Cases reported "Bone Resorption"

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1/10. Primary neonatal hyperparathyroidism. Report of a case and review of the literature.

    The seventh case in the world literature of primary hyperparathyroidism in a neonate is reported. This is the fifth case in which an autopsy was performed. The clinical and anatomic findings in all seven cases are reviewed and compared. Neonates with primary hyperparathyroidism show diffuse hyperplasia of the parathyroid glands. The bones show disturbed osteogenesis, bone resorption, and widespread fibrosis of the marrow cavities. Bony cysts are not appreciated. Pathologic fractures are common. Marked hypercalciuria or hyperphosphaturia is usually not observed, perhaps because the immature renal tubules fail to respond to the influence of excess parathormone. Aminoaciduria and anemia are commonly observed. The prognosis is grave, and the etiology of this syndrome remains unexplained.
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2/10. parathyroid hormone-related protein induced coupled increases in bone formation and resorption markers for 7 years in a patient with malignant islet cell tumors.

    parathyroid hormone-related protein (PTHrP) and PTH share the common PTH/PTHrP receptor. Although an elevated level of circulating PTHrP in patients with malignancies causes hypercalcemia as does PTH, chronic and systemic effects of PTHrP on bone metabolism in humans are not well understood because tumor-burden patients showing hypercalcemia usually have a poor prognosis. We investigated bone and calcium metabolism in a patient with malignant islet cell tumors showing hypercalcemia due to the elevated plasma PTHrP level for 7 years. hypercalcemia and hypercalciuria continued throughout the clinical course in spite of frequent infusions of bisphosphonates. bone resorption markers and a bone formation marker were consistently elevated as seen in primary hyperparathyroidism, a disease caused by an autonomous hypersecretion of PTH. Based on biochemical measurements including bone markers and serum 1,25-dihydroxyvitamin D, the clinical features of this case essentially are the same as those of primary hyperparathyroidism except for the elevated level of plasma PTHrP with suppressed intact PTH level. Therefore, it is suggested that chronic and systemic effects of PTHrP on bone as well as calcium metabolism are indistinguishable from those of PTH in human.
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3/10. Recurrent vesical calculi, hypercalciuria, and biochemical evidence of increased bone resorption in an adult male with paraplegia due to spinal cord injury: is there a role for intermittent oral disodium etidronate therapy for prevention of calcium phosphate bladder stones?

    STUDY DESIGN: Clinical case report with comments by colleagues from sweden, poland, spain, brazil, japan, belgium and switzerland. OBJECTIVES: To discuss the role of disodium etidronate therapy for prevention of calcium phosphate vesical calculi in persons with spinal cord injury, who have hypercalciuria and biochemical evidence of increased bone resorption. SETTING: Regional spinal injuries Centre, Southport, UK. methods: A 21-year-old male sustained paraplegia (T-10; ASIA scale: A) in a road traffic accident in June 2001. He had an indwelling urethral catheter until the end of August 2001, when he started self-catheterisation. He developed bladder stones and electrohydraulic lithotripsy (EHL) was performed in May 2002. All stone fragments were removed. recurrence of vesical calculi was noted in October 2002. These stones were fragmented by lithoclast lithotripsy in two sessions, in December 2002 and February 2003; all stone fragments were removed at the end of the second session. This patient reverted to indwelling catheter drainage when vesical calculi recurred. In September 2003, X-ray of the abdomen showed recurrence of vesical calculi. By February 2004, the stones had increased in size and number. EHL of vesical calculi was again performed in April 2004. Complete clearance was achieved. RESULTS: A 24-h urinalysis detected hypercalciuria--18.7 mmol/day (reference range: 2.5-7.5). Biochemical analysis of vesical calculus revealed calcium phosphate (85%) and magnesium ammonium phosphate (15%). plasma C-terminal telopeptide (CTX) was increased - 1.06 ng/ml (reference range: 0.1-0.5 ng/ml). Free deoxypyridinoline/creatinine ratio (fDPD/Cr) in urine was also increased - 20.2 (reference range: 2.3-5.4). In April 2004, this patient was prescribed disodium etidronate 400 mg day. Nearly 3 months after commencing therapy with etidronate, plasma CTX decreased to 0.87 ng/ml. fDPD/Cr in urine also decreased to 12.4. After 4 months of etidronate therapy, 24-h urinary calcium excretion had decreased to 6.1 mmol/day. CONCLUSION: Etidronate (400 mg daily) is a very effective inhibitor of calcium phosphate crystallisation. Etidronate decreased urinary excretion of calcium, an important factor in prevention of calcium phosphate bladder stones. Etidronate therapy is not a substitute for other well-established methods for prevention of vesical calculi in spinal cord injury patients, for example, large fluid intake, avoiding long-term catheter drainage. Intermittent therapy with etidronate may be considered in selected patients, in whom hypercalciuria persists after instituting nonpharmacological therapy for an adequate period, for example, early mobilisation, weight-bearing exercises, and functional electrical stimulation. However, possible side effects of etidronate, and the fact that etidronate is not licensed in United Kingdom for prevention of urolithiasis, should be borne in mind.
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4/10. Malignant osteoporosis and defective immunoregulation.

