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Calciphylaxis is characterized by progressive cutaneous necrosis associated with small- and medium­sized vessel calcification occurring in the setting of end-stage renal disease, diabetes mellitus, and hyperparathyroidism. Cutaneous involvement presents as initial painful geographic areas of ischemia that Progress to gangrene and ulceration of the subcutaneous fat, dermis, and epidermis; secondary infection and sepsis are common.


The pathogenesis is poorly understood. In animal models, calciphylaxis is described as a condition of induced systemic hypersensitivity in which tissues respond to appropriate challenging agents with calcium deposition. Calciphylaxis is associated with chronic renal failure, secondary hyperparathyroidism, and an elevated calcium phosphate end product. Implicated "challenging agents" include glucocorticoids, albumin infusions, intramuscular tobramycin, iron dextran complex, calcium heparinate, immunosuppressive agents, and vitamin D.


Patients usually experience unbearable pain, burning and sometimes itching at the lesion sites.

Calciphylaxis most often occurs on the lower limb especially in fatty areas. Lesions on the trunk, abdomen, buttocks or thighs, appear to be more dangerous than lesions on the lower legs and feet.

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