Cases reported "osteitis fibrosa cystica"

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1/67. osteitis fibrosa cystica generalizata with adult T-cell leukaemia: a case report.

    We report on a 62-year-old female initially suffering from extreme pain in both her lower extremities. Plain radiographs revealed multiple osteolytic lesions. Laboratory analyses indicated high levels of serum calcium and parathyroid hormone related protein (PTHrP) and detected HTLV-1 antibody. Histological examination of biopsied specimens which were obtained from osteolytic lesions indicated osteitis fibrosa cystica (OFC) without tumour cells. After the initial biopsy, a subcutaneous mass developed in the left thigh. Microsections of the biopsied mass disclosed adult T-cell leukaemia (ATL) neoplastic cells. Immunohistochemical findings revealed that PTHrP secreted from ATL neoplastic cells induced the OFC. ( info)

2/67. Brown tumour as a complication of secondary hyperparathyroidism in severe long-lasting vitamin d deficiency rickets.

    Brown tumour is a localised form of fibrous-cystic osteitis associated with primary or secondary hyperparathyroidism. Despite the fact that secondary hyperparathyroidism occurs in vitamin d deficiency rickets, no cases of rickets with brown tumour have so far been described. We present a 2.9-year-old girl who had brown tumour of the mandible due to severe vitamin d deficiency rickets. Treatment with vitamin D3 corrected the hyperparathyroidism rapidly which was followed by gradual regression in tumour size. CONCLUSION: Brown tumour can develop in severe, long-standing vitamin d deficiency rickets and responds to vitamin D treatment. ( info)

3/67. Documented hyperparathyroidism of thirty-six years' duration.

    The fascinating history of the first Memorial Hospital patient who was diagnosed as having hyperparathyroidism is reviewed. The illness presented as a cystic mass in a femur in 1929, which was treated with radiation. When the patient was first seen at Memorial Hospital in 1931, the diagnosis of osteitis fibrosa cystica was made; serum calcium was 14 mg/100 ml. In 1932, 6 years after Mandl performed the first parathyroidectomy ever for osteitis fibrosa cystica, this patient's neck was explored, and a right hemithyroidectomy was done, with removal of two normal parathyroid glands. The parathyroid tumor was finally located and partially removed in 1937 after a second failure at neck exploration in 1936. Correspondence between Dr. Edward D. Churchill at the massachusetts General Hospital and Dr. Bradley Coley at Memorial Hospital indicated the concern at that time about uncontrollable tetany, which had been fatal in some contemporary cases and which had led to the practice of only partially removing the tumor. Following this, the patient was observed with documented hypercalcemia and chemical evidence of hyperparathyrodism until age 79. The physical and chemical abnormalities over the years up to and including her last exam are presented. The case is important not only from the historical viewpoint, but because it lends a perspective to long-term parathyroid disease, which is becoming less appreciated in this day of the routine serum calcium by SMA-12 screening. The question of partial parathyroidectomy for adenoma or hyperplasia is reviewed, and the question of observation of patients with mild hypercalcemia who probably have parathyroid tumors is discussed. ( info)

4/67. Secondary hyperparathyroidism and brown tumor in dialyzed patients.

    Secondary hyperparathyroidism is one of the most common complications of chronic renal failure (CRF). Its pathogenesis is multifactorial and still not completely understood. Pathological mechanism of hypocalcemia, hyperphosphatemia and calcitriol deficiency are basic characteristics of CRF and main reason for morphological changes in parathyroid glands and hyperparathyroidism (HP). We present a case of a female patient born in 1975. At the age of 10, a urinary infection was diagnosed for the first time and treated. Six years later, as nausea and vomiting started, CRF based on bilateral reflux was diagnosed and the patient was included in the hemodialysis treatment. The patient was again examined in 1997, when biochemical parameters, including the level of parathyroid hormone, ultrasonography of the neck, scintigraphy of the skeleton and densitometry revealed secondary HP. Parathyreoidectomy was perfomed in 1998. During the follow up period, a tumefaction on a ramus mandibulae dex. was noticed, which was cytologically diagnosed as osteitis fibrosa, "brown tumor", a rare complication of the secondary HP. Surgery was performed and PHD was granuloma gigantocelulare. Prevention and therapy of secondary HP is a problem that demands early actions to avoid possible complications. ( info)

5/67. Tracheobronchopathia osteoplastica: incidental finding at tracheal intubation.

