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)

Fifteen cases of bone disease in primary hyperparathyroidism were investigated by comparing X-ray findings with metabolic data and histological features. Besides the usual features of subperiosteal resorption, diffuse demineralization and localized destruction, the less common features of osteosclerosis, and the infrequently described response of the growth plate were also demonstrated. The bone changes in roentgenographs were graded on a five point scale, 0-IV. All cases in Grade IV had parathyroid cancers and extremely high serum and urinary calcium values.
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PMID:Comparison of roentgenological and histological features of bone changes in primary hyperparathyroidism. 49 11

In early chronic renal failure, the state of the bones resembles that of type II primary hyperparathyroidism. Cortical bone becomes thinner and more porous, and there is increased extent of surface remodeling. These changes are followed in turn by osteomalacia and osteitis fibrosa, although sometimes these may be alternate rather than successive stages. Bone turnover is less than would be expected for the elevation of PTH level, probably because of 1,25 (OH)2D3 deficiency. The resorption velocity and lamellar bone appositional rates are depressed, but woven bone appositional rate may be increased, possibly because of hyperphosphatemia. Bone mass reflects the summation of three independent processes: loss of lamellar bone due to hyperparathyroidism (depending on the extent of insulation by osteoid); accumulation of partly mineralized osteoid because of osteomalacia; accumulation of woven bone because of osteitis fibrosa. Osteosclerosis may be growth-related metaphyseal, subchondral or diffuse axial, and periosteal neostosis may also occur. Some patients on hemodialysis lose bone because of planing rather than lacunar or dissecting resorption, combined with depression of both lamellar and woven bone formation. Hyperparathyroid bone disease tends to improve slowly after renal transplantation. Persistent hypocalcemia reflects a defect in the calcium homeostatic system and cannot be explained solely by the known stimuli to secondary hyperparathyroidism. The increment in plasma calcium in response to PTH infusion is subnormal, both in early chronic and in acute renal failure, probably because of 1,25(OH)2D3 deficiency. This is also the most likely explanation for the depressed level of blood-bone equilibrium. The activity of all three of the PTH responsive cell systems in bone is depressed in renal failure, probably because all three require 1,25(OH)2D3 in order to function normally. In pseudohypoparathyroidism, as in chronic renal failure, hypocalcemia results from a defect in the regulation of the blood-bone equilibrium. The bone-remodeling system shows all gradations of response, from slight depression of bone turnover to overt osteitis fibrosa, but bone turnover is never as low as in PTH deficiency. These differences may reflect the presence or absence of resistance to PTH of the osteoprogenitor cell as well as of the calcium homeostatic system, or may be due to varying degrees of 1,25(OH)2D3 deficiency, as in chronic renal failure. An increase in plasma calcium in response to PTH can occur either in the untreated state or after treatment with vitamin D because either the error-correcting or remodeling system remains responsive to PTH. Pseudohypoparathyroidism may be subdivided into three types, depending on whether the urinary cyclic-AMP response to PTH remains defective despite treatment with vitamin D, improves with treatment, or is normal before treatment. Only the former is associated with the genetic syndrome of Albright's hereditary osteodystrophy...
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PMID:The actions of parathyroid hormone on bone: relation to bone remodeling and turnover, calcium homeostasis, and metabolic bone disease. Part IV of IV parts: The state of the bones in uremic hyperaparathyroidism--the mechanisms of skeletal resistance to PTH in renal failure and pseudohypoparathyroidism and the role of PTH in osteoporosis, osteopetrosis, and osteofluorosis. 78 23

Osteosclerosis in adults with primary hyperparathyoidism is rare; the usual skeletal manifestation, when presented, is diffuse osteropenia. We describe a patient with generalized osteosclerosis in association with primary hyperparathyroidism. The findings are documented by conventional and fine-detail radiography, absorptiometric bone mineral analysis, quantitative microradiography and histologic examination of bone. The unique features are contrasted with the manifestations recorded in a recently studied group of 87 hyperparathyroid patients. The data presented here support a causal relationship in this patient between parathyroid hormone excess and the development of densely sclerotic bones.
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PMID:Osteosclerosis in primary hyperparathyroidism. 113 42

