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PubMed2000

[Renal osteodystrophy (1): invasive and non-invasive diagnosis of its pathologic varieties].

1. Renal osteodystrophy is a general term encompassing all the disturbances of the phosphocalcic metabolism and their associated bone and soft tissue abnormalities, which progressively occur in chronic renal failure. In this article we detail their main histopathological and etiopathogenic aspects as well as their invasive and non invasive diagnostic approach. 2. Osteitis fibrosa is characterized by extensive medullary fibrosis and osteoclastic hyperresorption linked to PTH hypersecretion. 3. Adynamic bone disease is mainly related to iatrogenic oversuppression of PTH secretion. It is favored by aluminum overload which directly inhibits the osteoblasts. It is characterized by a low bone formation rate without primary mineralization defect so that the osteoid seam thickness is normal or low, in contrast to osteomalacia in which by definition osteoid thickness is increased. 4. Osteomalacia is mainly due to aluminum intoxication, vitamin D insufficiency, hypocalcemia, acidosis and exceptionally to hypophosphatemia. 5. The differential diagnosis between the histopathological entities may be oriented on clinical, radiological and biochemical means. Only the bone biopsy can make the diagnosis with certainty. This latter is however necessary for appropriate treatment only in the patients who have been exposed to aluminum and who are symptomatic or hypercalcemic in order to distinguish severe osteitis fibrosa from aluminic bone disease, and more particularly from mixed osteopathy. Indeed surgical parathyroidectomy in patients with mixed osteopathy associating bone hyperremodeling and mineralization defect with inappropriately thick osteoid seam may induce fracturing low turn over aluminic bone disease.

Bone and Bones↗
PubMed2000

[Renal osteodystrophy (3); its treatment in dialysis patients].

The prevalence and the clinical gravity of the various histopathological varieties of renal osteodystrophy in dialysis patients depends on the severity of both the aluminium intoxication and that of hyperparathyroidism. The prevalence of bone pains, fractures and hypercalcemias are the highest in adynamic bone diseases (ABD) with severe aluminium intoxication, then in osteitis fibrosa and mixed osteopathy, in the ABD with moderate aluminium intoxication and rare in the mild lesion in spite of similar moderate aluminium intoxication. In the absence of aluminium intoxication, hypercalcemia and hyperphosphatemia prevalence is higher only when intact PTH is more that 4 times the upper limit of normal. When PTH is between 1 and 2 folds the ULN this prevalence is null and bone mineral density is the highest. 2. The low turnover aluminic bone diseases (osteomalacic or adynamic) will be cured by long term deferoxamine treatment. The hazards of such treatment justify the performance of a bone biopsy to ensure the diagnosis. Their prevention relies on adequate treatment of tapwater and definitive exclusion of long term administration of aluminum phosphate binders. 3. Non aluminic osteomalacia will be treated according to the same guidelines given for the uremic patients before dialysis. 4. Non aluminic adynamic bone disease will be cured by means aiming at stimulating PTH secretion as discontinuing 1 alpha hydroxylated vitamin D derivatives, and, if there is no hyperphosphatemia by discontinuation of calcium supplement. In case of hyperphosphatemia in dialysis patients CaCO3 doses have to be nevertheless increased after the dialysate calcium concentration (DCa) has been decreased in order to induce a negative perdialytic calcium balance for PTH secretion stimulation. In the near future substitution of CaCO3 by non calcemic non aluminic phosphate binders will suffice. 5. Osteitis fibrosa due to hyperparathyroidism will be treated first by securing an optimal vitamin D repletion (bringing plasma 25OH vitamin D around 30 and 60 ng/ml or 75-150 nmol/l) and by correcting hypocalcemia and hyperphosphatemia by CaCO3 at high doses (3-12 g/day) taken with the meals. In case of hypercalcemia dialysate calcium concentration will be decreased to correct it or, in a near future, CaCO3 will be decreased to 3 g/day and hyperphosphatemia will be controlled by non calcemic, non aluminic phosphate binders. When hyperphosphatemia is controlled whereas plasma calcium is normal or low, 1 alpha hydroxylated vitamin D derivatives can be administered. 6. Instrumental parathyroidectomy should be considered when plasma levels of intact PTH remain above 7 folds the upper limit of normal whereas hyperphosphatemia persists and hypercalcemia occurs in order to prevent thining of the corticals and subsequent fracture risk. In case of previous exposition to aluminum, a deferoxamine test and/or a bone biopsy will be performed to decide a long term DFO treatment before the parathyroidectomy in order to prevent the transformation of a mixed osteopathy into an aluminic adynamic bone disease. 7. The difficulty of hyperparathyroidism control in dialysis patients is due to poor compliance to phosphate binders and to irreversible parathyroid hyperplasia with occured before the dialysis stage. This stress the primary importance if its early prevention without iatrogenia by first CaCO3 and vitamin D repletion, as soon as the creatinine clearance decreases below 60 ml/min/1.73 m2.

