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Healing of skin necrosis and regression of anticardiolipin antibodies achieved by parathyroidectomy in a dialyzed woman with calcific uremic arteriolopathy.

AIM
To present the impact of parathyroidectomy on the spontaneous healing of necrotic lesions of the skin of the lower leg and on anticardiolipin antibodies regression in a 68-year-old female dialyzed patient with hyperparathyroidism and calcific-uremic arteriolopathy (CUA).


METHODS
After the occurrence of initial lesions of the lower leg skin, the intact parathyroid (iPTH) level, calcium (Ca) and phosphorus (P) product were measured, and on two occasions at 6-week intervals, the titer of anticardiolipin antibodies was determined, followed by a clinical monitoring of the progress of necrotic skin lesions. Two months after the occurrence of the skin lesions, the patient's right leg was amputated below the knee due to gangrene, and a histopathological analysis of the skin tissue sample of the amputated lower leg was made. After parathyroidectomy, iPTH, Ca x P product were measured, and on two occasions at 6 weeks' intervals, anticardiolipin antibodies titer was determined, followed by a clinical monitoring of lesions of the left lower leg skin.


RESULTS
Before parathyroidectomy, iPTH level and Ca x P product were increased, as well as IgG anticardiolipin antibody titer measured on two occasions 6 weeks apart. The histopathological analysis of the skin tissue sample of the amputated right lower leg showed mural calcification of artery walls and thrombotic occlusions of small arteries, arterioles, and dermal capillaries, in addition to epidermolysis. A week after parathyroidectomy, iPTH level and Ca x P product were within normal range. Two measurements 6 weeks apart revealed no anticardiolipin antibodies. Eight weeks after parathyroidectomy, spontaneous healing of necrotic skin lesions of the left lower leg was observed.


CONCLUSION
Regression of anticardiolipin antibodies, normalization of Ca x P product, and healing of the skin lesions after parathyroidectomy all pointed to the elevated PTH level as a crucial factor in the pathogenesis of CUA.