    The linkage between immune cells and the osteoclast has become partially understood in the laboratory, but the full spectrum of clinical disorders of this relationship remain to be elucidated. We report a 29-month-old girl with recurrent infections and multiple fractures. Immune evaluation showed normal quantitative serum immunoglobulins but absent antibodies to the respiratory viruses and tetanus toxoid and decreased in vitro polyclonal-induced immunoglobulin production. Further analysis in vitro with separated lymphocyte populations showed normal B cell function but markedly increased suppressor T cell activity. The bone evaluation showed diffuse osteopenia on x-ray. serum calcium, phosphorus, PTH, 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D were normal for age. Urinary calcium excretion (24 h) was, however, two times normal. An iliac crest biopsy confirmed the presence of extreme osteopenia with normal mineralization and numerous small atypical osteoclasts resorbing the bone. No circulating plasma resorptive activity was demonstrated. calcitonin therapy markedly diminished the patient's hypercalciuria. We speculate that this patient's increased bone resorption, decreased bone formation, and suppressor activity may be linked by a common pathway involving the abnormal function of immune cells. Since no similar constellation of findings has been previously reported, this case may represent a new congenital disorder: severe osteopenia associated with increased osteoclast activity in association with a defect in T cell immunoregulation.
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5/10. Calcium-oxalate-crystal-induced bone disease.

    A 13-year-old boy with primary hyperoxaluria and a successful renal allograft developed symptomatic bone disease, hypercalcemia, and hypercalciuria. Transiliac bone biopsy revealed calcium oxalate crystals in the marrow within mononuclear phagocytes and multinucleated giant cells. Deep resorption bays were seen adjacent to these crystal-cell aggregates. serum 1,25-(OH)2-vitamin d (calcitriol) and iPTH concentrations were low or normal. We suggest that hypercalcemia results from macrophage-mediated bone resorption initiated by Ca oxalate crystal deposition.
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6/10. Healing of osteitis fibrosa cystica after partial parathyroidectomy despite persistent parathyroid hyperfunction: a case report.

    The diagnosis of primary hyperparathyroidism was made in a 55-year-old female with marked hypercalcemia (15 mg/100 ml) and hypercalciuria and skeletal x-rays showing typical lesions of subperiosteal resorption and numerous cystic areas. At surgery a left lower parathyroid adenoma presumably was totally excised. serum calcium returned to normal levels immediately postoperatively, but 4 months after surgery hypercalcemia (11.5 mg/100 ml) was again found. During the following 18 months the patient was free of symptoms, and radiologic studies revealed complete healing of the subperiosteal resorption and repair of the bone cysts. Cortical bone mineral content also increased. However, elevated levels of serum parathyroid hormone (PTH) and calcium clearly indicated the persistence of primary hyperparathyroidism. Thus, a decrease in the degree of PTH hypersecretion permitted the repair of the skeletal lesions caused by a more severe level of parathyroid hyperfunction.
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7/10. Skeletal sarcoidosis with osteopenia.

