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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Brown tumor is a focal, bony lesion of hyperparathyroidism that results from parathyroid hormone on bone increasing osteoclastic activity with bone resorption and trabecular fibrosis. This leads to microfractures and hemorrhage and the appearance of brown tumors, which are seen most commonly in primary hyperparathyroidism and less frequently in secondary hyperparathyroidism. Rarely do these tumors involve the orbit. We report the sixth case, to our knowledge, of orbital involvement, in a patient with chronic renal failure (secondary hyperparathyroidism) and review the literature.
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PMID:Brown tumor and secondary hyperparathyroidism. 204 73

Brown tumor of bone (osteitis fibrosa cystica) should be included in the differential diagnosis of lesions that cause false-positive thallium-201 localization in patients with primary hyperparathyroidism. We report a case of a brown tumor of the upper sternum mimicking a superior mediastinal parathyroid neoplasm in a patient with persistent hyperparathyroidism 9 years after a negative neck exploration (with subtotal thyroidectomy and thymectomy). A 201TI/99mTc pertechnetate subtraction scintigram demonstrated complete subtraction of this 201TI focus.
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PMID:Brown tumor of bone: a potential source of false-positive thallium-201 localization. 273 7

This is a first report of primary hyperparathyroidism (HPT) masquerading as a destructive fibrous sphenoid sinus "Brown tumor" associated with progressive blindness and hypercalcemia. Diagnosis of a Brown tumor was delayed despite serial computerized tomography of the head and repeated transnasal and transethmoid sphenoid biopsies demonstrating diffuse fibrosis. Only detection and medical evaluation of hypercalcemia, demonstrating elevation of both serum calcium and C-terminal parathyroid hormone with an elevated chloride/phosphate ratio, prompted neck exploration, thus confirming a solitary left superior parathyroid adenoma. Postoperative normocalcemia occurred synchronously with the return of light perception and the arrest of sphenoid sinus and parasellar erosion. Although maxillary Brown tumors of secondary HPT have been reported, this is the first report of osteitis fibrosa of the sphenoid sinus. Differential diagnosis of an erosive sphenoid lesion with cranial nerve dysfunction, exclusive of inflammatory or vascular disease, should include sarcoidosis, primary and metastatic sphenoid carcinoma, fibrous dysplasia, giant cell reparative granuloma, midline lethal granuloma, chordoma, and chondrosarcoma. Furthermore, the bony destructive lesions with concomitant hypercalcemia of sarcoidosis and HPT are distinguishable by radiographic and laboratory analyses and by the Dent corticosteroid suppression test. Hypercalcemia of primary HPT is associated with elevated serum C-terminal parathormone, osteitis fibrosa, a negative Dent test, and a chloride/phosphate ratio greater than 33 in 94% of primary HPT patients. Hypercalcemia of sarcoidosis is associated with a normal or decreased C-terminal parathormone assay and a positive Dent test, as well as elevated serum immunoglobulins and erythrocyte sedimentation rate, and a positive angiotensin-converting enzyme assay.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sphenoid sinus brown tumor, hypercalcemia, and blindness: an unusual presentation of primary hyperparathyroidism. 379 83

Acute primary hyperparathyroidism is an unusual form of primary hyperparathyroidism characterized by life-threatening hypercalcemia. Forty-three cases reported in the literature since 1974 are reviewed, along with five new cases. The average age of the patients was 55 (27 to 82), with an even distribution between men and women. Marked hypercalcemia (17.5 +/- 2.1 mg/dl) was accompanied by parathyroid hormone levels 20 times normal. Virtually all patients had symptoms. Hyperparathyroid bone disease occurred in 53 percent of patients; even more (69 percent) had nephrolithiasis or nephrocalcinosis. Combined renal and skeletal involvement was seen in 50 percent. Only three deaths were recorded. The pathophysiology of the acute hyperparathyroid state is unknown but appears to consist of uncontrolled parathyroid hormone secretion followed by cycles of hypercalcemia, polyuria, dehydration, reduced renal function, and worsening hypercalcemia. These features of acute primary hyperparathyroidism are compared with the features reported in the literature antedating multichannel screening, and with the features of the common form of primary hyperparathyroidism. Clinical guidelines by which the diagnosis may be suspected are also reviewed.
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PMID:Acute primary hyperparathyroidism. 381 20

