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PubMed1975

What is tertiary hyperparathyroidism?

Five patients who had gross abnormalities of calcium and phosphorus metabolism due to long standing renal failure are described to illustrate the difficulties with the term "tertiary hyperparathyroidism". One patient who had unequivocal biochemical tertiary hyperparathyroidism was found histologically to have nodular hyperplasia of all four glands even though one gland weighed twice as much (12g) as the combined weight of the other three. Another patient was not hypercalcaemic but had all the other features of the condition including rapid onset of osteitis fibrosa, vascular calcification and a probable parathyroid adenoma, with hyperplasia of the three glands. The other three had hypercalcaemia only after a reduction in the plasma inorganic phosphorus due either to renal transplantation or aluminum hydroxide therapy. The bone histology of the five patients varied from severe osteomalacia to severe osteitis fibrosa. A consideration of the factors involved in causing hypercalcaemia in these patients and a review of the literature leads to the conclusion that the term tertiary hyperparathyroidism is often misleading and best avoided.

Adenoma↗

PubMed1993

Correlation of bone histology with parathyroid hormone, vitamin D3, and radiology in end-stage renal disease.

We analyzed transiliac bone biopsy specimens from 30 end-stage renal failure patients, taken at the time of admission for CAPD training. Results were compared with values of iPTH, bone alkaline phosphatase, 1,25-dihydroxyvitamin D3, skeletal survey, quantitative computed tomography (QCT) and single photon absorptiometry (SPA) bone density measurements. Osteitis fibrosa was the most common histological diagnosis, present in 15 of the 30 patients (50%), with eight classified as "severe" and seven as "mild." Eight patients (27%) had adynamic bone lesion, four mixed renal osteodystrophy (13%), and two (7%) osteomalacia. The mean age of the adynamic group was higher than the osteitis fibrosa group (41 +/- 12.1 vs. 56 +/- 10.2 years; P < 0.01), and than the mixed group (39 +/- 7.5 vs. 56 +/- 10.2 years; P < 0.02). Levels of iPTH enabled discrimination between groups, but not between individual patients, and values correlated with bone alkaline phosphatase (r = 0.62; P < 0.001). Erosion of the terminal phalanges was seen on the plain X-rays of 7 of 15 patients with mild or severe OF, and in three patients with another diagnosis. The majority of patients (> 90%) had bone density measurements within the normal range. No significant correlation existed between QCT or SPA scores and any of the histomorphometric parameters, or iPTH. We conclude that iPTH is the most helpful non-invasive investigation in this group of patients. Plain X-ray of the hands is the most useful radiological investigation, but single measurements of bone density are not diagnostic.

Adult↗

PubMed1977

Use of 1,25(OH)2-vitamin D3 to separate 'types' on renal osteodystrophy.

Patients with severe symptomatic renal osteodystrophy were treated with either 1,25(OH)2D3 or 1 alpha(OH)D3. In 39 instances, there was either reversal of symptoms and/or a marked fall in plasma alkaline phosphatase. Bone biopsies showed improvement of either osteomalacia or osteitis fibrosa, and serum iPTH often fell. In thirteen patients, no improvement occurred. In seven patients, bone biopsy disclosed osteomalacia, and serum iPTH was normal or only slightly elevated. Thus, there was a defect in mineralisation. apparently unrelated to the lack of 1,25(OH)2D3 and in the absence of evidence of phosphate depletion. The other 'treatment failure' group showed osteitis fibrosa on biopsy and iPTH levels were markedly elevated. They are presumed to have marked secondary hyperparathyroidism. These 'treatment failure' groups had higher pre-treatment levels of serum Ca and Mg than in those showing a favourable response; also, hypercalcaemia developed rapidly during 1,25(OH)2D3 treatment. Thus, 1,25(OH)2D3 is efficacious in treating symptomatic osteodystrophy in many uraemic patients, and in other patients, it may help identify bone disease of other, as yet unknown, pathogenesis.

