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 325 records · Page 18Linked to original sources

PubMed1999

Dominantly inherited isolated hyperparathyroidism: a syndromic association?

Dominantly inherited isolated hyperparathyroidism (DIIH) is rare in childhood. It may be the first biochemical abnormality in the multiple endocrine neoplasia type I (MEN I) and type II (MEN II) syndromes. Its clinical course is usually asymptomatic or of low morbidity. Radiographic examination is most often normal. We describe six members of a family with distinctive phenotype and DIIH. Limited systemic symptoms and severe radiographic osteitis fibrosa cystica were further unusual features in this family. The diagnosis of DIIH was made only after a 9-year-old girl developed hypercalcaemic crisis after a pathological femoral fracture. Distinctive phenotype, unusual clinical course and unparalleled radiographic changes suggest a not yet described syndromic association.

Acute Disease↗

PubMed1997

Familial hyperparathyroidism without multiple endocrine neoplasia.

Hyperparathyroidism occurs sporadically, in association with multiple endocrine neoplasia (MEN) types I and II, or rarely as familial hyperparathyroidism (FHPT) without other manifestations. We analyzed our experience in 16 FHPT patients from 14 families treated between 1934 and 1991 and reviewed 51 other FHPT patients reported in the literature to determine the clinical course of these patients. Among our 16 patients, 7 (44%) had a serum calcium level >/= 3.75 mmol/L, 5 (31%) presented with hypercalcemic crisis, 3 (19%) had osteitis fibrosa cystica, 5 (31%) had nephrolithiasis, 1 had pancreatitis, 12 (75%) had multiple abnormal parathyroid glands, 3 (19%) had supernumerary glands, and 7 (44%) required reoperation for persistent (n = 4) or recurrent (n = 3) hyperparathyroidism. Three patients (19%) also had papillary thyroid cancer, and 7 (44%) had other coexistent thyroid disorders. Among 51 patients with FHPT reported in the literature, 23 (45%) had serum calcium >/= 3.75 mmol/L, and 23 (45%) had multiple abnormal parathyroid glands; 10 (20%) had recurrent hyperparathyroidism. FHPT without other endocrinopathies is a distinct entity. Patients with FHPT have multiple abnormal parathyroid glands and are prone to both recurrent and persistent hyperparathyroidism. They frequently present with profound hypercalcemia or hypercalcemic crisis, in contrast to patients with MEN-associated hyperparathyroidism or sporadic hyperparathyroidism.

Adolescent↗

PubMed2003

Catabolic and anabolic phases of osteodystrophy in aged rats.

The aims of this study were to investigate the incidence and characteristics of osteodystrophy that occurred in rats which were maintained until death without experimental intervention. We defined and characterized catabolic and anabolic phases of osteodystrophy, based on the morphology of the cortical bone. During the catabolic phase, large resorption cavities appeared within the cortical bone. During the anabolic phase, progressively increased amounts of new bone was formed, which partially or completely filled previous resorption cavities and also extended into the medullary space. Contrary to previous experimental studies of renal failure in rats, which documented suppression of bone formation, the present studies found that the majority of rats displayed evidence of an anabolic phase with extensive new bone formation. The new bone originated within and around fibers that had formed adjacent to bone trabeculae or within resorption cavities. Hence, osteitis fibrosa was a preliminary stage to de novo bone formation. There was an association between the incidence of osteodystrophy and kidney failure as the cause of death, and it is proposed that the observed osteodystrophy had been a consequence of secondary hyperparathyroidism due to renal failure.

Aging↗

PubMed2004

Effect and safety of intermittent weekly administration of human parathyroid hormone 1-34 in patients with primary osteoporosis evaluated by histomorphometry and microstructural analysis of iliac trabecular bone before and after 1 year of treatment.

