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1/16. 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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2/16. calciphylaxis: a rare limb and life threatening cause of ischaemic skin necrosis and ulceration.

    calciphylaxis (uraemic gangrene syndrome) is a rare complication of chronic renal failure and secondary hyperparathyroidism. patients present with painful purple skin lesions which undergo necrosis and ulceration. The histology is specific. There is medial calcification with intimal hyperplasia and thrombosis of the lumen of small sized arteries in the underlying subcutaneous tissue. death frequently arises from overwhelming sepsis. Early recognition of this condition and prompt parathyroidectomy can lead to rapid relief of symptoms and ulcer healing and may be life saving.
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3/16. Spectrum of complications related to secondary hyperparathyroidism in a peritoneal dialysis patient.

    The index patient is a 23-year-old female with end-stage renal disease (ESRD) secondary to chemotherapeutic agents. Continuous cycling peritoneal dialysis (CCPD) has been the renal replacement therapy for the past 5 years since a failed cadaveric renal transplant. Past medical history was significant for diabetes mellitus, hypertension, anemia, bilateral subclavian vein thrombosis with superior vena cava syndrome, secondary hyperparathyroidism, leukemia (at age 8), and hyperlipidemia. On presentation, soft tissue nodules were noted in the anterolateral surfaces of the legs. After 3 months of continued low-calcium-dialysate CCPD, calcitriol, and oral phosphate binders, a 2 x 3 cm nodule was noted on the posterior aspect of the thorax at the scapula. The only complaint at this time was shoulder pain at the acromioclavicular joint. Radiological examination revealed a 3 x 4 cm soft tissue opacity in the superior segment of the left lower lobe laterally. Despite a prior subtotal parathyroidectomy, phosphate binders, and calcitriol, the parathyroid hormone levels continued to increase, with development of tumoral calcinosis, worsening renal osteodystrophy, and calciphylaxis. Computed tomography examination revealed extensive soft tissue calcification consistent with tumoral calcinosis. An ulcerative lesion (1 cm) developed on the lateral aspect of the upper thigh owing to warfarin necrosis versus calciphylaxis. At this time, the phosphate binder was changed from calcium acetate to sevelamer hydrochloride. Aggressive wound treatment and aggressive calcium and phosphate control added to the treatment regimen has resulted in healing of the single ulcer and a decrease in the size of the tumoral lesions. In conclusion, early recognition and aggressive treatment of calciphylaxis can result in reduced morbidity and mortality from calciphylaxis in ESRD patients.
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4/16. 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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5/16. Surgical treatment of mediastinal parathyroid adenoma.

    Ectopic parathyroid adenoma is a frequent cause of persistent or recurrent hyperparathyroidism after parathyroidectomy in patients with chronic renal failure on dialysis. An unusual anatomic localization of parathyroid adenoma may make the diagnosis and surgery difficult. In a 41-year-old woman with chronic renal failure, increased serum level of parathyroid hormone and symptoms of progressive renal osteodystrophy, mediastinal parathyroid adenoma was detected in the aorticopulmonary window by 99m Tc sesta MIBI scintigraphy and transmission computed tomography. Extirpation of adenoma, sized 3 x 2 cm, was performed through a left thoracotomy. serum parathormone level returned to normal and the patient steadily recovered.
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6/16. Successful ultrasonically guided percutaneous ethanol injection for secondary hyperparathyroidism.

    Ultrasonically guided percutaneous ethanol injection to all of four enlarged parathyroid glands, which were confirmed by fine-needle aspiration biopsy, was successfully performed in a hemodialysis patient with secondary hyperparathyroidism. In addition to marked reduction of serum parathyroid hormone, the size of parathyroid glands was significantly decreased after the procedure. As an adverse effect, the patient experienced a transient self-limiting dysphonia due to right recurrent nerve palsy after the first injection. This procedure may be an effective alternative to surgical treatment or administration of high-dose 1,25(OH)2 vitamin D3 in uremic patients with sonographically verified multiple enlarged parathyroid glands.
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7/16. A case of secondary hyperparathyroidism whose high turnover bone improved after the direct injection of acetic acid into the parathyroid glands.