Adolescent↗

PubMed1994

Biochemical markers of renal osteodystrophy in pediatric patients undergoing CAPD/CCPD.

Serum intact PTH [1-84] levels were evaluated as a potential non-invasive method for the diagnosis of renal osteodystrophy in children treated with CAPD/CCPD. Sixty-eight bone biopsy samples were obtained from 55 patients, aged 13 +/- 5 (X +/- SD) years, undergoing CAPD/CCPD for 29 +/- 13 months; osteitis fibrosa was present in 34 cases, mild lesions of secondary hyperparathyroidism in six, 15 had adynamic lesions, and 13 were classified as normal histology. Serum calcium levels were higher in patients with adynamic bone or normal bone histology than in those with secondary hyperparathyroidism, whereas serum phosphorus, alkaline phosphatase and PTH levels were greater in patients with osteitis fibrosa. The combination of a serum PTH level > 200 pg/ml and a serum calcium value < 10 mg/dl was 85% sensitive and 100% specific for identifying patients with high-turnover lesions of bone. Serum PTH values < 200 pg/ml were 100% sensitive but only 79% specific for patients with adynamic bone; specificity increased to 92%, however, using the combined criteria of a PTH level < 150 pg/ml and a serum calcium level > 10 mg/dl. Higher serum calcium levels and serum PTH values within or below the normal range characterize patients with the adynamic lesion of renal osteodystrophy. Serum PTH levels of approximately 200 pg/ml are useful for distinguishing patients with low-turnover lesions of renal osteodystrophy from those with secondary hyperparathyroidism.

Adolescent↗

PubMed1998

High frequency of iron bone deposits in a Mexican population with renal osteodystrophy.

Renal osteodystrophy (ROD) is a multifactorial disease. Aluminium deposits have been implicated in its physiopathology but iron deposits have seldom been described. The purpose of this study was to investigate the presence of iron on the mineralization front, in 70 patients with ROD. Their mean age was 48+/-16 years, 36 were female, 34 male, 55 were admitted on peritoneal dialysis (78.5%) and 15 to haemodialysis (21.5%), for a period of 28+/-22 months. A bone biopsy was obtained from each patient after double tetracycline labelling. Blood samples were also obtained at the time of bone biopsy. The histomophometric analysis was performed following the criteria of Sherrard et al., with slight modifications; beside the usual stains, aluminium, iron and amyloid stainings were done on all bone specimens. Biochemical findings were: Ca 8.8+/-0.9 mg/dl, P 6.1+/-1.5 mg/dl; total alkaline phosphatase 197+/-258; PTHm 4.9+/-4.05ng/ml (normal 0.4-0.7 ng/ml), calcitonin 11+/-6 pg/ml (normal 1-26 pg/ml). Osteitis fibrosa was found in 31 patients (44.28%), mixed bone disease in two patients (2.28%); mild bone disease in 20 subjects (28.57%), adynamic bone lesion in 15 cases (21.42%) and osteomalacia in two patients (2.28%). Iron deposits were found on the mineralization front in 43 patients (61.4%); in 17, the percentage was <25 and, in 26, >25%. The iron deposits in the osteitis fibrosa group were highly significant (25/31). The aluminium deposit at the mineralization front was observed in eight patients (11.4%); in all but one, the percentage of this metal was <10%. Amyloid deposits were negative in all cases. The results show: (i) a Mexican population with ROD, present a highly significant incidence of siderosis on the bone mineralization front; (ii) in contrast, the aluminium deposits in this group of patients is lower than that reported in other series, and (iii) the spectrum of RO in this Mexican population is similar to that reported in other studies.

Adult↗

PubMedDate not supplied

[Osteodystrophy in children with chronic renal insufficiency in dialysis therapy].

