Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Osteocalcin, also called bone gla-protein, is a bone matrix protein synthetized specifically by osteoblasts. It circulates in blood where it can be assayed by the radioimmune method. We measured osteocalcin serum levels in 169 adult controls and 161 patients with different disseminated or localized bone diseases. The normal concentration of 6.2 +/- 0.2 ng/ml increases significantly with age. Serum osteocalcin levels are considerably increased in renal osteodystrophy (114 +/- 23 ng/ml) and to a lesser degree in primary hyperparathyroidism (15.9 +/- 2.8 ng/ml) and Paget's disease (11.4 +/- 0.9 ng/ml), all diseases characterized by increased bone turnover. High levels are also encountered in osteomalacia (9.7 +/- 0.9 ng/ml). Conversely, serum osteocalcin levels are significantly decreased in patients under long-term corticosteroid therapy (4.3 +/- 0.5 ng/ml); they remain normal in patients with bone myeloma and bone metastases under treatment. Finally, osteocalcin is normal in patients with osteoporosis, but its level reflects that of bone turnover as evaluated by iliac bone biopsy. The circulating osteocalcin therefore is the first specific and sensitive marker for bone turnover. Serum osteocalcin measurements make it possible to evaluate the osteoblastic bone formation without biopsy and should provide information on the effectiveness of drugs acting on the bone-forming process.
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PMID:[Osteocalcin (or bone gla-protein), a new biological marker for studying bone pathology]. 293 33

In 6 of 8 adults with severe hypocalcemia and osteomalacia due to vitamin D depletion, basal excretion of nephrogenous cAMP (NcAMP) was increased, but the mean renal phosphate threshold (TmP/GFR) was normal, indicating that the steady state phosphaturic response to cAMP generated by endogenous PTH was impaired, as in pseudohypoparathyroidism type II. In all 6 patients, correction of hypocalcemia by administration of vitamin D and calcium restored the normal relationship between NcAMP and TmP/GFR. By contrast, in 13 patients with normocalcemic osteomalacia due to vitamin D depletion, TmP/GFR was reduced, with a significant negative regression on NcAMP, and rose to normal after treatment. Bone histomorphometry after double tetracycline labeling did not differ significantly between the 2 groups. In 72 patients with primary hyperparathyroidism, the slope of the negative regression of TmP/GFR on NcAMP was the same as in normocalcemic secondary hyperparathyroidism, but the adjusted mean for TmP/GFR was significantly lower. We conclude that the effect of endogenous PTH on phosphate reabsorption varies with the level of plasma calcium, and that dissociation between this effect and the generation of cAMP is nonspecific and can be a consequence of hypocalcemia. Exclusion of vitamin D depletion should be an additional diagnostic criterion for pseudohypoparathyroidism type II.
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PMID:Dissociation between the effects of endogenous parathyroid hormone on adenosine 3',5'-monophosphate generation and phosphate reabsorption in hypocalcemia due to vitamin D depletion: an acquired disorder resembling pseudohypoparathyroidism type II. 298 17

In the course of chronic renal failure, aluminium may deposit and accumulate in different tissues. The aluminium content of parathyroid glands was measured in 31 haemodialysis patients at the time of a parathyroidectomy. The values were compared with those obtained from ten control patients with primary hyperparathyroidism without renal failure, and were related to bone remodelling. Of the 31 patients, 27 had a bone biopsy after double tetracycline labelling, at the time of parathyroidectomy. Twenty-one patients had severe hyperparathyroidism, three patients had hyperparathyroidism associated with osteomalacia, three patients had mild hyperparathyroidism with reduced bone formation. Seven patients had bone aluminium deposits, associated with osteomalacia in one case. The parathyroid aluminium was 62 +/- 35.7 (mumol/g glandular dry weight) in haemodialysis patients and 14.3 +/- 6.3 in control patients (P less than 0.001). A significant positive correlation existed between parathyroid aluminium and serum aluminium (P less than 0.01). The parathyroid aluminium was not different in the patients with and without bone aluminium deposits. A weak correlation was found between parathyroid aluminium and plasma parathyroid hormone. A significant negative correlation existed between parathyroid aluminium and osteoblastic surfaces (P less than 0.05), but no correlation was found with bone formation rate at tissue and bone multicellular units levels. We conclude that aluminium accumulates in parathyroid glands of dialysed patients. Severe hyperparathyroidism may coexist with aluminium overload of parathyroid glands. A marked aluminium overload, however, may cut short the course of hyperparathyroidism and may decrease parathyroid function and cellular activity in bone.
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PMID:Aluminium overload of parathyroid glands in haemodialysed patients with hyperparathyroidism: effect on bone remodelling. 314 Jan 27