    Diffuse osteopenia is not generally recognized as a radiological manifestation of skeletal sarcoidosis. Furthermore, the pathologic correlates of the skeletal abnormalities in sarcoidosis are poorly characterized. We quantitated the histomorphometric parameters of bone formation and resorption in a transiliac crest biopsy specimen from a patient with sarcoidosis, diffuse osteopenia, hypercalcemia, and hypercalciuria, who was treated only intermittently with corticosteroids and thiazides. Peritrabecular granulomas were associated with the histologic features of accelerated bone remodeling, namely: excess osteoid; increased numbers of osteoclasts and osteoblasts; increased osteoclastic resorbing surfaces; and increased bone formation rate. We conclude that the peritrabecular granulomas of skeletal sarcoidosis may result in rapid bone turnover with diffuse osteopenia which may contribute to the abnormalities of mineral metabolism.
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8/10. Successful treatment of immobilization hypercalcemia using calcitonin and etidronate.

    hypercalcemia of immobilization may present in patients with spinal cord injury, multiple fractures, or Landry-guillain-barre syndrome. It is attributed to an increase in bone resorption and diminished bone formation characterized clinically by elevated serum calcium levels, hypercalciuria, increased risk of urinary lithiasis, and renal failure. Traditional treatment methods can interfere with the intensive level of therapy provided in the comprehensive rehabilitation program. Other treatments, less disruptive of the rehabilitation milieu, are possible. Reported are six patients with hypercalcemia of immobilization who were successfully treated with combination therapy of salmon calcitonin and sodium etidronate. The patients developed hypercalcemia an average of 69 days after the onset of illness. serum calcium levels dropped an average of 2.8mg/dL (12.3mg/dL, SD 1.33 to 9.5mg/dL, SD 0.42) within eight days after initiation of treatment. In two patients, 24 hour urine excretions of calcium decreased by 414 and 210mg/day, respectively. All patients had a reduction in serum calcium levels noted within two days of treatment, and a normal serum calcium levels within one week. patients were usually changed to a single medication maintenance regimen, sodium etidronate, within a few days. Full therapies in the treatment gyms were given to all patients within a day of initiation of the combined treatment. These two drugs appear to have a rapid and combined effect on the treatment of hypercalcemia of immobilization, and allow full participation in a comprehensive rehabilitation program.
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9/10. Infantile hypophosphatasia: treatment options to control hypercalcemia, hypercalciuria, and chronic bone demineralization.

    A 2-month-old child with infantile hypophosphatasia had hypercalcemia (3.49 mmol/L (14 mg/dl)), nephrocalcinosis, and diminished bone mineral content. hypercalcemia was corrected with calcitonin. hypercalciuria and bone demineralization abated with chlorothiazide. hypercalcemia is hypothesized to be related to normal bone resorption in conjunction with impaired bone mineralization. chlorothiazide may alleviate this impairment.
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10/10. Interleukin 1beta mediated calciotropic activity in serum of children with juvenile rheumatoid arthritis.

    OBJECTIVE: To detect the presence and source of calciotropic activity in the serum of children with juvenile rheumatoid arthritis (JRA). methods: Metabolic evaluation of an adolescent with polyarticular JRA and hypercalcemia/hypercalciuria included testing with a bone disc bioassay. The bioassay detects calciotropic activity (increased bone resorption or reduced bone formation) in serum. Interleukin 1 receptor antagonist (IL-1RA) was added to patient sera to test the role of IL-1beta. The results in this index case prompted additional study in 9 children with JRA. Correlation of calciotropic activity with disease activity score, erythrocyte sedimentation rate (ESR), and urinary calcium excretion was by Spearman rank correlation. RESULTS: Calciotropic activity was found in 2 consecutive samples from the index patient. This activity was eliminated by addition of IL-1RA (p < 0.001 compared to serum alone). Testing of the other 9 children showed calciotropic activity at least once in 7/9 and 10/15 samples studied. Addition of IL-1RA completely (6/8) or partially (2/8) neutralized calciotropic activity (p < 0.001 compared to serum alone) in the specimens available for testing. Calciotropic activity did not significantly correlate with disease activity score, ESR, or urine calcium. CONCLUSION: Our data indicate the presence of IL-1beta mediated calciotropic activity in the sera of children with JRA, and suggest a role for IL-1beta in JRA associated osteopenia.
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