    Subglottic papillomatous growths were observed on routine tracheal intubation for a scheduled colorectal procedure. Fibreoptic bronchoscopy revealed that the lesions extended down to the carina and into the main bronchi. The diagnosis of tracheobronchopathia osteoplastica was made after subsequent bronchoscopy and biopsy in the post-operative period. A brief review of this rare benign condition is given. ( info)

6/67. Disseminated brown tumors from hyperparathyroidism masquerading as metastatic cancer: a complication of parathyroid carcinoma.

    osteitis fibrosa cystica (brown tumors) can be a skeletal manifestation of advanced hyperparathyroidism, including parathyroid cancer. Severe osteitis fibrosa cystica can mimic metastatic bone diseases especially in patients with a history of cancer. Because the treatment and prognosis of these two problems differ greatly considering hyperparathyroidism in the differential diagnosis of patients found to have osteolytic lesions is critical for the appropriate management of these patients. In this case report we describe a patient with a history of renal cell cancer and presumed osteolytic bone metastases. During prophylactic intramedullary rodding to prevent pathologic fracture of her femur she was found to have a benign lesion related to her previously undiagnosed hyperparathyroidism caused by an underlying parathyroid cancer. A detailed review of this disease and the associated bone changes is also included to underscore the importance of an adequate differential diagnosis as well as optimal management. patients with hypercalcemia or bony lesions should not automatically be treated palliatively for metastatic disease just because of a past medical history of cancer. hyperparathyroidism is a readily curable problem if properly diagnosed. ( info)

7/67. Primary hyperparathyroidism: what every orthopedic surgeon should know.

    The diagnosis of hyperparathyroidism should rarely by missed by the orthopedic surgeon. When a patient presents with a pathologic fracture, routine serum calcium should be obtained. If there is evidence of elevated serum calcium or any of the pathognomonic findings of primary hyperparathyroidism on plain radiographs, total and ionized calcium and an intact parathyroid hormone levels should be obtained to make the diagnosis (Figure 5). When patients require surgical treatment for an orthopedic condition and also need surgery for hyperparathyroidism, the procedures can be safely performed simultaneously. Simultaneous parathyroidectomy corrects the underlying endocrinopathy, thereby improving the outcome of the orthopedic procedure. In addition, these procedures can easily be performed simultaneously under one anesthetic and thereby minimize cost and length of hospitalization. ( info)

8/67. Brown tumor of the maxilla associated with primary hyperparathyroidism.

    Brown tumors represent the terminal stage of the remodeling processes during primary or secondary hyperparathyroidism. During the last three decades primary hyperparathyroidism has been recognized much more commonly and the increase has generally been attributed to the routine determination of calcium by new automated methods and the advent of new and more objective parathyroid hormone radioimmunoassay techniques. early diagnosis and successful treatment of the disease have made clinical evidence of bone disease uncommon. While, the mandible is the most frequently involved bone in the head and neck region, maxillary involvement is extremely rare. A case of brown tumor on the maxilla associated with primary hyperparathyroidism is reported. This patient presented multiple skeletal lesions, which are uncommonly seen nowadays. The diagnosis was suggested by the clinical history and confirmed by biochemical, radiological and histopathological determinations. Excision of a parathyroid adenoma normalized the metabolic status. Excision of the maxillary mass led both histopathological confirmation of the disease and early masticator rehabilitation. ( info)

9/67. Brown tumor of the sternum.

    The skeletal changes of severe hyperparathyroidism, known as osteitis fibrosa cystica, are now rarely encountered, because hyperparathyroidism is currently being diagnosed and treated at an early stage. Herein, a case of brown tumor of the sternum is reported; our report adds histologic data on this type of tumor to the literature. ( info)

10/67. Sensorineural deafness due to osteitis fibrosa.

    A 91-year-old woman with deafness died from renal failure. autopsy revealed osteitis fibrosa cystica generalisata, chronic myeloid leukemia, renal atrophy, and hyperplastic parathyroid glands. The temporal bones showed senile osteoporosis, osteitis fibrosa, and chronic myeloid leukemia. The inner ears showed extensive degeneration of cochlear sensorineural elements. The perilymph showed a general increased staining reaction with hematoxylin-eosin that was most evident in localized areas, where marrow spaces of osteitis fibrosa communicated directly with perilymph. It appears that the active diseased marrow exerted a toxic effect on the sensorineural elements of the cochlea by diffusion through the perilymph. ( info)
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