A simple method of quantifying skeletal uptake of 99Tcm-methylene diphosphonate, using a rectilinear scanner and a simultaneously image standard, is described. The pattern of quantified uptake in ten regions of the skeleton, the sacro-iliac joints and kidneys in 57 controls and 54 patients with various metabolic bone disease is presented. This method distinguishes patients with primary hyperparathyroidism and osteomalacia from controls with a sensitivity adequate for clinical purposes. In primary hyperparathyroidism the increased skull uptake of tracer correlated well with levels of serum alkaline phosphatase, plasma parathyroid hormone, urinary hydroxyproline excretion and the degree of intracortical resorption in the metacarpal bones. The skull uptake in oestoporosis was normal or moderately elevated and correlated well with bone mass density measurements of the radius. Patients with osteomalacia also showed the greatest increase in tracer uptake in the skull. Patients with thyrotoxicosis differed from most other patients by showing moderately increased uptake in shafts of long bones. We propose our method of quantitative bone uptake as a useful noninvasive test to detect metabolic bone disease and to monitor responses to therapy of bone disease.
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PMID:Quantitative radionuclide scanning in metabolic bone disease. 315 46

Three noninvasive indices of bone formation, serum alkaline phosphatase (s-AP), 24-h whole body retention of diphosphonate (WBR), and serum osteocalcin (s-OC), the two lastnamed clearance-corrected, were compared in 121 patients with various bone disorders and in 50 patients with thyroid disease. In conditions with qualitatively normal matrix formation and mineralization, i.e. thyrotoxicosis, primary hyperparathyroidism, myxoedema and osteoporosis, the three indices deviated from average normal by about the same extent: 134%/128%/200%, 120%/113%/133%, 105%/100%/79% and 89%/86%/69%, respectively. A disproportionately marked deviation of s-AP was observed in states of abnormal matrix formation or mineralization, i.e. osteomalacia and Paget's disease: 430%/145%/282% and 348%/145%/202%, respectively. Furthermore, the formation indices correlate differently with s-calcium in hyper- and hypocalcaemic conditions. In primary hyperparathyroidism the respective r-values were 0.32/0.62/0.68, while an inverse pattern was observed in osteomalacia: -0.60/-0.51/-0.47. As very little is known about the secretion of AP and OC and their role in bone formation and mineralization, the cause(s) for the observed differences remain(s) uncertain.
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PMID:Non-invasive evaluation of bone formation: measurements of serum alkaline phosphatase, whole body retention of diphosphonate and serum osteocalcin in metabolic bone disorders and thyroid disease. 326 12

Osteopenia in the elderly is responsible for 1.3 million fractures per year in the United States. The acute care costs associated with this disorder are between $6 and $10 billion dollars annually. Although much has been learned over the last few years of the factors that predispose patients to osteoporosis and how these factors may be avoided, the precise pathophysiologic mechanisms for bone loss remain obscure. Significant technological advances have been made in the 1980s in the development of noninvasive methods for measuring bone mineral density that give indirect assessments of bone mass. However, these methods are very controversial, are not suitable for mass screening for detecting subjects potentially at risk, and have a limited place in routine clinical care. Osteoporosis is characterized by thinning and fragmentation of trabecular bone, which is probably irreversible when it is far advanced. The most reasonable therapeutic approach may be prevention, which can be achieved in many patients by estrogen therapy in the perimenopausal years and insuring an adequate dietary calcium intake, particularly in adolescents and in the elderly. Physical activity throughout life is also likely to be important in maintaining adequate bone mass. It is important to differentiate osteoporosis from other causes of osteopenia, for example, osteomalacia, primary hyperparathyroidism, and malignant diseases such as myeloma, since these bone diseases have a different natural history, pathophysiology, and treatment.
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PMID:Osteopenia. 331 29