One of the most important complication of patients with chronic renal failure is osteodystrophy. This causes skeletal deformities, growth failure, bone pain and decreased physical activity. Osteodystrophy is more frequent among children than uraemic adults. In fact, 50-80% of children with chronic renal failure may occur in metabolic bone disease and the incidence tends to be higher in those children who have been in uraemic state for a long time before starting chronic haemodialysis. Osteodystrophy is a result of: 1) lesions of rickets; 2) lesions of osteitis fibrosa: 3) osteosclerosis. In contrast to adult, metastatic calcifications are virtually never observed in uraemic children. Hyperphosphoraemia, that is secondary to the reduction of G.F.R., may be the principal responsible of hyperparathyroidism that is the main cause of osteodystrophy. Hyperparathyroidism is also maintained and increased by deficit of 1,25(OH)2D3 which is responsible for lesions of rickets. Haemodialysis may markedly improve osteitis fibrosa and it is efficacious in reversing the mineral defect. Dialysate calcium concentration should be maintained at approximately 3,5 mEq/l. In this case we can raise serum calcium. On the contrary dialysate has to be lacking in phosphorus to correct hyperphosphoraemia. It must be noted that we have to prepare a dialysate with deionized water lacking in aluminum to avoid encephalopathy compliance.

Aluminum Hydroxide↗

PubMed1998

Bone marrow immunoscintigraphy (BMIS): a new and important tool for the assessment of marrow fibrosis in renal osteodystrophy?

One of the classic histologic forms of renal osteodystrophy is osteitis fibrosa, and its distinguishing characteristic is bone marrow (BM) fibrosis, caused by the activation of marrow parenchymal cells. A bone biopsy must be performed in order to establish the diagnosis of renal osteodystrophy. The clinical use of bone biopsy is restricted, however, due to the invasiveness of the procedure. In recent studies, bone scans have provided information useful for the differential diagnosis between osteomalacia and osteitis fibrosa. However, bone scans can not provide information on the bone marrow status. Bone marrow immunoscintigraphy (BMIS) using Tc-99m anti-granulocyte antibody (AGA), a highly sensitive test for the detection of bone marrow abnormalities which is also a noninvasive method, has rarely been reported in chronic renal failure (CRF). BMIS can provide information in patients with myelofibrosis. The purpose of this study was to evaluate the usefulness of BMIS in CRF patients with special regards to biochemical parameters. Nineteen CRF patients (13 men, 6 women; mean age: 48 +/- 11 years) in whom bone scintigraphy using Tc-99m MDP (methylene diphosphonate) showed the so-called superscan pattern were included in the study. Their primary renal diseases were chronic glomerulonephritis (n = 14), diabetes (n = 4), and polycystic kidney disease (n = 1). Modes of therapies were continuous ambulatory peritoneal dialysis (CAPD) (n = 13; mean duration: 9.5 months), HD (n = 5; mean duration: 7.8 months), and conservative treatment (n = 1). BMIS using Tc-99m labeled anti-granulocyte monoclonal mouse antibody BW250/183 was performed, and the results were compared with the biochemical parameters of the patients. According to the presence of BM expansion, which may represent marrow fibrosis, the 19 patients were divided into two groups: Group I (n = 7) with BM expansion and Group II (n = 12) with normal marrow distribution. The biochemical parameters and bone markers of Group I were compared with those of Group II. There was no significant difference in biochemical parameters (blood hemoglobin, serum ferritin, erythropoietin, BUN, creatinine) between the two groups. There were no significants difference in serum calcium, phosphorus, tartate-resistant acid phosphatase (TRAP), and intact parathyroid hormone (iPTH) between the two groups. Serum alkaline phosphatase (ALP) and osteocalcin were significantly (P < 0.05) higher in Group I than in Group II. These results suggest that patients with bone marrow expansion in BMIS have increased levels of ALP and osteocalcin, indicating an increased osteoblastic activity. BMIS may be useful for the detection of bone marrow expansion due to marrow fibrosis in renal osteodystrophy, and for the evaluation of the extent of bone marrow fibrosis.

Biomarkers↗

PubMedDate not supplied

Pseudohypohyperparathyroidism: a case study of differential resistance to parathyroid hormone.