Aluminum↗
PubMed2000

Effect of 22-oxacalcitriol on bone histology of hemodialyzed patients with severe secondary hyperparathyroidism.

To examine the effectiveness of 22-oxacalcitriol (OCT) injection on the improvement of severe osteitis fibrosa, we studied 10 hemodialyzed patients (age, 59 +/- 12 years). The initial OCT dose was 5 microg and was administered three times weekly at the end of each hemodialysis session. OCT doses (1, 3, 5, 10, 15, and 20 microg) were changed in subsequent weeks to maintain serum calcium levels at less than 11.5 mg/dL. Administration of OCT significantly suppressed serum intact parathyroid hormone (PTH) from an initial level of 1,193 +/- 584 to 775 +/- 552 pg/mL in the 24th week (n = 10). OCT increased PTH levels again to 857 +/- 635 pg/mL in the 48th week (n = 7). Among the 10 patients, 5 patients (high responders) showed more than a 50% suppression of serum intact PTH levels at the end of the study. The rest of the patients had hypercalcemia and did not receive increased OCT doses (low responders). At the start of the treatment, the only difference between high and low responders was serum calcium level. Serum calcium levels (adjusted for serum albumin level) increased from 9.7 +/- 0.7 mg/dL (n = 10) at the beginning to 10.5 +/- 0.6 mg/dL (n = 10) in the 24th week and to 11. 1 +/- 0.7 mg/dL (n = 7) in the 48th week. Six patients (1 to 6) agreed to undergo a second bone biopsy in the 24th week of OCT administration. In bone histomorphometric measurements, OCT significantly changed bone marrow fibrosis, mineralization (labeled mineralizing surface and bone formation rate), and osteoid formation (osteoid volume and thickness). In conclusion, intravenous OCT effectively suppressed PTH secretion and improved the bone histological characteristics of severe osteitis fibrosa, especially in patients with initial serum calcium levels less than 10 mg/dL. With concerns about OCT causing adynamic bone, additional bone histological data are needed to ensure the long-term safety of OCT.

Adult↗
PubMed2006

Calcimimetics for secondary hyperparathyroidism in chronic kidney disease patients.