In order to evaluate the efficacy and safety of intermittent subcutaneous administration of 1-34 N-terminal peptide of human parathyroid hormone (hPTH 1-34), 100 units of hPTH 1-34 was subcutaneously injected once a week for 1 year in ten patients with primary osteoporsis (one male and nine females) with no qualitative abnormality of the bone according to the results of iliac crest biopsy performed previously, followed by a second biopsy after the end of the 1-year administration. Written consent of the patients for participation in the study was obtained. The mean lumbar bone mineral density (LBMD) definitely increased, by 1.8%, 3.4%, and 4.6% after 12, 24, and 48 weeks of hPTH administration, in accordance with previous clinical studies. Histomorphometric analysis after double-tetracycline labeling was completed in six patients (one male and five females) after the exclusion of those who dropped out because of adverse events unrelated to the test drug, or refusal of continuation. Examination of thin hard-tissue sections revealed no qualitative abnormalities of bone tissue or bone marrow cavity, such as osteomalacia, woven bone, or osteitis fibrosa, precluding the contribution of qualitatively abnormal tissue elements to any changes of LBMD in response to hPTH 1-34 administration. Histomorphometric measurement in the second biopsy revealed a tendency for an increase of bone volume, a significant increase of osteoid surface, and a tendency for an increase in other parameters of bone formation, compared with values obtained in the preadministration biopsy. Indices of two-dimensional microstructure obtained by microfocus computed tomography (CT) and results of node-strut analysis indicated improvement of trabecular continuity. In five patients in whom three-dimensional reconstruction images were analyzed, there were significant increases of bone volume and trabecular thickness, and a significant decrease in the trabecular bone pattern factor, a parameter related to the continuity, suggesting an improvement of the three-dimensional trabcular microstructure. Intermittent weekly subcutaneous injections of hPTH (1-34) for 48 weeks increased trabecular bone volume and improved microstructure, without causing the appearance of abnormal bone elements in primary osteoporosis.

Aged↗

PubMed2002

Rheumatic manifestations of primary hyperparathyroidism and parathyroid hormone therapy.

A frequent manifestation of severe primary hyperparathyroidism was the bone disease osteitis fibrosa cystica. Rarely, excess parathyroid hormone (PTH) was associated with gout and calcium pyrophosphate crystal deposition disease. Surgical cure of primary hyperparathyroidism was occasionally associated with pseudogout. Today, primary hyperparathyroidism is generally asymptomatic. Clinically overt rheumatologic and skeletal effects are mainly of historical interest. Skeletal disease is still detectable by more sensitive techniques. In certain circumstances, PTH may be protective and anabolic for the skeleton.

Bone Diseases↗

PubMed1978

The effect of 1alpha(OH)D3 and 1alpha,25(OH)2D3 on the bone in patients with renal osteodystrophy.

Six patients with chronic renal disease and variable degrees of renal osteodystrophy were treated for three weeks with either 1alpha,25-dihydroxyvitamin D3 (1alpha25(OH)D3) or 1alpha,hydroxyvitamin D3 (1alpha(OH)D3) and both the biochemical and osseous responses measured. The most consistent changes seen were an increase in serum calcium concentration to normal, a decrease in immunoreactive parathyroid hormone toward normal, an increase in the extent of the calcification front and a decrease in the extent of fibrous dysplasia in the marrow cavity. Two important parameters which did not change significantly were serum alkaline phosphatase activity and the osteoid volume. These data, in conjunction with that from previous studies, indicate that therapy with 1alpha,25(OH)2D3 or 1alpha(OH)D3 does not heal the osteomalacia of renal osteodystrophy, but that it does suppress the secondary hyperparathyroidism, and ameliorate the osteitis fibrosa seen in patients with chronic renal disease. They raise the likelihood that additional factors, such as metabolites of vitamin D other than 1alpha,25(OH)2D3, play a role in regulating bone formation and/or mineralization.

Aged↗

PubMed1984

Evidence of increased parathyroid activity on discontinuation of high-aluminum dialysate in patients undergoing hemodialysis.

High-aluminum dialysate exposure has been incriminated in the pathogenesis of vitamin D-resistant osteomalacia in patients undergoing long-term hemodialysis. Parathyroid-mediated osteitis fibrosa is rare in these patients. Thirteen patients undergoing longterm hemodialysis were transferred from a center (Unit A) where water used to prepare dialysate was high in aluminum (100 to 450 micrograms/liter) to a new center (Unit B) where dialysate was highly purified (aluminum concentration less than 10 micrograms/liter), and changes in calcium metabolism were studied over a 12-month period. After transfer of patients to Unit B, serum aluminum levels fell (p less than 0.01), whereas serum immunoreactive parathyroid hormone levels rose (p less than 0.01) over 10 months. Over this time, predialysis serum calcium levels did not alter significantly, whereas postdialysis serum calcium levels declined slightly (p less than 0.05). Serum phosphate levels did not alter. Serum alkaline phosphatase levels rose progressively in Unit B (p less than 0.001). Discontinuation of dialysate high in aluminum in patients undergoing long-term hemodialysis may facilitate a rise in parathyroid activity.