OBJECTIVE: To present a rare case of a combination of hyperparathyroidism and hypoparathyroidism in a 30-year-old woman. METHODS: We review the laboratory, radiographic, and pathologic findings in a healthy-appearing woman who sustained a patellar fracture after a simple fall at home. RESULTS: Our patient had features of hypoparathyroidism--that is, tetanic crises and hypocalcemia--and also hyperparathyroidism--fracture of the patella, multiple bone cysts, and confirmed osteitis fibrosa cystica on bone biopsy specimens. These features were associated with a high serum level of intact parathyroid hormone (PTH) and parathyroid hyperplasia. A lack of response of nephrogenic cyclic adenosine monophosphate (cAMP) to PTH stimulation was observed along with subnormal serum cAMP responses. In contrast, urine phosphate excretion increased after administration of PTH. CONCLUSION: These results demonstrate a state of renal PTH resistance in a patient with osteitis fibrosa cystica.

Journal Article↗

PubMed1975

Back pain and vertebral crush fractures: an unemphasized mode of presentation for primary hyperparathyroidism.

During a 3-year period, 14 of 319 patients (4.4%) with surgically proved primary hyperparathyroidism had spinal rarefaction with vertebral crush fractures but no unequivocal roentgenographic evidence of osteitis fibrosa generalisata. All complained of back pain, and this was the presenting complaint in 9 of the 14 patients. This incidence was significantly higher (P less than 0.001 for women; P less than than 0.01 for men) than the incidence of similar roentgenographic findings among patients of the same age undergoing operation for protruded intervertebral disks during this same time period. Although tradition equates roentgenographically evident bone disease in primary hyperparathyroidism with the classis findings of osteitis fibrosa generalisata, our observations emphasize that patients with primary hyperparathyroidism occasionally may present in a manner that is indistinguishable symptomatically and roentgenographically from that of postmenopausal or senile osteoporosis.

Age Factors↗

PubMedDate not supplied

Sphenoid sinus brown tumor, hypercalcemia, and blindness: an unusual presentation of primary hyperparathyroidism.

This is a first report of primary hyperparathyroidism (HPT) masquerading as a destructive fibrous sphenoid sinus "Brown tumor" associated with progressive blindness and hypercalcemia. Diagnosis of a Brown tumor was delayed despite serial computerized tomography of the head and repeated transnasal and transethmoid sphenoid biopsies demonstrating diffuse fibrosis. Only detection and medical evaluation of hypercalcemia, demonstrating elevation of both serum calcium and C-terminal parathyroid hormone with an elevated chloride/phosphate ratio, prompted neck exploration, thus confirming a solitary left superior parathyroid adenoma. Postoperative normocalcemia occurred synchronously with the return of light perception and the arrest of sphenoid sinus and parasellar erosion. Although maxillary Brown tumors of secondary HPT have been reported, this is the first report of osteitis fibrosa of the sphenoid sinus. Differential diagnosis of an erosive sphenoid lesion with cranial nerve dysfunction, exclusive of inflammatory or vascular disease, should include sarcoidosis, primary and metastatic sphenoid carcinoma, fibrous dysplasia, giant cell reparative granuloma, midline lethal granuloma, chordoma, and chondrosarcoma. Furthermore, the bony destructive lesions with concomitant hypercalcemia of sarcoidosis and HPT are distinguishable by radiographic and laboratory analyses and by the Dent corticosteroid suppression test. Hypercalcemia of primary HPT is associated with elevated serum C-terminal parathormone, osteitis fibrosa, a negative Dent test, and a chloride/phosphate ratio greater than 33 in 94% of primary HPT patients. Hypercalcemia of sarcoidosis is associated with a normal or decreased C-terminal parathormone assay and a positive Dent test, as well as elevated serum immunoglobulins and erythrocyte sedimentation rate, and a positive angiotensin-converting enzyme assay.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗

PubMed1962

Phosphatase activity in the limb bones of monkeys (Lagothrix humboldti) with hyperparathyroidism.