BACKGROUND: Calcimimetic agents have recently been evaluated in the treatment of secondary hyperparathyroidism (SHPT) as add-on therapy to calcitriol and vitamin D analogues and dietary phosphate binders. OBJECTIVES: To evaluate the benefits and harms of calcimimetics for the prevention of secondary hyperparathyroid bone disease (including osteitis fibrosa cystica and adynamic bone disease) in dialysis patients with chronic kidney disease (CKD). SEARCH STRATEGY: MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials and conference proceedings were searched for randomised controlled trials (RCTs) evaluating any calcimimetic against placebo or another agent in pre-dialysis or dialysis patients with CKD. SELECTION CRITERIA: We included all RCTs of any calcimimetic agent, cinacalcet HCl (AMG-073, Sensipar), NPS R-467 or NPS R-568 administered to patients with CKD for the treatment of SHPT. DATA COLLECTION AND ANALYSIS: Data were extracted on all relevant patient-centred and surrogate outcomes. Analysis was by a random effects model and results expressed as relative risk (RR) or weighted mean difference (MD) with 95% confidence intervals. MAIN RESULTS: Eight studies (1429 patients) were identified, which compared a calcimimetic agent plus standard therapy to placebo plus standard therapy. The end of treatment values of parathyroid hormone (pg/mL) (MD -290.79, 95% CI -360.23 to -221.34), serum calcium (mg/dL) (MD -0.85, 95% CI -1.14 to -0.56), serum phosphorus (mg/dL) (MD -0.29, 95% CI -0.50 to -0.08) and the calcium by phosphorus product (mg(2)/dL(2))(MD -7.90, 95% CI -10.25 to -5.54) were significantly lower with calcimimetics compared to placebo. No significant effects on patient-based endpoints were demonstrated except for the risk of hypotension which was significantly reduced with calcimimetics compared to placebo (RR 0.53, 95%CI 0.36 to 0.79). AUTHORS' CONCLUSIONS: Calcimimetic treatment of SHPT leads to significant improvements in biochemical parameters that observational studies have shown to be associated with increased mortality, cardiovascular risk and osteitis fibrosa, but patient-based benefits have not yet been demonstrated in trials. For patients with SHPT, the benefits of calcimimetics over standard therapy remain uncertain until further RCTs become available.

Calcium↗
PubMedDate not supplied

Progress of brown tumors in patients with chronic renal insufficiency undergoing dialysis.

In a group of 73 patients, affected by chronic renal insufficiency, whose skeleton was periodically checked, three cases of brown tumors were found. These cases demonstrated a variety of locations that were involved, especially the pelvis, ribs and mandible. During therapeutic treatment the brown tumors presented a different behavior; while some lesions tended toward complete sclerosis, others increased in size and in both instances new lesions appeared. Parathyroidectomy, carried out in two patients, determined a definitive sclerosis of these lesions. Brown tumors also correlate with high PTH levels and with lesions from osteitis fibrosa.

Adolescent↗
PubMed1986

A survey of bone disease in the Alpk/AP rat.

Bone disease in an outbred colony of Alpk/AP rats over a period of more than 20 years is recorded. The incidence of most conditions, including fracture, necrosis, osteomyelitis, osteitis deformans, renal osteitis fibrosa cystica and neoplasia is rare compared with other species and possible reasons for this low incidence are discussed.

Animals↗
PubMed1975

Secondary hyperparathyroidism. Conservative management in patients with renal insufficiency.

In three patients with advanced renal disease (inulin clearance, 4.6 to 9.1 ml/min) and systemic manifestations of secondary hyperparathyroidism, concentrations of serum calcium and phosphorus were maintained within our normal limits (9 and 3.5 mg/100 ml, respectively) with phosphate-binding antacids and orally given calcium carbonate. The result was progressive disappearance of symptoms related to secondary hyperparathyroidism, healing of osteitis fibrosa, and normalization of serum concentrations of immunoreactive parathyroid hormone.

Administration, Oral↗
PubMedDate not supplied

[Brown tumors in the technetium-99m methyldiphosphonate bone scan mimicking metastases of parathyroid carcinoma].

This is a case of a 78 year old male with parathyroid carcinoma and multiple bone lesions in the technetium-99m methyldiphosphonate ((99m)Tc-MDP) bone scan, initially interpreted as metastatic bone disease, but finally proved to be brown tumors. The interest of this case lies on the rarity of the disease, as well as the co-existence of osteitis fibrosa cystica, which often resembles metastatic bone disease and leads to diagnostic pitfalls.

Adenoma↗
PubMed1982

Patellofemoral abnormalities in renal osteodystrophy.

Seven patients with renal osteodystrophy demonstrated characteristic abnormalities of the patellofemoral compartment of the knee. The abnormalities consisted of narrowing of the patellofemoral space and ill-defined osseous erosions on the posterior surface of the patella, which in some cases were accompanied by similar alterations on the anterior surface of the femur. Clinical manifestations were not infrequent, including restriction of joint motion and a traumatic synovitis with accumulation of intra-articular fluid. The mechanism accounting for the patellofemoral alterations appears to be subchondral fracture of weakened trabeculae due to the presence of osteomalacia or osteitis fibrosa cystica, or both. Calcium pyrophosphate dihydrate crystal deposition is not required to produce these characteristic abnormalities.