Adult↗

PubMed1985

Asymptomatic long-standing idiopathic hypoparathyroidism discovered following delivery of a healthy infant.

A case of long-standing idiopathic hypoparathyroidism that remained asymptomatic during pregnancy is described in a 25-year-old primipara. Clinical signs including carpopedal spasm, convulsions, and acute psychosis developed after the patient gave birth to a healthy infant. In contrast to previous reported cases, no signs of osteitis fibrosa cystica were found in the infant. This is believed to be the first such case described.

Adult↗

PubMed1985

Pseudohyperparathyroidism. Syndrome associated with aluminum intoxication in patients with renal failure.

Aluminum intoxication is an increasingly frequent complication of chronic renal failure. Because hypercalcemia, elevated parathyroid hormone levels, and radiologic changes said to be typical of osteitis fibrosa commonly occur with aluminum intoxication, it is frequently confused with hyperparathyroidism. In this report, examples of this dilemma are described. The pathophysiology leading to the confusing clinical picture is discussed, with a suggested approach to the problem.

Adolescent↗

PubMed1987

Controlled study of renal osteodystrophy in patients undergoing dialysis. Improved response to continuous ambulatory peritoneal dialysis compared with hemodialysis.

To assess the effect of different dialysis modalities on renal osteodystrophy, a controlled study was performed in six patients undergoing continuous ambulatory peritoneal dialysis and six hemodialysis-treated patients. All patients were enrolled at the initiation of dialysis, and age, sex, cause of renal failure, prior treatment of renal osteodystrophy, and baseline serum and bone histologic variables were similar in the two groups. After initial blood samples and bone biopsy specimens (with double-tetracycline labels) were obtained, renal osteodystrophy in both groups received comparable treatment with aluminum hydroxide to maintain serum phosphorus levels between 3.5 and 5.5 mg/dl, and with calcium carbonate and calcitriol to maintain total serum calcium levels between 10 and 11 mg/dl. Blood and bone samples were obtained again after nine months. All patients were asymptomatic at the beginning and end of the study. Phosphorus values were well controlled, and total calcium increased similarly in both groups. Although ionized calcium levels increased in both groups, the final level was higher in hemodialysis-treated patients than in patients undergoing continuous ambulatory peritoneal dialysis (2.82 +/- 0.07 meq/liter and 2.5 +/- 0.05 meq/liter, respectively; p = 0.005). Amino-terminal parathyroid hormone levels normalized in both groups, and histologic improvement of osteitis fibrosa occurred in a similar proportion of patients in both groups; however, quantitative improvement was greater in the hemodialysis-treated patients. Osteomalacia, assessed qualitatively and by dynamic histomorphometric measurements, was ameliorated to a much greater degree in patients undergoing continuous ambulatory peritoneal dialysis compared with hemodialysis-treated patients. Bone aluminum staining was absent in all biopsy specimens. Overall, bone histologic findings improved to a greater degree in patients undergoing continuous ambulatory peritoneal dialysis. When patients undergoing continuous ambulatory peritoneal dialysis or hemodialysis and receiving similar treatment for renal osteodystrophy were compared, patients treated with continuous ambulatory peritoneal dialysis appeared to have a greater improvement in their metabolic bone disease.

Aluminum Hydroxide↗

PubMed1987

Long-term intracaval calcium infusion therapy in end-organ resistance to 1,25-dihydroxyvitamin D.