Radionuclide imaging with Tc-99m diphosphonates is not an effective method for detecting or ruling out most osteoporotic diseases including senile osteoporosis or accelerated postmenopausal osteoporosis, and the slow loss of bone tissue generally remains undetected by this modality. Nonetheless, it frequently surpasses or supplements radiographic findings in evaluating the focal complications of metabolic bone disease, including fractures, microfractures, stress fractures, vertebral compressions, Milkman-Looser zones, aseptic necrosis, and acute infarction. In contrast to its secondary role in osteoporosis, bone imaging is of prime importance in investigating hypercalcemia, because the major cause of this abnormality is skeletal metastatic malignancy. In defective bone mineralization due to hyperparathyroidism or osteomalacia, a general increase in diphosphonate skeletal uptake is detected more frequently than radiographic abnormalities. However, normal skeletal images do not rule out metabolic bone disease. Biochemical testing is more reliable in detecting primary hyperparathyroidism. On the other hand, in renal osteodystrophy, biochemical abnormalities are variable and bone imaging is helpful in assessing the severity of skeletal involvement, but not its etiology. Many methods of quantitating the kinetics of Tc-99m diphosphonates have been explored, such as plasma clearance, bone-to-soft-tissue ratios, 24-hour total body retention and 24-hour urinary excretion. None of these have been widely accepted. The value of bone imaging is established in other systemic diseases, most notably in Paget's disease, hypertrophic pulmonary osteoarthropathy, sickle cell disease, fibrous dysplasia, and sympathetic dystrophy.
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PMID:Radionuclide imaging in metabolic and systemic skeletal diseases. 331 47

An 86-year-old woman with a history of treated hyperthyroidism and a 20-year history of untreated primary hyperparathyroidism developed generalized bone pain and a pseudofracture of the midshaft of the left femur. Laboratory examinations revealed elevated serum calcium, alkaline phosphatase, and C-terminal parathyroid hormone levels. Serum inorganic phosphate was below normal and 25-hydroxyvitamin D levels were low-normal. An undecalcified transiliac bone biopsy specimen following tetracycline double labeling revealed osteomalacia and osteitis fibrosa. Following treatment with vitamin D and phosphate, the serum inorganic phosphate level rose to normal. There was a decrease in bone pain, and the pseudofracture healed. However, the serum calcium, alkaline phosphatase, and C-terminal parathyroid hormone levels remained elevated. Longstanding primary hyperparathyroidism causes chronic hypophosphatemia and may lead to osteomalacia. Osteomalacia and its consequences may be part of the spectrum of bone disease seen in patients with longstanding primary hyperparathyroidism.
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PMID:Osteomalacia as a very late manifestation of primary hyperparathyroidism. 334 77

Results are presented of measurements of skeletal blood flow made in 80 patients with painful benign or malignant diseases of the skeleton, excluding patients with Paget's disease. In crush fracture osteoporosis, total bone blood flow was slightly lower than normal although skeletal perfusion was normal. High values of bone blood flow were seen in 14/20 patients with osteomalacia and 3/12 patients with primary hyperparathyroidism. Very high values, comparable to those seen in the most severely affected patients with Paget's disease, were seen in polyostotic fibrous dysplasia, 2 out of 4 cases of Engelmann's disease and 1 out of 3 cases of renal osteodystrophy. Results were less elevated in myositis ossificans, secondary skeletal involvement with breast and prostatic carcinomata, myelomatosis and sympathetic osteodystrophy.
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PMID:Skeletal blood flow in metabolic disorders of the skeleton. 342 88

In a 71-year-old patient with osteomalacia, masked primary hyperparathyroidism was detected by vitamin D therapy for hypercalcemia. Surgery revealed a parathyroid tumor. Interpretation of total plasma calcium may be difficult unless the 25-hydroxyvitamin D levels are outside the normal range.
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PMID:[Hyperparathyroidism masked by osteomalacia. Is vitamin D administration in every case of osteomalacia problem-free?]. 371 42


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