Adult↗
PubMed1994

Jaw enlargement complicating secondary hyperparathyroidism in three hemodialysis patients.

Over a period of two years we saw three patients with longstanding chronic renal failure in whom the size and shape of the jaws had gradually changed. Clinical, metabolic, and radiologic observations suggested that secondary hyperparathyroidism had caused the disfigurement, and bone histology supported this conclusion in each case. The appearance of our subjects resembled that of patients morbidly afflicted with osteitis fibrosa before its association with hyperparathyroidism was widely known. Jaw enlargement is a potential consequence of secondary hyperparathyroidism in dialysis patients.

Adult↗
PubMed2004

Hyperparathyroid crisis in a pediatric patient.

Primary hyperparathyroidism is rarely found in the pediatric population. Delays in diagnosis due to vague symptoms can lead to severe disease manifestations such as osteitis fibrosa cystica. We report a rare case of primary hyperparathyroidism in a 13-year-old girl who presented with a pathological femur fracture and numerous brown tumors.

Adenoma↗
PubMed2004

[Role of vitamin D in the pathogenesis of renal osteodystrophy].

Renal osteodystrophy was occurred in patients with chronic renal failure and the biopsied patients had various forms of bone disease. Active vitamin D has an important role of calcium regulation and bone metabolism. In patients with end-stage renal disease, decreased levels of active vitamin D, reduced number of vitamin D receptors and calcium sensing receptors in parathyroid gland pay a major role in the development of hyperparathyroidism. It was invited osteitis fibrosa, high bone turnover. The parathyroid function is suppressed by active vitamin D, it was considered that lower parathyroid hormone levels was one of the cause of low bone turnover, adynamic bone disease.

Bone and Bones↗
PubMed2001

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.

Adult↗
PubMed1976

Bone disease in long-term haemodialysis: the association of radiological with histological abnormalities.

The radiological findings in the skeletal surveys of 70 patients receiving long-term haemodialysis for chronic renal failure have been correlated with histological findings in a specimen obtained by biopsy of the iliac crest. Many significant associations were found, and the ones presented are those thought to be most useful in the interpretation of the radiological abnormalities. The main conclusions are that fractures and severe medullary rarefaction appear to be most commonly the result of osteomalacia; subperiosteal erosions are associated with the more severe grades of osteitis fibrosa; cortical striations and sclerosis are associated with an increased amount of osteoid, and sclerosis is diagnosed more frequently by radiological means than by iliac-crest biopsy.

Adult↗
PubMed2002

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.

Adenoma↗
PubMed1977

Effect of renal transplantation on marrow mast cell hyperplasia of chronic renal failure.

Marrow mast cells have been counted in iliac bone from patients with chronic renal failure treated by renal transplantation. Mast cell numbers were initially increased but returned to the normal range in many patients after renal transplantation. Improvement in osteitis fibrosa and osteomalacia after transplant was not clearly related to this diminution in the number of mast cells. The use of prednisone in renal transplant patients may have some effect in reducing the numbers of mast cells. There is no fully acceptable explanation for the increase in marrow mast cells which occurs in chronic renal failure.

Bone Marrow↗
PubMed1996

Tc-99m sestamibi imaging of brown tumors of primary hyperparathyroidism.

Double-phase scintigraphy using Tc-99m sestamibi MIBI is the study of choice for detecting parathyroid adenoma in patients with primary hyperparathyroidism. However, before parathyroid imaging, these patients may uncommonly present with multiple osteolytic lesions and bone scan findings consistent with metastatic disease. By excluding malignancy, the diagnosis of osteitis fibrosa cystica and parathyroid adenoma may subsequently be confirmed. The authors describe the case of an elderly patient who presented with imaging findings initially masquerading as metastatic disease. When parathyroid adenoma was finally diagnosed with Tc-99m MIBI imaging, radiopharmaceutical uptake was also noted within several brown tumors, including clinically significant brown tumors of the left lower extremity, a finding that has not been previously reported.

Adenoma↗