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 397 records · Page 22Linked to original sources

PubMed2005

Which vitamin D derivative to prescribe for renal patients.

PURPOSE OF REVIEW: It is possible to control the secondary hyperparathyroidism and osteitis fibrosa of patients with chronic kidney disease by calcitriol when given early and in appropriate doses. However, this control is often achieved at the price of unacceptably high plasma calcium and phosphorus levels, the induction of adynamic bone disease, and soft tissue calcification. To avoid these side effects, so-called 'nonhypercalcemic' vitamin D analogs have been developed. Their possible advantages and their precise place in the treatment and prevention of secondary hyperparathyroidism remain a matter of debate. RECENT FINDINGS: A large US multicenter study showed that the administration of the vitamin D analog paricalcitol to hemodialysis patients, as compared with calcitriol, was associated with better survival. In a subsequent large US multicenter study paricalcitol-treated hemodialysis patients experienced fewer hospitalizations and hospital days compared with calcitriol-treated patients. In a third, smaller study from Japan, regular alfacalcidol users among hemodialysis patients had better cardiovascular survival than nonusers. Finally, in a recent historical control study the mortality of a large hemodialysis patient cohort was analyzed as a function of previous vitamin D treatment. Patients on active vitamin D compounds at any time had a 2-year survival advantage over vitamin D-naive patients. It must be pointed out, however, that all four studies were retrospective in nature. SUMMARY: The development of vitamin D analogs with less side effects than with calcitriol is of major theoretical interest. Practically speaking, however, we still need to be convinced that this goal can be achieved in chronic kidney disease patients.

Animals↗

PubMed2006

Bone disease in long-term renal transplant recipients with severe osteopenia: a cross-sectional study.

BACKGROUND: Fracture is a disabling clinical outcome after transplantation, but there is little histopathological information on long-term renal recipients with severe osteopenia. METHODS: Twenty kidney recipients (8.3+/-1.9 years after transplantation), 13 males and 7 females (five postmenopausal) with nearly normal renal function, affected by severe osteopenia (T-score: males= -4.9+/-0.28; females= -5.08+/-0.47) underwent bone biopsy and morphometric X-ray absorptiometry to evaluate vertebral fractures. RESULTS: Histopathological diagnosis was osteoporosis-osteopenia in seven patients, osteitis fibrosa in six, prevalent osteomalacic lesion in six, and "normal" bone in one patient. Significant increases in osteoid volume (OV/BV), osteoid surface, osteoblastic surface (ObS/BS) and osteoid thickness were observed. OV/BV and Obs/BS ratios were inversely correlated to cumulative doses of MPRED (r2=0.85 P<.0001 for both ratios), whereas age, sex, time after transplantation, iPTH levels, and cumulative cyclosporine A dose were not related to osteoblastic indices. Osteoclast surface was slightly increased. Widened mineralization lag times were observed, with normalcy of the bone formation rate. Half of the patients showed fractured vertebrae. No differences in T scores were found when patients were subdivided into groups "with" or "without" vertebral fractures. A higher prevalence of fractures was observed in patients with osteoporosis-osteopenia compared to other osteopathies (P<0.02). No relationships between bone volume versus T-scores were observed. CONCLUSIONS: In long-term renal transplant recipients, severe osteopenia does not predict osteoporosis alone. The main abnormality we found was an increase in osteoblastic activity with a slight mineralization defect. The heterogeneous bone illness we observed would suggest performing bone biopsy in these patients.

Adult↗

PubMed1977

Measurement of whole body calcium in chronic renal failure: effects of 1alpha-hydroxyvitamin D3 and parathyroidectomy.