Two boys aged six and four with the syndrome of hereditary resistance to 1,25-dihydroxyvitamin D3 with rickets alopecia and growth retardation are presented. After unsuccessful therapeutic trials with pharmacologic doses of vitamin D or its active metabolites, the patients were treated by long-term intracaval infusions of calcium through an implantable catheter. A total of 0.5 to 0.9 g of elemental calcium was infused daily for 18 months and the serum calcium concentration was maintained at 9 to 10 mg/dl. Bone pain subsided within one week of treatment. Serum phosphorus, immunoreactive parathyroid hormone, and 1,25-dihydroxyvitamin D concentrations and alkaline phosphatase activity were normalized within four to nine months. Radiographs of the knees and hands revealed progressive healing of rickets with complete resolution after one year of treatment. The patients gained 12 cm and 8 cm per year in height as compared with 3 cm and 2 cm, respectively, in the previous year. A transilial bone biopsy obtained from one patient prior to treatment revealed severe osteomalacia associated with osteitis fibrosa. A follow-up biopsy examined after 12 months of therapy showed almost complete healing of osteomalacia and normal mineralization. These observations indicate the following: (1) Long-term intracaval calcium infusions are an effective mode of therapy for these patients, and (2) When adequate serum calcium and phosphorus concentrations are maintained, healing of rickets and normal growth rate could be achieved even in the absence of a normal 1,25-dihydroxyvitamin D3 receptor-effector system.

Biopsy↗

PubMed1991

Multiple recurrent giant cell lesions associated with high circulating levels of parathyroid hormone-related peptide in a young adult.

Parathyroid hormone-related peptide (PTHrP, PLP) has previously been identified and assays are now available which can be used in clinical situations. A case is reported of a normocalcaemic young adult female in whom multifocal recurrent giant cell osteolytic lesions in the maxilla and elsewhere were associated with a raised plasma level of parathyroid hormone-related peptide. The lesions were histologically identical to reparative giant cell granuloma of the jaws and to osteitis fibrosa cystica associated with hyperparathyroidism.

Adult↗

PubMed1995

A history of the parathyroid glands.

Diseases of the parathyroid glands have always existed, affecting occasional individuals in every period and culture of the past. The significant changes in body build associated with their dysfunction must have attracted in the popular mind bewildering connotations that can be gleaned from their mythology. Although their associated clinical features were described in the medical literature, the presence of the parathyroid glands and their function went long unrecognized. In the relatively slow evolution of endocrinology, compared with that of other medical disciplines, the parathyroid glands and their diseases were one of the last to be defined. It was only in the latter part of the nineteenth century that the glands were identified in humans by Ivar Sandström (1852-1889). Their subsequent experimental extirpation by Eugene Gley (1857-1930), as well as others, led to the differentiation of the neuromuscular symptoms that theretofore had been attributed to removal of the thyroid glands. That these symptoms were the result of the hypocalcemia that ensues parathyroidectomy was suggested in 1908 by W. G. MacCallum (1874-1944) and Carl Voegtlin (1879-1960). The possibility that parathyroid pathology may be associated with skeletal abnormalities was made in 1914 by Jacob Erdheim (18874-1937), and in the following year documented by Z. Schlagenhaufer from the observation that in patients with osteitis fibrosa cystica, only one parathyroid gland is enlarged. This was to set the stage for parathyroidectomy beginning in 1925, for the alleviation of bone disease of hyperparathyroidism.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Relationship between intact 1-84 parathyroid hormone and bone histomorphometric parameters in dialysis patients without aluminum toxicity.

With the markedly reduced usage of aluminum salts in renal failure, parathyroid hormone (PTH) has become the major determinant of currently seen bone disease. Clinicians now must consider what PTH level should be sought. Too low a level may lead to the aplastic bone lesion (low turnover bone), and too high a level may cause osteitis fibrosa. Furthermore, conventional normal PTH levels may not be a suitable target because of the well-known resistance to PTH in uremic patients. In this report, we derive the PTH levels that best distinguish patients with low and high bone formation states from those with normal bone formation in a group of 175 dialysis patients without aluminum toxicity. Using bone histological parameters, we propose that ideally PTH levels should be maintained between 10 pmol/L (100 pg/mL) and 20 to 30 pmol/L (200 to 300 pg/mL) in chronic dialysis patients, levels two to four times the upper limit of values found in normal subjects.

Adult↗

PubMed1994

Renal osteodystrophy and dialysis artifacts as indicators of identification.

