylaxis--both financial and in terms of incidence and severity of complications--remain to be defined. An individual approach to each patient with renal impairment seems at present appropriate.
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PMID:Prevention of renal osteodystrophy. 181 86

Phosphonoformate (PFA), a monophosphonate pyrophosphate analog, caused plasma biochemical and bone histomorphologic abnormalities in cats given 1,000 mg/kg/day as a continuous intravenous infusion for 14 days. Plasma biochemical alterations observed in young cats (10 weeks old) treated with PFA included increased calcium and decreased phosphorus, alkaline phosphatase, and calcitriol. Young cats treated with PFA developed rickets-like lesions characterized by widened growth plates, increased osteoid, and failure of mineralization. In addition, area of mineralized trabecular bone was decreased. Osteoclast size was increased whereas osteoclast perimeter and number were unaffected in young PFA-treated cats. Plasma alkaline phosphatase was decreased in adult cats (greater than or equal to 1 year old) treated with PFA but changes in calcium, calcitriol, and immunoreactive parathyroid hormone were highly variable and not significantly different. Adult cats treated with PFA exhibited osteomalacia characterized by increased osteoid area, perimeter, and width with failure of mineralization. In addition, static resorption indices were increased in PFA-treated adult cats but area of mineralized trabecular bone was not decreased. The monophosphonate PFA inhibited bone mineralization in young and adult cats similar to bisphosphonate treatment in other species. Because PFA is currently in phase I trials for use in AIDS, results of this study suggest a need to evaluate patients treated with PFA for metabolic bone disease.
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PMID:Age-related differences in phosphonoformate-induced bone toxicity in cats. 182 19


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