SEARCH · PubMed Health

Results for “OSTEITIS FIBROSA”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources

PubMed1985

Metabolic bone disease in pseudohypoparathyroidism: radiologic features.

We reviewed the radiographs of six patients with pseudohypoparathyroidism (PHP) manifested by variable renal and skeletal resistance to parathyroid hormone (PTH). Features compatible with hyperparathyroid bone disease, osteomalacia, and rickets were observed. Skeletal changes of hyperparathyroidism included (a) subperiosteal bone resorption, (b) radiolucent lesions, caused by either brown tumors or bone cysts, (c) slipped capital femoral epiphyses, (d) focal areas of osteosclerosis, (e) periosteal neostosis, and (f) osteopenia with reduced cortical and trabecular bone volume. Histologic bone features were compatible with osteitis fibrosa in all patients, which suggests that the skeleton responded to the bone-remodeling effects of PTH despite hormonal resistance at other target sites. Skeletal changes of rickets included metaphyseal irregularities, cupping, and widening of the growth plates. Osteomalacia was indicated by Looser zones in one patient and confirmed by histologic evidence in three patients.

Adolescent↗

PubMed1984

Renal-nonresponsive, bone-responsive pseudohypoparathyroidism. A case with normal vitamin D metabolite levels and clinical features of rickets.

Clinical signs of rickets developed in a previously healthy 13-year-old girl with normal features. She had hypocalcemia, hyperphosphatemia, elevated alkaline phosphatase and parathyroid hormone levels, and normal vitamin D metabolite levels, with osteitis fibrosa cystica on bone biopsy specimen. Her renal function was normal. Treatment with 1 microgram of calcitriol each day resulted in symptomatic and clinical relief and improvement of the serum chemical values. This patient probably has pseudohypoparathyroidism type 1, with renal nonresponsiveness and bone responsiveness. This disorder has the clinical features of rickets, but represents hyperparathyroid bone disease.

Adolescent↗

PubMed2003

[Brown tumors in multiple locations: manifestation of severe renal osteodystrophy. Case report].

We report a 25 years old woman with a four years history of end stage renal disease on hemodialysis. During the last two years of follow up, multiple tender nodules appeared in the left clavicle and ribs. These were diagnosed as brown tumors, secondary to osteitis fibrosa cystica, in the context of a secondary hyperparathyroidism. A subtotal parathyroidectomy was performed and a homologous parathyroid implant was done in the right forearm. The pathological study of the surgical pieces confirmed the presence of the brown tumors and parathyroid hyperplasia. Nine months after surgery, parathormone levels and brown tumor calcifications decreased significantly and bone mineral density increased by 20%.

Adult↗

PubMed1986

Toxicity of parathyroid hormone in uremia.

The most significant complication of elevated parathyroid hormone (PTH) levels in uremia is the development of osteitis fibrosa cystica. The hormone also appears to play a role in soft-tissue and organ calcification, metabolic abnormalities (glucose, lipids), and electroencephalographic changes seen in uremic patients. Its role in the hematological abnormalities of uremia (anemia, bleeding) is controversial. A role for PTH in heart and skeletal muscle dysfunction in uremia has not been clearly established. Further studies are required to establish PTH as a "universal" toxin in uremia.

Anemia↗

PubMed1989

Brown tumor of bone: a potential source of false-positive thallium-201 localization.

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.

Bone and Bones↗

PubMed2005

Multiple brown tumors of the ribs simulating malignancy.

Bone disease associated with primary hyperparathyroidism, known as osteitis fibrosa cystica, is now very rarely encountered, since the parathyroid disorder is most often diagnosed at the early stage of asymptomatic hypercalcemia. Here, we report the case of a patient with multiple pleural-based masses and hypercalcemia, which led to the presumptive diagnosis of malignancy. However, histological and laboratory data were consistent with the development of brown tumors of the ribs due to underlying severe hyperparathyroidism.

Aged↗

PubMedDate not supplied

[Hyperparathyroidism due to parathyroid carcinoma located in the mediastinum].

Parathyroid gland carcinoma is a rare cause of primary hyperparathyroidism. The authors discuss the case of a 56-year-old man who presented with hypercalcemia and multiple bone lesions suggestive of tumor metastases. Laboratory and radiological investigations revealed primary hyperparathyroidism in a patient with evidence of osteitis fibrosa cystica, sustained by carcinoma of a mediastinal parathyroid gland. Early titration of parathyroid hormone (PTH) levels in all patients with hypercalcemia of unclear cause is important for early diagnosis of cases that are tumor-sustained and prevention of the most severe complications. The role of immunostaining with anti-PTH antibodies in demonstrating parathyroid gland tissue in ectopic and/or non-functioning primary tumors, as well as metastases, is also discussed.

Bone Neoplasms↗

PubMed1989

Computed tomographic features of renal osteodystrophy.

