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1/53. Brown tumour as a complication of secondary hyperparathyroidism in severe long-lasting vitamin d deficiency rickets.

    Brown tumour is a localised form of fibrous-cystic osteitis associated with primary or secondary hyperparathyroidism. Despite the fact that secondary hyperparathyroidism occurs in vitamin d deficiency rickets, no cases of rickets with brown tumour have so far been described. We present a 2.9-year-old girl who had brown tumour of the mandible due to severe vitamin d deficiency rickets. Treatment with vitamin D3 corrected the hyperparathyroidism rapidly which was followed by gradual regression in tumour size. CONCLUSION: Brown tumour can develop in severe, long-standing vitamin d deficiency rickets and responds to vitamin D treatment.
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keywords = rickets, vitamin
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2/53. Severe ectopic calcification of the intestinal wall in a patient on long-term continuous ambulatory peritoneal dialysis therapy.

    We report autopsy findings of a 69-year-old man on long-term CAPD therapy for 13 years who showed linear peritoneal calcification. Continuous ambulatory peritoneal dialysis (CAPD) was started in 1982. He has been administered excessive amounts of vitamin D(3) derivatives (VitD) (2.0 to 2.5 microg daily) and calcium carbonate (4 g daily) for secondary hyperparathyroidism since initiation of CAPD. In May 1995, his intact parathyroid hormone (PTH) level increased over 1,000 pg/mL. Immediately after VitD was changed from pill to liquid, the dose was increased to 5 microg daily. Although the serum calcium level remained between 4.5 and 4.9 mEq/L, and serum phosphate level was 5.0 to 7.2 mg/dL, plain abdominal radiography and computed tomography showed continuous calcification along the intestinal wall in October 1995. In spite of the continuation of CAPD therapy, he remained asymptomatic until he died of congestive heart failure in January 1997. He experienced eight episodes of peritonitis during his clinical course. autopsy showed that numerous calcified plaques were present on the submucosal portion between the thickened serosa and the longitudinal layer of the muscularis externa. The remainder of the subserosa was fibrotic, and the small arteries had markedly thickened intima and severely narrowed lumina.
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ranking = 0.019102685000198
keywords = vitamin
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3/53. 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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ranking = 0.019102685000198
keywords = vitamin
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4/53. 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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ranking = 0.057308055000594
keywords = vitamin
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5/53. Treatable lower motor neuron disease due to vitamin d deficiency and secondary hyperparathyroidism.

    vitamin d deficiency and osteomalacia are frequently associated with muscle weakness and atrophy. We present a 78-year-old man with complaints of progressive painless weakness who was referred to us with a diagnosis of suspected motor neuron disease. Results of the neurological examination were remarkable, showing diffuse limb weakness and atrophy, rare fasciculations, normal sensory examination, no bulbar weakness, and no upper motor neuron signs. electromyography revealed mild chronic changes, denervation and re-innervation, without fibrillations or positive waves. serum laboratory studies showed an elevated serum parathyroid hormone and markedly reduced vitamin D level. Although the etiology of the vitamin d deficiency was not determined, the patient made a substantial clinical improvement following vitamin D therapy. vitamin d deficiency and secondary hyperparathyroidism need to be included in the differential diagnosis of patients presenting with a progressive lower motor neuron disease.
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ranking = 0.13371879500139
keywords = vitamin
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6/53. Maxillary brown tumor in secondary hyperparathyroidism requiring urgent parathyroidectomy.

    Brown tumors are unusual but serious complications of renal osteodystrophy, and can be successfully treated by parathyroidectomy or by pharmacological treatment of hyperparathyroidism. Brown tumors in patients with severe hyperparathyroidism (HPT) secondary to renal failure have been increasingly reported. We describe an unusual case of brown tumors at the maxillary bone and the seventh right rib, in a 57-year old man with a long history of hemodialysis. The maxillary lesion caused serious local discomfort due to its rapid growth. In this setting, surgical total parathyroidectomy was chosen as the most adequate therapeutic approach, given the previous unsatisfactory response to calcitriol. After successful parathyroidectomy, rapid healing was achieved with sclerosis of both brown tumors, as documented by serial computerized tomograms. In conclusion, although vitamin D therapy has been beneficial in several cases of secondary hyperparathyroidism complicated by brown tumors, we propose that whenever regression of the tumor bulk is urgently needed, as in our case, parathyroidectomy should be the first treatment choice.
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ranking = 0.019102685000198
keywords = vitamin
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7/53. Oral doxercalciferol therapy for secondary hyperparathyroidism in a peritoneal dialysis patient.