In vivo neutron activation analysis was used to measure changes in whole body calcium in patients with chronic renal failure. Eight patients, not treated by haemodialysis, showed losses of calcium in contrast to increases noted in twenty-one patients treated by haemodialysis. Changes in whole body calcium were independent of pre-existing renal bone disease. Treatment of bone disease by total parathyroidectomy (six patients) or 1alpha-hydroxyvitamin D3 (eleven patients) resulted in large increases in total body calcium. In patients given 1alpha-hydroxyvitamin D3, changes in total body calcium correlated with histological and radiological indices of response but variable changes in forearm bone mineral content were observed. Neutron activation analysis provides a convenient method for measuring skeletal mass and may also be useful in the assessment of response to 1alpha-hydroxyvitamin D3 of patients with osteitis fibrosa and osteomalacia.

Adult↗

PubMed1995

Vitamin D status in primary hyperparathyroidism in India.

OBJECTIVES: Primary hyperparathyroidism is a syndrome with variable clinical expression, presenting as asymptomatic hypercalcaemia in Western countries and with predominant bone disease in developing countries. Vitamin D deficiency has been implicated as the cause of bone disease. There is a paucity of information on the vitamin D (25-OHD3) status of patients with primary hyperparathyroidism presenting with bone disease. The present study aims to evaluate the vitamin D status in patients with primary hyperparathyroidism and to correlate it with the bone disease. DESIGN: Twenty consecutive patients with primary hyperparathyroidism admitted to the endocrinology and metabolism wards of the All India Institute of Medical Sciences were analysed to assess their clinical, radiological and biochemical features, as well as parathyroid hormone (mid-molecular, PTH-MM) and 25-OHD3 levels. MEASUREMENTS: PTH-MM levels and 25-OHD3 levels were measured using RIA kits. RESULTS: Bone disease (osteitis fibrosa cystica) was the mode of presentation in 90%. Radiologically, sub-periosteal resorption was present in 90% of the total group of patients, brown tumours in 60%, and pathological fractures in 40%. Renal stones and/or nephrocalcinosis was present in 50% of patients. Mean serum calcium, phosphate and alkaline phosphatase concentrations (mean of 3 days values) were 2.72 +/- 0.24 mmol/l; 1.01 +/- 0.28 mmol/l and 425 +/- 249 IU/l respectively. The 24-hour (mean of 3 days values) urine calcium and phosphate excretions were 8.0 +/- 4.2 mmol and 19.0 +/- 13 mmol. Only 50% of the patients had hypercalcaemia ( > 2.7 mmol/l). However, 90% of the whole group of patients had hypercalciuria. The mean serum creatinine concentration of patients with hypercalcaemia was 108 +/- 38 mumol/l and of those with normocalcaemia 89 +/- 33 mumol/l. The mean serum PTH-MM was 438 +/- 350 pmol/l (the detection limit for the kit was 34 pmol/l). Ultrasound examination detected adenomas in 72% of the cases and computerized tomography of the neck localized adenomas in 71% of the cases. The median weight of the adenoma was 4.6 g (range 0.125-25 g). Two patients had coexistent hyperplasia of the other parathyroid glands and two had recurrent adenomas. 25-OHD3 levels were assessed in all 20 patients under fasting conditions. The mean value of 25-OHD3 observed (8.4 +/- 5.1 micrograms/l) was comparable to the mean value measured in 14 healthy age and sex matched controls (8.3 +/- 2.5 micrograms/l). CONCLUSION: Patients with primary hyperparathyroidism in India presented with bone and renal diseases; half were normocalcaemic. All the patients had hypercalciuria despite the bone disease. The PTH-MM levels were increased and 25-OHD3 levels were low. The predominant bone disease is probably due to prolonged primary hyperparathyroidism coexisting with low calcium intake and/or 25-OHD3 deficiency. The mean weight of the adenoma was higher than that reported for patients in the Western literature.

Adenoma↗

PubMed2005

Overproduction of an amino-terminal form of PTH distinct from human PTH(1-84) in a case of severe primary hyperparathyroidism: influence of medical treatment and surgery.