The spectrum of musculoskeletal abnormalities seen on routine computed tomographic (CT) examinations of five patients with renal osteodystrophy are described. CT findings included multiple brown tumors, osteitis fibrosa cystica, abnormal sacroiliac joints, periarticular tumoral calcifications, prominent Schmorl's nodes, and slipped capital femoral epiphyses. In this small group of patients, the musculoskeletal abnormalities ranged from the subtle to the dramatic. Although CT examination is rarely used as a screening test for renal osteodystrophy, it is important to be familiar with its many appearances on CT, in order not to confuse the CT changes of renal osteodystrophy with metastatic disease, osteomyelitis, or inflammatory arthritis.

Adolescent↗

PubMed1985

Parathyroidectomy in chronic renal failure.

In order to establish whether parathyroidectomy altered the natural history of ectopic calcification in patients with renal failure we undertook a detailed analysis of 62 patients with hyperparathyroidism secondary to chronic renal failure who were submitted to parathyroidectomy. Biochemical data (61 patients) and radiological skeletal surveys (42 patients) were studied before and after parathyroidectomy. Transiliac bone biopsies were obtained at (or some time in the previous six months before) parathyroidectomy in 30 and in 36 patients after surgery. Paired bone biopsies were available from 17 of these patients. In the majority of patients secondary hyperparathyroidism was controlled after parathyroidectomy although in seven patients (11 per cent), who underwent subtotal parathyroidectomy, it relapsed after initial improvement. Non-visceral soft tissue calcification disappeared or decreased in 60 per cent of the patients after parathyroidectomy. However, despite marked improvement in subperiosteal erosions and histological osteitis fibrosa, with significant reductions in iPTH and Ca X P product after parathyroidectomy, small peripheral arterial calcification developed or progressed in 56 per cent of the patients. Histological osteomalacia after parathyroidectomy developed after operation in two patients. Both had positive aluminium stains for excess aluminium in their bone. Numbers of osteoclasts and the amount of marrow fibrosis declined in parallel following parathyroidectomy, but woven bone persisted for months or years.

Adult↗

PubMed1985

Renal osteodystrophy--pathogenesis and treatment.

Histologic bone changes of osteitis fibrosa and osteomalacia are commonly present in patients with end-stage renal disease. Although many patients are not symptomatic from these bone changes, some patients are severely disabled. Altered metabolism of vitamin D, calcium, phosphorus, and parathyroid hormone occurs in renal failure and contributes to the development of uremic bone disease. This article reviews the current theories of pathogenesis and treatment of renal osteodystrophy. In addition, the clinical presentation, pathogenesis, and treatment of the various aluminum-associated osteomalacic syndromes in uremia are discussed.

Aluminum↗

PubMed1986

Review: Renal osteodystrophy--pathogenesis and treatment.

Aluminum↗

PubMed1976

Diphosphonate therapy in nephrocalcinosis.

4 patients with nephrocalcinosis were treated with disodium ethane 1-hydroxy-1, 1-diphosphonate (EHDP) for a period of 13 months. No clinical side-effects were observed and growth proceeded normally. Radiographic changes of osteitis fibrosa cystica developed in 1 child and bone biopsy in 2 children showed defective osteoid mineralisation. It is suggested that EHDP prevented further crystal deposition in 3 children but did not prevent non-calcium stone formation in the 4th child. In view of this and the development of histological and radiographic evidence of osteomalacia and/or secondary hyperparathyroidism in these patients the value of EHDP remains dubious. On the other hand its use may be justified when rapidly increasing calcification is expected, as for example in hyperoxaluria.

Bartter Syndrome↗

PubMed1989

Multiple forms of parathyroid hormone-like proteins in a human tumour.

The extensive chromatographic characterization of four parathyroid hormone (PTH)-like proteins in a human bronchial carcinoid tumour associated with humoral hypercalcaemia and severe osteitis fibrosa is described. PTH-like bioactivity was detected in acetic acid extracts of the tumour using an in-vitro osteo-sarcoma cell bioassay. The active tumour proteins were positively charged at physiological pH and had apparent Mr of approximately 29,000, 16,000, 4000-9000 and less than 4000. The proteins were immunologically distinct from PTH, but each stimulated PTH-sensitive adenylate cyclase in cultured osteoblastic cells. There was no evidence of PTH gene expression by the tumour. These proteins represent different molecular forms of PTH-related protein.

Biological Assay↗

PubMed1991

Renal osteodystrophy in CAPD.