Evidence of rare disease may be useful in the identification of unknown remains. Osteodystrophy is a condition commonly associated with chronic renal failure. The presence of renal osteodystrophy and medical artifacts associated with the treatment of kidney failure in human remains may provide information about the individual's medical history. Currently, there are more than 100,000 patients with end stage renal disease in the United States receiving dialysis treatments to replace kidney function, and hundreds of thousands more who have significant chronic kidney failure and are not yet treated with dialysis. Chronic renal failure frequently leads to disorders in the metabolism of vitamin D, calcium, and parathyroid hormone which are extremely difficult to correct. At least three patterns of skeletal change may result: osteitis fibrosa, characterized by increased bone remodelling, increased osteoclastic activity, peritrabecular fibrosis, and a normal mineralization pattern; osteomalacia, with a markedly increased osteoid surface and volume, and impaired mineralization; and mixed osteodystrophy, with increased bone remodelling and moderately impaired mineralization. While these bone changes may not have any clinical manifestations in most patients, they can been seen radiographically and histologically. This evidence may be useful in identifying remains which have been skeletonized, burned, decomposed, or dismembered. Medical artifacts associated with dialysis treatment, such as catheters, polytetrafluoroethylene grafts, and evidence of surgical procedures, are also useful for identification.

Adult↗

PubMed1992

Non-aluminic adynamic bone disease in non-dialyzed uremic patients: a new type of osteopathy due to overtreatment?

Adynamic bone disease, characterized by a low bone formation rate with normal or reduced amount of unmineralized osteoid, is supposed to be the consequence of aluminum intoxication in uremic patients. However, the emergence of adynamic bone disease has been recently reported in hemodialyzed patients in the total absence of aluminum overload. This study was aimed to assess whether such a histological pattern of adynamic bone disease was already present in uremic patients not yet on dialysis. Twenty-seven asymptomatic uremic patients (mean age +/- SD 43 +/- 10 years, mean creatinine clearance 19 +/- 3 ml/mm) were studied and bone biopsies were repeated in 16 of them after 18 +/- 10 months of treatment with oral calcium carbonate (1-3 g of elemental calcium/day) and calcidiol (21 +/- 14 micrograms/day). None of the patients received aluminum hydroxide, and the search for bone aluminum deposits was negative in all patients both before and after treatment. Two patients fulfilled the criteria of adynamic bone disease on their post-treatment biopsies. They originated from patients classified as having normal bone histology before treatment. Comparison with the other patients showed that they had comparable plasma C-terminal PTH but higher plasma creatinine than patients with normal bone histology and lower plasma C-terminal PTH than patients with osteitis fibrosa but comparable plasma creatinine. The plasma levels of 1,25(OH)2D reached values above normal after treatment in these two patients. It is suggested that adynamic bone disease not related to aluminum intoxication can develop in uremic patients independently of dialysis, and is favored by a relative hypoparathyroidism for the degree of renal failure, possibly induced by elevated plasma concentrations of calcitriol.

Adult↗

PubMedDate not supplied

Malignant hypercalcemia associated with a parathyroid macrocyst and the early genesis of a giant cell tumor.

Parathyroid cysts rarely cause primary hyperparathyroidism. In most cases, the resultant hypercalcemia is mild and detected before any significant skeletal disease develops. We report a patient with severe hypercalcemia, a synchronous brown tumor (osteitis fibrosa cystica) of the maxilla, and a large benign functional parathyroid cyst. The unusual patient presentation and management are described and illustrated. The pertinent literature is reviewed.

Biopsy, Needle↗

PubMed2004

Management of calcium and bone abnormalities in hemodialysis patients.

In chronic renal failure, hyperphosphatemia, hypocalcemia, hyperparathyroidism, reduced activation of vitamin D, decreased level of calcium-sensing receptor, osteitis fibrosa, and osteomalacia are features related to calcium abnormalities. Hyperparathyroidism is a risk factor for survival of hemodialysis patients as well as hypoparathyroidism, which is another feature in hemodialysis patients. Treatment of these abnormalities includes control of parathyroid hormone (PTH) secretion, counteracting hyperphosphatemia, correction of hypocalcemia, and others. Various kinds of vitamin D analogs have been introduced recently in addition to calcitriol and alfacalcidol, which have a rather long history (eg, maxacalcitol and falecalcitriol). Sevelamer is a newly developed phosphate binder to treat soft-tissue calcification.

Bone Diseases↗