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1/80. Localization of a bone imaging agent in a calcified hematoma.

    A patient with chronic renal failure and secondary hyperparathyroidism had iliac bone biopsy. The procedure was complicated by a soft-tissue hematoma, which had calcified. A 3-4-cm palpable mass was visible in the lower left abdominal wall. Intense uptake of 99mTc-HMDP corresponded with the location of the calcified hematoma in this patient.
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2/80. Post-gastrectomy bone disease undiagnosed for forty years.

    Polya partial gastrectomy was performed for peptic ulcer in a previously healthy woman aged 28 years. She complained afterwards of a variety of non-specific symptoms including weakness, tiredness, debility, slowness of walking, poor appetite and constipation. Within ten years her back became bent. She was treated for intercurrent hypertension and epilepsy. Bone fractures on low-impact trauma occurred in her fifties. At 57 years, she was unable to care for herself and had to be admitted to a nursing home. She could still walk slowly with the aid of a stick. For three months at the age of 65 years, she was unable to rise from her chair. Investigations disclosed severe post-gastrectomy bone disease. At no time had she complained of bone pains.
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3/80. Mobilization of lead from bone in end-stage renal failure patients with secondary hyperparathyroidism.

    BACKGROUND: It is now recognized that long-term exposure to even low levels of lead may increase bone lead content. lead can then be released in toxicologically significant amounts during critical states of increased bone turnover. methods: Two patients with end-stage renal failure, one on haemodialysis and the other on continuous ambulatory peritoneal dialysis (CAPD), had been exposed to lead and developed secondary hyperparathyroidism. An edetate calcium disodium (EDTA) test was performed in combination with haemofiltration or CAPD before and after parathyroidectomy. RESULTS: Before parathyroidectomy, both patients had low delta aminolaevulinic acid dehydrase (ALA-D) and high concentrations of chelated lead. After parathyroidectomy, there was a dramatic decrease in chelated lead and the ALA-D returned to normal. CONCLUSION: Secondary hyperparathyroidism increases mobilization of bone lead in dialysis patients with an elevated lead burden. This may cause toxic effects.
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4/80. 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.
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5/80. The role of bone scanning in the detection of metastatic calcification: a case report.

    Metastatic calcification associated with renal failure is well described. Bone scanning agents accumulate to various degrees within extraskeletal sites of metastatic calcification. The authors describe a patient with polycystic kidney disease resulting in renal failure, with the subsequent development of secondary hyperparathyroidism and metastatic calcification. Bone scintigraphy revealed abnormal uptake in both lungs, the right leg, and the right hand.
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6/80. Brown tumour of hyperparathyroidism in the mandible associated with atypical parathyroid adenoma.

    The brown tumour of hyperparathyroidism is a localized bone tumour and an uncommon manifestation of hyperparathyroidism. A 27-year-old woman presented with a mandibular 8 x 10 cm solid mass diagnosed as central giant cell granuloma. Chemical blood analysis revealed increased serum calcium levels of 12.46 mg/dL and the parathyroid hormone level was 124 pg/dL. The patient underwent surgery with removal of a parathyroid mass. Histologically, this parathyroid tissue was seen to be limited by a fibrous capsule with morphological features consistent with atypical parathyroid adenoma. The mandibular tumour has receded and the patient declined further procedures. This is the first case reported of brown tumour as the primary manifestation of an atypical parathyroid adenoma, a lesion that shares some features with parathyroid carcinoma without the unequivocal properties of malignancy.
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7/80. gastrectomy and osteomalacia: an association not to be forgotten.

    Metabolic bone disease due to calcium and vitamin d malabsorption is a well-defined consequence of gastrectomy and to a lesser extent of pancreatic insufficiency. The diversity of its presentation, however, can be misleading, resulting in delayed diagnosis or a thorough investigation for possible underlying neoplasias being undertaken. We describe the case of a man with partial gastrectomy and pancreatectomy with osteomalacia and secondary hyperparathyroidism.
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8/80. fanconi syndrome following bowel surgery and hepatitis reversed by 25-hydroxycholecalciferol.

    A permature male infant required intravenous alimentation for six weeks following extensive surgery for ileal and cecal necrosis. At 3 months he developed evidence of hepatitis. Subsequently osteoporosis and the fanconi syndrome appeared. urine phosphate clearance was 83 percent of creatinine clearance at a serum phosphate concentration of 1.6 mg/dl. Concentration of plasma immunoreactive parathyroid hormone was elevated at 550 pg/ml. 25-Hydroxycholecalciferol was given at 240 mug/day. Aminoaciduria disappeared and bone healing occurred. serum phosphate rose to 6.5 mg/dl and phosphate clearance fell to 2 percent of creatinine clearance. Upon cessation of 25-OHCC therapy, the fanconi syndrome recurred despite administration of vitamin D2. 25-OHCC was then administered at 40 mug/day, and the urine abnormalities were reversed. The patient probably developed hyperparathyroidism, secondary malabsorption, and hepatitis. The fanconi syndrome was the consequence of the hyperparathyroidism. 25-OHCC therapy was more effective than vitamin d in reversing the disordered state, possibly because of impaired hepatic metabolism of vitamin D2.
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9/80. Secondary hyperparathyroidism: evidence for an association with papillary thyroid cancer.

    The association between primary hyperparathyroidism and nonmedullary thyroid malignancies is well known. There is also, however, some evidence for an association between secondary hyperparathyroidism (SHPT) and thyroid cancer. We report three patients in whom invasive papillary thyroid carcinoma (PTC) was diagnosed before (one case) or at the time of (two cases) parathyroidectomy for SHPT. Three women (ages 23, 54, and 64 years) presented with bone pain and pruritis typical of SHPT. All three patients had biopsy-proven parathyroid bone disease and elevated parathormone levels (664, 1674, and 2051 pg/mL). All underwent subtotal parathyroidectomy and total thyroidectomy without complications. pathology revealed diffuse parathyroid hyperplasia with multifocal invasive papillary thyroid carcinoma (two cases) and follicular variant of papillary thyroid carcinoma (one case). Two cases were associated with metastatic disease to local lymph nodes. The patients received adjuvant radioactive 131I, and remained tumor free 24 to 36 months after surgery with complete resolution of SHPT. We conclude: 1) PTC may accompany SHPT, 2) PTCs associated with SHPT may be locally aggressive although usually they are early tumors, 3) surgeons need to have an index of suspicion for thyroid tumor when operating on patients with SHPT, and 4) routine removal of the thymus as part of the operation for SHPT may have a secondary benefit in diagnosing PTC in the occasional patient.
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10/80. Brown tumor of the thoracic spine in a patient on long-term hemodialysis.

    A 39-year-old woman on long-term hemodialysis presented with a history of rapidly progressive paraplegia. Radiological examination showed a compression fracture of seventh thoracic vertebra and expansive mass lesion in the posterior elements of the fourth thoracic vertebra. Laboratory tests on admission showed serum calcium of 11.9 mg/dl, phosphate 6.0 mg/dl, and the high-sensitive parathyroid hormone level of 139,191 pg/ml measured by radioimmunoassay. Percutaneous biopsy of the expansive mass showed a large number of multinucleated giant cells in a fibroblastic stroma containing abundant hemosiderin. Tumor resection and anterior interbody fusion with artificial bone graft was performed on 14th hospital day. paraplegia gradually improved postoperatively. Total parathyroidectomy and autotransplantation of parathyroid gland were subsequently performed. Nodular hyperplasia was evident in the parathyroid glands by light microscopy. Brown tumor is rarely found in vertebral bone and this is the sixth case of such tumor in secondary hyperparathyroidism.
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