At start of dialysis most patients have histological bone abnormalities. These can be divided into two groups--high turnover and low turnover bone disease. Low turnover aplastic disease was previously attributed to aluminum accumulation but is now known to occur even in patients with less than 5% surface stainable aluminium. It is characterised by a mineralisation defect, thin osteoid seams, decreased numbers of osteoclasts and osteoblasts and absent aluminium staining. We have avoided aluminium containing phosphate binders (ACPBs) completely, with a combination of oral calcium carbonate and "low calcium" (1.25 mMol/l) dialysis fluid. Phosphate control has been good (mean less than 1.6 mMol/l) and over the first twelve months serum PTH levels have fallen significantly. Transient asymptomatic episodes of hypercalcaemia have occurred but no patient required ACPBs. Bone biopsies at the start of CAPD in 34 patients showed over 50% to have osteitis fibrosa (OF) but in five cases (15.6%) the aplastic lesion was found without aluminium staining. In seven follow-up biopsies OF improved in 3 cases, osteomalacia improved in 1, became aplastic in 1, while aplastic bone worsened in 1 and changed to mild OF in 1. We conclude that the predominant bone lesion in our patients at start of CAPD is OF, but 15% already have aplastic bone. "Low calcium" dialysis fluid enables ACPBs to be avoided in the majority of CAPD patients.

Adult↗

PubMed1987

Muramidase, alpha-1 antitrypsin, alpha-1 antichymotrypsin, and S-100 protein immunoreactivity in giant cell lesions.

A spectrum of giant cell lesions was evaluated for muramidase, alpha-1 antitrypsin, alpha-1 antichymotrypsin, and S-100 protein immunoreactivity using an avidin-biotin-complex immunoperoxidase method. Peripheral giant cell granuloma, central giant cell granuloma, giant cell tumor, osteitis fibrosa cystica, cherubism, and giant cell tumor of tendon sheath showed similar patterns of reactivity. Granulomatous inflammatory lesions stained more intensely for muramidase than did noninflammatory lesions. Alpha-1-antichymotrypsin was a slightly better marker of giant cell lesions than was alpha-1-antitrypsin. Positive S-100 protein staining in half the lesions was thought to be due to the presence of Langerhans cells. The results supported the belief that giant cell lesions of bone and tendon sheath are differentiated toward cells of the mononuclear-phagocyte system and that multinucleated giant cells are derived from macrophages.

Cherubism↗

PubMed1985

Elevated bone aluminum content in dialysis patients without osteomalacia.

In almost all dialysis patients, bone aluminum content (BAC) is elevated in comparison with levels in normal subjects. Extremely high BAC (200 micrograms or more of aluminum per gram of bone) is significantly associated with classic aluminum-related osteomalacia. We noted three patients with elevated BAC but without histologic evidence of typical osteomalacia. Two of the patients had moderately severe osteitis fibrosa (hyperparathyroidism), and one patient had mixed uremic bone disease--predominantly hyperparathyroidism but some impairment of bone mineralization as well. As has recently been reported by others, the deferoxamine infusion test yielded unusual results in these patients. On the basis of our observations, we believe that an isolated measurement of BAC to determine whether aluminum-related osteomalacia is present has certain limitations. Aluminum-related bone disease can be accurately diagnosed only with use of bone histomorphometry. Elevated levels of immunoreactive parathyroid hormone may offer protection from the toxic effects of aluminum.

Adult↗

PubMedDate not supplied

Parathyroid apoplexy manifesting as fever of unknown origin.

OBJECTIVE: To describe a rare clinical presentation of necrosis of a parathyroid adenoma, manifesting as fever of unknown origin. METHODS: We present a case report, including detailed clinical and laboratory data, of a patient with previously undiagnosed primary hyperparathyroidism in whom necrosis of a parathyroid adenoma developed during a psychiatric admission for depression. RESULTS: A 40-year-old woman was admitted with severe depression. During her hospitalization, she was found to have osteitis fibrosa cystica, pathologic fractures of her left femur, and primary hyperparathyroidism. Shortly after her admission, spontaneous necrosis of her parathyroid adenoma developed, in association with high-grade fever, acute hypercalcemic crisis, neck pain, hypophonia, and shortness of breath. Findings on extensive evaluation of the fever remained unremarkable, with persistent high-grade temperatures that resolved postoperatively. CONCLUSION: Spontaneous necrosis of a parathyroid adenoma is a rare but well-documented complication of primary hyperparathyroidism. Fever, a previously undocumented associated finding, might be a part of the clinical syndrome of this complication.

Adenoma↗

PubMed2004

[Severe primary hyperparathyroidism and vitamin D deficiency].

Primary hyperparathyrodism is a common disease, often asymptomatic. A young post-partum woman was hospitalized for functional impotence of the upper right limb and poor health status. Laboratory tests revealed severe primary hyperparathyroidism (osteitis fibrosa cystica and nephrolithiasis) associated with vitamin D deficiency. Technetium 99m and thallium parathyroid scintigraphy showed increased uptake under the left thyroid lobe. After surgical resection of a parathyroid adenoma, serum calcium fell markedly and parathyroid levels declined but remained above normal. Calcium and 25(OH)-vitamin D supplementation led to normal calcium and vitamin D levels in three Months, with marked improvement in the bone lesions visualized on the six-Month x-rays. Based on this observation, we describe the many radiological aspects of bone involvement in long-standing hyperparathyroidism aggravated by vitamin D deficiency. Early diagnosis of hyperparathyroidism is crucial.

Adenoma↗