The term "renal osteodystrophy" is used to include skeletal disorders of patients with chronic renal failure: osteitis fibrosa, osteomalacia, osteosclerosis, osteoporosis and the frequently associated extraskeletal calcifications. It is the chronic glomerular disease with phosphate retention and resultant hyperphosphatemia on one hand and deficient 1,25 (OH)2 D3 and resultant hypocalcemia on the other to induce secondary hyperparathyroidism. The three most common causes of chronic renal failure in our patients are chronic glomerulonephritis, diabetic nephropathy, hypertensive nephropathy in decreasing frequency, polycystic renal disease occurs in five patients. Other miscellaneous causes include nephrotic syndrome, chronic pyelonephritis, systemic lupus erythematosus, periarteritis nodosa, interstitial nephritis and renal stones. The bone changes are similar in primary and secondary hyperparathyroidism and the incidence of brown tumor is about 3% in the former and 1.5 to 1.7% in the latter. We present one among the 94 dialyzed patients who has long-standing severe chronic renal failure from polycystic kidney disease and develops brown tumor in the mid ulna after 7 years on maintenance hemodialysis. The incidence of brown tumor in our series is about 1.1%. Because of increased longevity of the dialyzed patients, brown tumor from secondary hyperparathyroidism is now more commonly observed. Hyperphosphatemia with serum calcium-phosphate products exceeding plasma solubility of 60 to 75 mg/dl may induce soft tissue and vascular calcification. This explains the much higher incidence of soft tissue calcification in secondary than primary hyperparathyroidism; two of our patients with generalized Monckeberg's type arterial calcification and multiple periarticular calcifications in five patients have been observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal osteodystrophy. 164 77

The metabolic bone disease associated with chronic renal failure has been described collectively by the terms "renal osteodystrophy" or "renal-glomerular-osteodystrophy" and consists of osteomalacia, osteitis fibrosa, and osteosclerosis. The skeletal abnormalities may occur either alone or in combination with one another. An increased concentration of circulating immunoreactive-parathyroid hormone (i-PTH) is a recognized feature of patients with chronic renal failure, and the values are usually much higher than those found in patients with primary hyperparathyroidism associated with a parathyroid adenoma. It must, however, be recognized that the high circulatory concentrations of parathyroid hormone found in patients with chronic renal failure are of immunoassayable material which may or may not be of biological significance in respect of activity. A disturbance in the homeostatic control mechanism governing parathyroid hormone, the secretion rate, its metabolism, and target organ resistance to its action are of major importance in the pathogenesis of some aspects of the metabolic bone disease in patients with chronic renal failure. The pathogenesis of the secondary hyperparathyroidism of chronic renal failure, however, also involves disturbances in cholecalciferol metabolism, phosphate retention, and the uremic state per se.
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PMID:Secondary hyperparathyroidism in chronic renal failure. 626 38

The basis for this study is two children with primary hyperparathyroidism (PHPT) who radiographically manifested both marked subperiosteal resorption and prominent osteosclerosis. We hypothesize that the parathyroid hormone (PTH) elevation not only increased osteoclastic resorption of cortical bone but also simultaneously enhanced cancellous bone formation, giving rise to osteosclerosis. In this report, we describe the changes in trabecular and cortical bone density, as measured by quantitative computed tomography (QCT), in these two young patients with severe PHPT, before and after removal of a parathyroid adenoma. Before surgery, the radiographic findings of subperiosteal resorption and osteosclerosis were associated with low cortical and high cancellous bone density values in both children. Within 1 week of surgery, both cortical and cancellous bone density values increased and serum concentrations of calcium and, to a lesser degree, phosphorus decreased due to the "hungry bone syndrome." Twelve weeks after parathyroidectomy, QCT bone density values and skeletal radiographs were normal in both patients. The findings suggest that in patients with severe PHPT, the catabolic effect of PTH on cortical bone may be associated with a simultaneous anabolic effect on cancellous bone, and PTH may cause a significant redistribution of bone mineral from cortical to cancellous bone.
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PMID:Decreased cortical and increased cancellous bone in two children with primary hyperparathyroidism. 854 81

Hyperparathyroidism is an endocrine abnormality that frequently causes diffuse osteopenia in the bones. Osteosclerosis is a rare phenomenon in adults with primary hyperparathyroidism since the usual skeletal manifestation is generalized osteopenia. We describe a patient with generalized osteosclerosis in the jaws and skull in association with primary hyperparathyroidism, while the other skeletal bones had normal or decreased density.
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PMID:Osteosclerosis in a thirty-four-year-old woman with primary hyperparathyroidism. 2590 Dec 65

Primary hyperparathyroidism is the first differential diagnosis when a patient presents with asymptomatic hypercalcemia. The symptoms of hyperparathyroidism can be as grave as skeletal, cardiovascular, and neuropsychological changes. Skeletal manifestations are relatively common, and patient may present with generalized or focal bone pains, fragility fractures, subperiosteal bone resorption, and osteolytic lesions like brown tumors and salt and pepper appearance of the skull. However, focal osteosclerotic lesions of the skull are rare findings in hyperparathyroidism. Only a few cases of associated osteosclerosis are reported in the literature. Here, we report a case of Tc99m SestaMIBI positive parathyroid adenoma with coexisting osteolytic and osteosclerotic skull lesions on Tc99m methylene diphosphonate bone scan.
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PMID:Osteosclerotic and osteolytic manifestations of hyperparathyroidism in a case of Tc99m SestaMIBI positive parathyroid adenoma. 2617 May 73