Brown tumour is one of the forms in which fibrous-cystic osteitis, which represents the terminal stage of the bone remodelling processes during primary or secondary hyperparathyroidism, is manifested. For years brown tumour was regarded as a typical lesion of primary hyperparathyroidism, but cases of brown tumours in patients with hyperparathyroidism secondary to renal failure were increasingly often reported in the literature. From an epidemiological point of view, the frequency of brown tumours in patients with renal insufficiency is extremely variable, as is the bone site affected. Several bone segments can be affected at once, but the ethmoid and frontal sinus are rarely reported. Symptoms are caused by the considerable dimensions of the brown tumour and its localisation: in the jawbones it may present sometimes painful, hard and clearly palpable swellings; if large, the tumour may deform the appearance of the bone segments affected or alter the function of the masticatory apparatus. In other cases, there is a complete absence of clinical symptoms and diagnosis may be totally coincidental during the radiological examinations. In histological terms, brown tumours are made up by a cell population consisting of rounded or spindle-like mononucleate elements, mixed with a certain number of plurinucleate giant cells, resembling osteoclastic cells, among which recent haemorrhagic infiltrates and hemosiderin deposits (hence the brown colour) are often found. The aim of this study was to report three cases from a population of 107 patients undergoing haemodialysis at the Turin University Centre. In conclusion, the localisation of maxillary brown tumours appears to prefer a young, female population; brown tumours are rarely an early sign of hyperparathyroidism in haemodialysis patients, but they often appear in conditions of advanced hyperparathyroidism which have escaped medical control either owing to unsuitable therapy or scant patient compliance; they are rapidly evolving lesions whose regression may be very slow or not occur even after total parathyroidectomy; the severity of the lesion caused by a brown tumour may lead to evident osteolysis in the maxillofacial district, thus suggesting the need for early and regular radiological screening; in the event of lesions which are already present, from the authors' point of view, the choice of treatment must be oriented towards parathyroidectomy.
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PMID:[Brown tumor of the jaws]. 902 91

Fibrous-cystic osteitis is a bone metabolic disorder related to hyperparathyroidism. This pathological condition shows a bone catabolism enhancement, due to increased level of PTH. Brown tumour is a uni- or multi-focal bone lesion, which represents the terminal stage of the hyperparathyroidism-dependent bone pathology. This focal lesion is not a real neoplasm showing itself as a cellular reparative process, mainly interesting the jaws, specially the mandible. Because of the similar radiological features (cyst-like radiolucency) showed by other lesions, the diagnosis can be difficult. Histology cannot guarantee a certain diagnosis, some lesions, such as giant cell tumour, giant cell granuloma, aneurysmal bone cyst and cherubism, show a similar macroscopical and microscopical features. Differential diagnosis is possible only by comparative evaluation of clinical, radiological and biochemical evidences. Personal experience with a patient affected by maxillary expansive lesion previously diagnosed as GCT is reported. Radiological examinations showed another cyst-like lesion involving the mandible. Clinical history and multifocality of lesions were suggestive for the presence of a systemic disease, laboratory data allowed a primary hyperparathyroidism diagnosis. Parathyroid scintigraphy was performed and detected a parathyroid adenoma. In first instance the patient underwent to surgical operation on the jaws in order to stop the rapid progression of bone lesions, and then another operation for the removal of parathyroid adenoma was performed.
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PMID:[Differential diagnosis in a case of brown tumor caused by primary hyperparathyroidism]. 1076 15

Brown tumor of the larynx is extremely rare. We describe a patient with long-standing primary hyperparathyroidism and severe skeletal involvement associated with brown tumors of the axial and appendicular skeleton and of the thyroid cartilage. Ossification of the laryngeal skeleton may explain the presence of this process in this unusual location.
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PMID:Brown tumor of the thyroid cartilage: CT findings. 1287 99

Brown tumor is a rare clinical entity complicating hyperparathyroidism. It may occur in the head and neck, with the mandible being the most frequent site. Hyperparathyroidism is usually associated with hypercalcemia. We report a case of madibular Brown tumor secondary to primary hyperparathyroidism. In this case in spite of hyperparathyroidism and the bony lesion the serum calcium level was within normal range. The case managed by surgical excision of the mandibular tumor with an en-bloc hemithyroidectomy with inclusion of the diseased parathyroid gland. This case demonstrates that in osteolytic bony lesions a hyperparathyroid complication can be expected even with normal serum calcium level. The presence of normocalcemia in primary hyperparathyroidism should prompt the physician to look for vitamin D deficiency.
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PMID:Normocalcemic hyperparathyroidism presented with mandibular brown tumor: report of a case. 1536 68

Brown tumor of the paranasal sinuses is rare. It is a benign fibro-osseous lesion, typically presenting as an expansile mass that leads to a cortical defect. We presented the radiological findings of a brown tumor of the right maxillary sinus in a 13-year-old boy who presented with complaints of swelling in the right maxillary region, headache, and epistaxis. Biochemical findings were compatible with primary hyperparathyroidism. The lesion was removed by partial parathyroidectomy. No recurrences or residual mass were detected during a six-month follow-up period.
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PMID:[Brown tumor of the maxillary sinus: a case report]. 1549 41


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