    Control of hyperphosphatemia and the administration of vitamin D are the primary treatment modalities for the prevention and management of secondary hyperparathyroidism. Vitamin D therapy for secondary hyperparathyroidism has been limited by the development of hypercalcemia and/or hyperphosphatemia due to increased intestinal absorption of these minerals. Recently, selective vitamin D analogs specifically designed to suppress parathyroid hormone (PTH) without causing hypercalcemia or hyperphosphatemia have shown promise for the treatment of secondary hyperparathyroidism in uremia. This case report describes the successful use of doxercalciferol to treat severe secondary hyperparathyroidism in an adult male patient undergoing chronic peritoneal dialysis, with a follow-up period of 9 months. During this period, the patient's hyperparathyroidism was rapidly and easily controlled. Treatment was complicated by a single incident of over suppression of PTH, with concomitant hypercalcemia. This quickly resolved upon temporary discontinuation of doxercalciferol therapy, after which therapy was resumed without further incident.
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ranking = 0.038205370000396
keywords = vitamin
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8/53. Radiographic follow-up of a phalangeal brown tumor.

    We report the 6-year radiographic follow-up of a phalangeal brown tumor in a patient with severe hyperparathyroidism secondary to chronic renal failure treated with hemodialysis. The phalangeal lesion increased in size during the first 3 years, until the patient finally accepted to undergo parathyroidectomy. The initial radiographic change was a small intracortical lytic area. Two years later, an expansile cystic lesion was visible in the phalanx, and computed tomography showed a cortical defect. Ossification of the lesion occurred over the 2.5 years following parathyroidectomy. The epidemiology, radiographic changes and post-treatment evolution of brown tumor in dialysed patients is reviewed. Surgical parathyroidectomy is the standard treatment for brown tumor complicating secondary hyperparathyroidism. The usefulness and limitations of treatment with vitamin D analogs, recently reported in a few case reports, are discussed.
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ranking = 0.019102685000198
keywords = vitamin
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9/53. Decreased cutaneous vitamin D-synthesis in heavily melanized individuals: a rare cause for pathologic fractures of the hip.

    Painful pathological fractures of the femoral neck and the subtrochanteric region of the femur are reported in two women originating from india. After exclusion of renal or intestinal causes, laboratory data on bone metabolism, scintigraphic and radiographic examinations were characteristic for the presence of secondary hyperparathyroidism. Based on vitamin deficiency and low calcium absorption, disturbed mineralization of bone and increased osteoclastic resorption have apparently led to osteomalacia and subsequent fracturing. Fracture localization necessitated surgical fixation in one patient; conservative treatment including protected weightbearing was effective in the other women. After supplementation of calcium and vitamin D3, levels of parathyroid hormone and scintigraphic alterations returned to normal in both patients. In these two cases, pathological fractures of the hip could be attributed to the presence of secondary hyperparathyroidism based on decreased cutaneous vitamin D synthesis.
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ranking = 0.13371879500139
keywords = vitamin
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10/53. Derman necrosis due to thrombosis in severe secondary hyperparathyroidism.

    Two patients had gangrenous dermal necrosis associated with chronic renal disease and secondary hyperparathyroidism. Thromobosed and heavily calcified small arteries were underlying the infarcted areas. One patient had severe hypotension secondary to hemorrhage, which immediately preceded the appearance of dermal lesions. Both patients had notably elevated serum parathyroid hormone and serum alkaline phosphatase levels, as well as severe hyperphosphatemia. Therapy with phosphate binders and calcium and vitamin D supplementation corrected the hyperphosphatemia and reduced serum alkaline phosphatase levels. One patient died; the other patient's dermal lesions healed completely. Localized thrombosis, rather than obliterative intimal proliferation, represents a unique cause of dermal necrosis in this condition.
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ranking = 0.019102685000198
keywords = vitamin
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