OBJECTIVE: Rare patients with severe primary hyperparathyroidism present with large parathyroid tumours, severe hypercalcaemia, very high PTH levels and osteitis fibrosa cystica. Some of these patients display a large amount of C-PTH fragments in circulation and present with a higher C-PTH/I-PTH ratio than seen in less severe cases of primary hyperparathyroidism. We wanted to determine how PTH levels and circulating PTH high-performance liquid chromatography (HPLC) profiles analysed with PTH assays having different epitopes could be affected by medical and surgical treatment in such patients. DESIGN: A 55-year-old man with severe hypercalcaemia (Ca(2+): 2.01 mmol/l), very high PTH levels (CA-PTH 82.1 and T-PTH 72 pmol/l) caused by a large parathyroid tumour (7.35 g) and accompanied by significant bone involvement (alkaline phosphatase of 185 UI/l and subperiostal bone resorption of hands) was referred to us. Blood was obtained at various time points during his medical treatment, before and after surgery, to measure parameters of calcium and phosphorus metabolism, and of bone turnover. HPLC separations of circulating PTH molecular forms were performed and analysed with PTH assays having 1-4 (CA), 12-18 (T), 26-32 (E) and 65-84 (C) epitopes. RESULTS: Before surgery, serum Ca2+ was nearly normalized with hydratation, intravenous (IV) pamidronate and oral vitamin D administration. Despite a decrease in Ca2+ to 1.31 mmol/l, CA-PTH and T-PTH levels decreased by half in relation to a threefold increase in basal 1,25-dihydroxyvitamin D [1,25(OH)2D] level (94 to 337 pmol/l). After this initial positive response, hypercalcaemia and elevated CA- and T-PTH levels recurred even if 1,25(OH)2D levels remained elevated. The tumour was removed surgically and proved to be poorly differentiated with nuclear atypia and mitosis. After surgery, the Ca2+ level and PTH secretion normalized. The higher CA-PTH level relative to the T-PTH level observed before surgery in this patient was related to the oversecretion of an amino-terminal (N) form of PTH recognized by PTH assays with (1-4) or (26-32) epitopes but not by the T-PTH assay with a (12-18) epitope. This molecular form represented 50% of CA-PTH measured in this patient, but only 7% in less severe cases of primary hyperparathyroidism. It was unaffected by medical therapy and disappeared after surgery. CONCLUSION: The relationship between the overexpression of this N-PTH molecular form and severe primary hyperparathyroidism remains unclear. Further studies will be required in these rare patients to see whether N-PTH is a marker of less well differentiated parathyroid tumours and/or relates to the overproduction of C-PTH fragments in the presence of severe hypercalcaemia.

Adenoma↗

PubMed1978

Twenty years' experience with parathyroid exploration.

Eighty-four patients have undergone surgical exploration following a clinical diagnosis of hyperpathyroidism over a 20-year period. Urinary tract calculi were the major indication for exploration, and 90% of these patients had recurrent calculi. Osteitis fibrosa was a rare presentation of hyperparathyroidism. Lethargy, sometimes profound, was an important symptom, in some instances the dominant feature. Persistent hypercalcaemia remains the chief diagnostic investigation, with helpful confirmation from estimation of the parathyroid hormone level. Little attempt was made in this series to utilize preoperative localization techniques, reliance being placed on meticulous bloodless surgery to find normal and abnormal parathyroid tissue. Eighty-five explorations were carried out in the 84 patients. Seventy-four of the explorations were successful, converting the patient to a normocalcaemic state. Of these, 63 had a single adenoma (86%).

Adenoma↗

PubMed1976

The use of high calcium dialysate in the treatment of renal osteomalacia.