The paper reports a study of the distribution of phosphatases in the femora of three specimens of Humboldt's woolly monkey (Lagothrix humboldti) suffering from chronic hyperparathyroidism. Bone structure ranged from the apparently normal to extreme osteitis fibrosa. Most marked changes were found in the distribution of alkaline phosphatase, which reached at least 10 times the normal levels in the bone of the second monkey in the series, dropping to levels still well above normal in that of the most severely affected animal. Very high concentrations were found in the deeper layers of hypertrophied growth cartilage and in the osteoblasts lining poorly calcified trabeculae, and high concentrations in the fibre bone of the third animal. Lack of mineralization and the development of osteitis fibrosa are thus associated with a marked increase in alkaline phosphatase activity. Osteoclasts reacted strongly for acid phosphatase but were negative for alkaline phosphatase. Acid phosphatase levels were comparatively high in fibre bone, but overall levels ranged from 1/20 to less than 1/100 those of alkaline phosphatase. Some slow staining for acid phosphatase probably represents residual activity at acid pH of the markedly increased alkaline phosphatase. There may be some association between a failure of mineralization and the presence of acid phosphatase in osteoclasts and osteoid. The aetiology of the monkeys' condition is discussed. It seems likely that the parathyroid hypertrophy and rachitic changes were caused by low blood calcium dependent on a low calcium diet and lack of vitamin D, in which the requirements of New World monkeys are reputedly high.

Acid Phosphatase↗

PubMed1993

Renal bone disease in pediatric and young adult patients on hemodialysis in a children's hospital.

Renal bone disease has been well defined in adult patients receiving chronic dialysis and in children on peritoneal dialysis/continuous ambulatory peritoneal dialysis. However, little is known about the histologic features in patients undergoing chronic hemodialysis in a children's hospital center. Twenty one patients, aged 17.5 +/- 1.5 yr, on hemodialysis for 35 +/- 6 months underwent iliac crest bone biopsies and deferoxamine infusion tests. Nineteen of 21 patients were receiving oral calcitriol. The 21 patients were classified by histomorphometry as follows: osteitis fibrosa, 5; mild hyperparathyroidism, 3; normal histology, 3; aplastic, 6; and mixed lesions, 4. Four of 21 patients were surface positive for aluminum, and seven other patients stained positive for iron in bone. Serum parathyroid hormone (PTH) levels correlated directly with the bone formation rate (r = 0.84) and with eroded bone perimeter (r = 0.67). Eight of the nine patients with serum PTH levels above 125 pg/mL had marrow fibrosis. All patients with serum calcium levels < 10.0 mg/dL and serum PTH levels > 125 pg/mL had either osteitis fibrosa or mixed bone lesions--a group of patients that might benefit from aggressive vitamin D therapy. In contrast, an examination of patients with serum calcium levels > 10.0 mg/dL and serum PTH levels < 65 pg/mL correctly identified three out of three patients with aluminum-related bone disease. These findings suggest that measurements of serum intact PTH levels by the immunoradiometric assay method may be valuable in distinguishing high-turnover lesions from normal or low-turnover skeletal lesions in this population.

Adolescent↗

PubMed1995

Risk factors for renal osteodystrophy: a multivariant analysis.

