For end stage renal failure patients secondary hyperparathyr

For end-stage renal failure patients, secondary hyperparathyroidism followed by hyperphosphatemia is not uncommon. According to the 2012 United States Renal Data System Annual Data Report, the prevalence of ESRD patients in Taiwan is highest in the world, at 2584 per million population. Additionally, improving dialysis care quality and National Health Insurance coverage has led to better survival rates for these patients. Hence, although the incidence of TC in this patient cohort is still unclear, surgeons should be aware of potentially increasing presentations of this disease, and become familiar with the pathogenesis and treatments associated. Due to the benign presentation of the mass, TC is often misdiagnosed by inexperienced surgeons, resulting in incomplete excision and disease recurrence. Pathogenically, TC is a result of two concurrent events: (1) trauma that initiates a multistepped reaction to injury in soft tissues and skin; and (2) a multifactorial elevation of the serum calcium phosphate product principally caused by hyperphosphatemia. The pathologic lesion is specific, exhibiting features distinguishable from other calcifying entities, but is similar pathologically for all three TC types. In general, pathology characteristics demonstrate a foreign body granulomatous reaction with infiltrations by giant hcv protease inhibitor and lymphocytes. This response is inaugurated by histiocytes and their derivatives, synovial intimal cells and dysmorphic osteoclasts. The histiocytes aggregate, phagocytize lipids, and undergo necrosis, while, concurrently, a complex calcifying process occurs. Treatments for TC include surgery, phosphate deprivation, or a combination of both. Surgery is recommended for patients with functional impairment, pain, or skin erosion. Complete excision is effective for early primary normophosphatemic TC, and has a low recurrence rate. However, the recurrence rates are higher for the other two types, and are an important concern for the surgeon for proper surgical management. In addition, recurrent masses are more likely to be progressive, particularly for incompletely excised lesions. In cases that require wide excision resulting in large tissue defects, flaps or other reconstructive measures may become necessary. For the present case, the large mass with skin breakage resulted in local pain and severe functional impairment, requiring reconstruction with gluteal maximus rotational flap after excision. To our knowledge, TC cases requiring the use of flaps to cover the defect are rarely report in the literature. Medically, phosphate lowering interventions are also important in the management of TC in ESRD or patients with chronic renal failure, because calcium and phosphorus metabolism abnormalities are common in this cohort. Methods to decrease phosphate concentration include a low calcium and phosphate diet plus use of phosphate binding antacid, e.g., aluminum/magnesium hydroxide. Other methods such as large oral doses of calcium or vitamin D sterols may aggravate hypercalcemia and hyperphosphatemia, and can be unsuitable for patients with calcifying lesions. Parathyroidectomy to control hypercalcemia and hyperphosphatemia may also be performed, with reports of TC regression after subtotal parathyroidectomy, although this procedure may be controversial. For our case, due to the occurrence of skin breakage and large size of the tumor, primary excision was performed with local reconstruction, and the patient refused further intervention on the parathyroid glands. Otherwise, complete resolution of the lesion has been reported through medical management alone. For TC secondary to ESRD, complete resolution also has been reported after renal transplantation. Currently the most effective treatment is believed to be a combination of surgical excision and medical management, including phosphate deprivation therapy or long-term use of acetazolamide. Therefore, our patient was treated with surgical management due to the size and interference with common daily activities of the TC lesion, and further management with phosphate-binding antacid and consultation with her nephrologist.