Four chronic haemodialysis patients suffering from osteomalacia were treated by increasing their dialysate calcium concentration from 1-40 to 2-15 mM/I. Bone biopsies were taken before and after 22 weeks of this treatment and a further biopsy was taken in one patient after 52 weeks. Symptomatic cure occurred in one patient with mild osteomalacia and some improvement osteomalacia and hyperparathyroidism. Bone biopsies showed slight improvement in the patient with mild osteomalacia after 22 weeks, and considerable improvement after 25 weeks. In the patient with mixed histology, the osteitis fibrosa subsided and the osteomalacia became a little worse after 22 weeks. There was no histologic improvement in the two patients with severe osteomalacia after 22 weeks. It is concluded that high calcium dialysis is not an effective treatment for renal osteomalacia.

Aged↗

PubMed1976

Calcium metabolism after renal transplantation.

Calcium metabolism was studied in four patients who had undergone renal transplantation from eight to 19 months previously. The studies included conventional biochemical and radiological parameters, undecalcified bone histology and metabolic balances. The only abnormality found was biochemical and histologic evidence of mild hyperparathyroidism. All patients were in approximate calcium balance, and there was no evidence of osteoporosis, osteomalacia or osteitis fibrosa. It is suggested that transplantation patients with stable, well functioning grafts and normal biochemical and radiologic parameters are unlikely to have or to be at risk of developing metabolic bone disease.

Adult↗

PubMed2005

Parathyroid interventions for secondary hyperparathyroidism in hemodialyzed patients.

Although parathyroidectomy (PTX) is the ultimate treatment for secondary hyperparathyroidism (SHPT) that is resistant to medical treatment, recent advances in ultrasonographic techniques have increased the treatment options in Japan. Percutaneous ethanol injection therapy (PEIT) of the parathyroid was approved under the national health insurance system in 2004, and there have been trials of direct injection of vitamin D (VD) preparations. We followed 30 patients for at least 1 year who had undergone PEIT at the same institution. The overall mean concentration of intact parathyroid hormone (PTH) fell from 865.3+/-388.4 pg/mL to 291.9+/-277.8 pg/mL, or 34% of the pretreatment value. The effect was even more pronounced for one or two glands, with 68.4% reaching the target of intact PTH<or=300 pg/mL recommended in the K/DOQI guidelines, in comparison with 36.4% of cases of hypertrophy of three or four glands. The average time taken to achieve the target PTH concentration was 4 months. No correlation was found between the response to PEIT and the total parathyroid volume, or the volume of glands with suspected nodular hyperplasia. Cases in which PTH does not fall sufficiently after five or more injections should be considered refractory to PEIT and evaluated for PTX. Following PEIT, PTH falls relatively slowly, whereas after total PTX with forearm autograft the PTH concentration falls immediately and may still be less than 60 pg/mL 4 or 5 years later. Bone biopsies performed 1 year after total PTX with autograft showed a change from an osteitis fibrosa pattern to an adynamic bone disease pattern. In some cases of hypertrophy of three to four glands, markers of bone metabolism kept decreasing more than did PTH, corresponding to marked improvement in the patients' quality of life. Important considerations for treatment selection include: (i) ultrasonography of the cervical region as screening; (ii) earlier recognition of the limits of medical therapy; and (iii) the number of affected glands, the age of the patient, and the likely course postintervention.

Adult↗

PubMed2005

Parathyroid cell growth in patients with advanced secondary hyperparathyroidism: vitamin D receptor, calcium sensing receptor, and cell cycle regulating factors.