To assess the risk factors associated with renal osteodystrophy, we examined the database of 256 patients who were prospectively studied in three Toronto dialysis centers between October of 1987 and 1989. The potential risk factors examined included age, sex, type and duration of dialysis, type and dose of phosphate binders, vitamin D treatment, and history of diabetes mellitus, renal allograft failure, parathyroidectomy, and bilateral nephrectomy. All patients had undergone a bone biopsy and were categorized into one of four disease groupings: (1) osteitis fibrosa and mixed bone disease, (2) aluminum bone disease, (3) mild bone disorder, and (4) aplastic bone disorder. The mean (+/- SD) age of the patients at bone biopsy was 57 +/- 15 years, and 62% were men. Forty-five percent of patients were treated by hemodialysis and 55% by peritoneal dialysis. The mean duration of dialysis was 4 +/- 4 years. Twenty-five percent were also diabetic. The most common disorder was the aplastic (or "adynamic") bone disorder, found in 34% of patients. Aluminum bone disease was found in 27%, osteitis fibrosa or mixed bone disease in 27%, and mild bone disorder in 12% of patients. Cumulative intake of aluminum gels was associated with aluminum bone disease, whereas peritoneal dialysis with supraphysiologic calcium concentrations, ingestion of calcium carbonate, and diabetes mellitus were associated with both mild bone disorder and aplastic bone disorder. These three latter risk factors may be important in predisposing patients to a low bone turnover state through modulation of parathyroid hormone secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

Low turnover bone disease is the more common form of bone disease in CAPD patients.

CAPD is considered a risk factor for low turnover bone disease. This was previously attributed to aluminum accumulation. We evaluated by biochemical and histomorphometric parameters (including double tetracycline labelling), 26 patients maintained on CAPD for 12-14 months. Three (11.5%) showed mild hyperparathyroidism, 5 (19.2%) osteitis fibrosa, 3 (11.5%) mixed forms, 4 (15%) osteomalacia and 11 (42.3%) adynamic bone disease. Only one patient with diabetes mellitus showed an aluminum stained bone surface > 10%. Intact PTH serum levels were lower in LTBD (133.2 +/- 128 vs 468.2 +/- 451 pg/ml; p < 0.05). We also evaluated prospectively 11 patients who underwent a bone biopsy at start of dialysis and after 12 months of CAPD treatment. Bone biopsies pre CAPD demonstrated normal-high bone turnover disease in 8/11 (72.7%) and low turnover bone disease in 3/11 (27%). In the follow-up biopsies, 2 patients showed osteitis fibrosa and other two mild forms. Low turnover bone disease was found in 7 patients (3 osteomalacia and 4 adynamic bone disease). We conclude that the predominant bone lesion in our CAPD patients is low turnover bone disease, predominantly adynamic forms, and aluminum does not seem to play a role on its genesis. Low intact PTH serum levels may be a predictor of low turnover bone disease.

Bone and Bones↗

PubMedDate not supplied

Primary hyperparathyroidism in women: a tale of two cities--New York and Beijing.

The Western world has been used to describing disease on its terms, as if it is a prototype for the same disease found anywhere else in the world. It is unusual that one can test the hypothesis that a common disease can present in markedly different ways, depending on the country in which it is studied. We have had the opportunity to compare and contrast primary hyperparathyroidism in the United States and in China as seen in New York City and in Beijing. The cohort of subjects in each case was well over 100, and the experience extends to well over a decade of observations. In the United States, primary hyperparathyroidism typically presents as asymptomatic hypercalcemia in women within 10 years of menopause. Most often, it is discovered accidentally in the course of a routine multichannel chemistry screening test. The serum calcium is 10.5 + 0.1 mg/dL, within 1 mg/dL above the upper limit of normal, 10.2; the serum parathyroid hormone level is 118 + 9 pg/mL (within 1.5-2-fold above the normal limit, 65). The average 25-hydroxyvitamin D level is 21 ng/mL, in the lower range of normal. The classical clinical manifestations of primary hyperparathyroidism, stone and bone disease, have become much less common than earlier descriptions of the disease in the United States through the 1950s. Overt radiological bone disease (osteitis fibrosa cystica) is almost never seen, whereas stone disease is reduced in incidence from a high of 60% in the 1940s to current estimates of 15-20% now. Most patients are asymptomatic; skeletal involvement is detected only by measuring skeletal calcium by bone densitometry. Primary hyperparathyroidism in China presents much differently. Patients are younger, with an average age of 37. The serum calcium level is much higher, averaging about 12 mg/dL. PTH is over 20 times the upper limits of normal. The average 25-hydroxyvitamin D concentration is much lower than in the United States population, 8.8 ng/mL. Radiological evidence for osteitis fibrosa cystica is seen in 60% of patients; virtually all patients have osteoporosis. Thirty-five percent of patients suffer pathological fractures, most often of the femur or humerus. Forty-two percent demonstrate kidney stones, with half showing bilateral disease. Constitutional features of weakness and easy fatigability are always present. There are both facile and rather subtle explanations for this dramatically different presentation of the same disease in the United States (New York City) and China (Beijing).