    A 48-year-old male was admitted to our hospital because of increasing knee pain and thigh muscle weakness. He had been undergoing hemodialysis for 15 years. His serum intact PTH value was 1,600 pg/ml with elevated ALP (387 IU/l) and osteocalcin (400 ng/ml). Ultrasound (US) examination disclosed 2 enlarged parathyroid glands. Because of poor cardiac function, an US-guided acetic acid injection into the enlarged parathyroids (percutaneous acetic acid injection therapy; PAIT) was performed. Soon after the PAIT, his arthralgia disappeared. serum PTH fell to 220 pg/ml with the regression of bone marker 1 year following the PAIT. The size of his parathyroid glands dramatically regressed and 1 of the enlarged glands finally disappeared. Repeated bone biopsies following double tetracycline labeling showed a significant improvement from osteitis fibrosa to the mild lesion. This is the first known case report of severe secondary hyperparathyroidism whose PTH and high turnover bone was successfully managed by the direct injection of acetic acid into the parathyroid glands. As long as we pay attention to avoiding recurrent nerve palsy induced by acetic acid, US-guided PAIT may be an alternative to percutaneous ethanol injection therapy (PEIT) or surgical parathyroidectomy (PTx).
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8/16. Hypothesis: the case for quaternary hyperparathyroidism.

    We report the case of a young woman with hyperparathyroidism due to a large parathyroid adenoma associated with severe vitamin d deficiency. The case is noteworthy for the size of the parathyroid adenoma and for the young age at presentation, and is more typical of the presentation of hyperparathyroidism seen in developing countries where the prevalence of vitamin d deficiency is high. Vitamin D is known to have a suppressive effect on parathyroid cell proliferation and parathyroid hormone synthesis. vitamin d deficiency may result in a compensatory increase in the secretion of parathyroid hormone (secondary hyperparathyroidism) which involves hyperplasia of all four parathyroid glands. Secondary hyperparathyroidism can become autonomous and this has been termed tertiary hyperparathyroidism, the underlying pathology of which has been variably described in the literature as adenoma formation or four gland hyperplasia. The pathogenesis of parathyroid adenoma formation in vitamin d deficiency remains unclear. It is possible that a proportion of cases represent the coincidence of primary hyperparathyroidism in patients with vitamin d deficiency. Alternatively, we hypothesise that autonomous four gland hyperplasia or tertiary hyperparathyroidism may progress to adenoma formation and that this should be termed 'quaternary hyperparathyroidism'.
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9/16. infarction of mediastinal parathyroid gland causing spontaneous remission of secondary hyperparathyroidism.

    Secondary hyperparathyroidism is a serious complication in long-term hemodialysis patients. The authors report on 2 patients on long-term hemodialysis who suffered from persistent secondary hyperparathyroidism due to missed mediastinal parathyroid gland after total parathyroidectomy with forearm autograft. reoperation was planned. In both cases, severe hypocalcemia suddenly developed; serum parathyroid hormone (PTH) level decreased markedly after this episode. The serum calcium level increased gradually in response to administration of vitamin D and calcium carbonate, but serum PTH level remained low. A follow-up computed tomography scan showed that the formerly enlarged mediastinal parathyroid gland was markedly reduced in size. Moreover, a hot spot formerly detected by technetium 99m-MIBI (methoxy-isobutyl-isonitrile) scintigraphy in the mediastinum disappeared after this episode. The authors considered that necrosis of the enlarged ectopic parathyroid gland, probably due to infarction, resulted in hypocalcemia. To the authors' knowledge, this is the first case report of spontaneous mediastinal parathyroid autoinfarction after parathyroidectomy in hemodialysis patients.
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10/16. Brown tumor of the mandible associated with secondary hyperparathyroidism: a case report and review of the literature.

    Brown tumors are rare lesions that can develop in persistent cases of hyperparathyroidism (HPT). Therefore, identification of these lesions by diagnostic imaging is important during the follow-up of patients with HPT. This report describes a 45-year-old woman who developed HPT-induced brown tumors that appeared initially as an oral lesion. The diagnosis, treatment, and control of the disease--as well as the histopathological characteristics--are emphasized.
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