The parathyroid gland (PTG) is a unique endocrine organ in which the quiescent glandular cells begin to proliferate in response to the demand for maintaining calcium (Ca) homeostasis in the progressive course of renal failure, leading to secondary hypereparathyroidism (SHPT). SHPT is characterized with continuous over-secretion of parathyroid hormone (PTH) and high turn-over bone disease, osteitis fibrosa, and the major factors include a deficiency of active vitamin D, hypocalcemia, and phosphate retention. With long-term end-stage renal failure, SHPT becomes resistant to conventional medical treatment such as phosphate binders and active vitamin D supplementation, and the growth of the PTG accelerates with the pattern of hyperplasia changing from diffuse to nodular type. In this process, the sigmoid curve between extracellular Ca concentration (exCa) and the plasma level of PTH shifts to the upper-rightward, indicating both an absolute increase in PTH secretion and the resistance of PT cells to exCa. Many experimental and human studies have revealed down-regulation of vitamin D receptor (VDR), calcium-sensing receptor (CaSR), and retinoid X receptor (RXR) in PT cells. The sustained proliferation of PT cells after obtaining autonomicity is another characteristic feature of SHPT. In this context, it has been demonstrated that the cell cycle is markedly progressed, where the expression of cyclin-dependent kinase inhibitor (CDKI), p21 and p27, is depressed in a VDR-dependent manner. These pathological features are most evident in nodular hyperplasia, in which monoclonal proliferation is obvious, indicating the phenotypic changes have occured in PT cells. It has been observed by Fukagawa and colleagues that pharmacologically high dose of active vitamin D administered orally can cause small-size PTG hyperplasia to regress in patients with advanced SHPT. Successful renal transplantation may also restore VDR and CaSR expressions in the diffuse type, in association with increasing TUNEL-positive cells. Thus, it is important to vigorously treat SHPT when the PT cell proliferation is in the reversible stage of diffuse hyperplasia.

Cell Cycle Proteins↗

PubMed1970

Hypocalcaemic primary hyperparathyroidism.

A patient with many symptoms and signs of primary hyperparathyroidism had hypocalcaemia when first seen. Bone section histology showed osteomalacia and osteitis fibrosa, and the hyperparathyroidism at this stage was considered to be secondary to osteomalacia with postgastrectomy steatorrhoea. On treatment with vitamin D (with disappearance of her bone pains and weakness) she developed hypercalcaemia. She regained her health after removal of a 6-g. parathyroid adenoma. Normal histology was shown in another parathyroid gland.We believe that the initial hypocalcaemia was due to vitamin-D deficiency, which produced ineffective hyperparathyroidism until it was corrected. A review of the few reports of patients with autonomous hyperparathyroidism with steatorrhoea and osteomalacia does not support the argument that these patients had "tertiary" disease. It suggests that most of them, like our patient, had primary hyperparathyroidism.

Adult↗

PubMed1978

Osteomalacic dialysis osteodystrophy: a trial of phosphate-enriched dialysis fluid.

To assess whether phosphate depletion is an aetiological factor in osteomalacic dialysis osteodystrophy we undertook a prospective trial of phosphate-enriched dialysis fluid, in association with oral 1alpha-hydroxycholecalciferol, for this condition. Thirty patients started the trial; of the 27 who completed more than 6 months' treatment, 14 had iliac crest bone biopsies at the beginning and end of the treatment period. Side effects included pruritus, stiffness, and increase in corneal and vascular calcification. Only one patient showed histological improvement of osteomalacia, and eight deteriorated; in seven the osteitis fibrosa worsened. Myopathy showed some improvement in four patients, but became worse in four. This treatment does not seem to have a place in the routine management of non-hypophosphataemic patients on dialysis.

Adolescent↗

PubMed1976

Whole-body in-vivo neutron activation analysis in assessing treatment of renal osteodystrophy with 1-alpha-hydroxycholecalciferol.

Four selected adults with different patterns of osteodystrophy receiving regular dialysis were treated with 1-alpha-hydroxycholecalciferol (1-alpha-OHD3) 0-5-2 mug/day for 10 to 12 months. In two patients, one with osteitis fibrosa and the other with osteomalacia, significant biochemical, radiological, and histological improvements occurred, and total body calcium measured by in-vivo neutron activation analysis increased. In two patients, in whom there were no increases of whole-body calcium, neither biochemical improvement nor healing of bone lesions occurred during the study; in one of these patients the effect of 1-alpha-OHD3 on bone resorption may have contributed to loss of body calcium and deterioration of bone disease. 1-alpha-OHD3 may therefore be a valuable adjunct in the treatment of only some patients with renal osteodystrophy. Whole-body in-vivo neutron activation seems to provide a sensitive and non-invasive index of early response to treatment.