Adult↗

PubMed1978

Renal-resistant hormonoplethoric hypoparathyroidism with evidence for a defective response to cAMP.

A 15.5-yr-old black male is reported with hypocalcemia, hyperphosphatemia, and severe osteitis fibrosa cystica. While hypocalcemic and hyperphosphatemic, the circulating parathyroid hormone (PTH) level and urinary cAMP excretion were increased. An infusion of exogenous PTH produced a normal maximal excretion of urinary cAMP but failed to increase phosphate excretion. Correction of the hypocalcemia by administration of 200,000 U vitamin D daily lowered the endogenous PTH level and basal excretion of cAMP to normal; at that time, infusion of PTH produced both a normal rise in urinary cAMP and a normal phosphaturic response. This pattern of response suggests pseudohypoparathyroidism with a calcium-sensitive defect in renal phosphate transport distal to the PTH receptor adenyl cyclase mechanism, producing hyperphosphatemia, hypocalcemia, and secondary hyperparathyroidism. The osteitis fibrosa cystica was presumably due to the increased PTH, suggesting that resistance to PTH was present in kidney but not bone.

Adolescent↗

PubMed1982

Therapeutic effects of 25-hydroxycholecalciferol and sodium etidronate on renal osteodystrophy.

The effects of long-term treatment with 25-hydroxycholecalciferol (25OHD3) and disodium ethane-1-hydroxydiphosphonate, or 25OHD3 alone on biochemical parameters, and radiographic and quantitative histomorphometry of bone tissue were evaluated in 17 dialysis patients. They all displayed evidence of bone disease consisting of osteitis fibrosa and defective mineralization of varying degree and predominance. 100 micrograms/day of 25OHD3 significantly improved the state of bone mineralization in many patients with a pronounced fall in the osteoid volume and surface and produced a small reduction in the active resorption surface. Serum parathyroid hormone (iPTH) and alkaline phosphatase levels decreased in some patients. The combination of 25OHD3 with EHDP caused the healing of bone mineralization as did 25OHD3 alone and produced a significant fall in serum alkaline phosphatase and iPTH. The mean magnitude of the reduction in iPTH was higher in patients treated with 25OHD3 and EHDP than with 25OHD3 alone. Treatment with 25OHD3 and EHDP seems more effective for the improvement of osteitis fibrosa than is 25OHD3 alone.

Adult↗

PubMed1996

The renal bone diseases in children treated with dialysis.

Renal osteodystrophy represents a spectrum from high- to low-turnover bone lesions. The specific pattern, however, may change during selected therapeutic interventions. As in the past, osteitis fibrosa remains the most frequent histologic lesion in pediatric patients on dialysis, although recently the prevalence of low-turnover bone lesions without aluminum toxicity has been increasing in the pediatric population. This may be a consequence of aggressive calcitriol and calcium therapy. The different factors involved in the development of secondary hyperparathyroidism include hyperphosphatemia, hypocalcemia, altered vitamin D synthesis, impairments in parathyroid hormone (PTH) secretion and metabolism, and, recently, possible downregulation of renal PTH/PTH-rP messenger RNA receptor. New developments in molecular biology have demonstrated the relationship between vitamin D and PTH. The use of high-dose pulse intravenous, intraperitoneal, and oral calcitriol therapy has significantly decreased serum PTH levels and retarded the progression of osteitis fibrosa. These therapeutic interventions, however, may have led to the development of adynamic bone lesions. The impact of adynamic bone lesions in the young and growing skeleton remains to be determined.

Bone Diseases↗