Adult↗

PubMed1984

Long term follow up of untreated primary hyperparathyroidism.

Fourteen patients with primary hyperparathyroidism and whose initial serum calcium concentrations were 2.75 mmol/l (11.0 mg/100 ml) or more were followed up for five to 23 years without operative treatment. One had osteitis fibrosa when seen and died with a fibrosarcoma 22 years later. The remaining 13 patients, who were followed up for a mean of 10 years, came to little obvious harm from not being operated on. Their serum calcium concentrations did not rise and there was no evidence of progressive renal impairment. In four patients who presented originally with renal calculi there were three further episodes of renal colic in 54 patient years of follow up. Conservative management of primary hyperparathyroidism is not an unreasonable option, and patients who do not have symptoms need not necessarily be pressed to accept surgery.

Aged↗

PubMed1972

Effects of haemodialysis on bone in chronic renal failure.

Quantitative histological studies have been done on 80 sequential bone biopsies taken at yearly intervals from 37 patients with chronic renal failure on long-term haemodialysis treatment. Twenty-three patients were studied at the start of dialysis, and in about half the bone was abnormal. During dialysis mean osteoid area and the maximum number of unmineralized osteoid lamellae increased, and mineralized bone area decreased. The loss of bone during dialysis was also reflected in reduction of the width of individual trabeculae. These trends were less obvious in patients already established on dialysis at the time of the initial biopsy. The course of osteitis fibrosa appeared to be unaffected by dialysis.

Adult↗

PubMed1987

Tetany despite normocalcaemia and normomagnesaemia following parathyroidectomy.

Two patients with long-standing hyperparathyroidism due to a parathyroid adenoma are described. Both had severe osteitis fibrosa cystica and a proximal myopathy. Both were treated with alfacalcidol (2 micrograms/day) prior to and following parathyroidectomy, and infused with calcium gluconate following the operation. Plasma total and ionized calcium and magnesium concentrations were maintained within the normal range. However, both developed tetany in the postoperative period in spite of normal ionized calcium and magnesium concentrations. Tetany continued for 4 weeks in one patient and for longer in the other. Prolonged hypercalcaemia may result in a state of neuromuscular excitability following parathyroidectomy even at high normal concentrations of ionized calcium.

Adenoma↗

PubMed1997

Bone disease in moderate renal failure: cause, nature and prevention.

There are two primary types of bone disorders observed in patients with end-stage renal disease: a high-turnover osteodystrophy characterized by osteitis fibrosa, and a low-turnover osteodystrophy characterized initially by osteomalacia and, more recently, by adynamic or aplastic bone disease. This article reviews the clinical presentation, pathogenesis, and laboratory findings of patients with these two disorders. It discusses the important roles of phosphorous binding, vitamin D administration, and correction of acidosis in prevention and treatment of bone disease in patients with moderate renal insufficiency.

Aluminum↗

PubMed1976

Subchondral resorption of bone in renal osteodystrophy.

In a radiographic-pathologic study of the spine and several axial joints in a cadaver with renal osteodystrophy, subchondral resorption of bone is described as an important mechanism of osseous abnormality. Widening and irregularity of the sacroilliac and sternoclavicular joints and symphysis pubis are related predominantly to trabecular destruction beneath cartilage surfaces, substitutive fibrosis, and new bone formation. Subperiosteal abnormalities at these locations produce juxta-articular erosions. The presence of osteitis fibrosa cystica about multiple Schmorl's nodes within the thoracic vertebral bodies suggests that subchondral resorption beneath the cartilage end-plates of the spine may be associated with disk protrusions and represents one further example of hyperparathyroid joint disease.

Aged↗