SAT-803 - Calcinosis Cutis as A Rare Presentation of Primary Hyperparathyroidism

Introduction
Calcinosis cutis is characterized by calcium deposition in the skin and subcutaneous tissue and typically occurs in autoimmune or renal disease. Metabolic causes are rare. We describe a patient who developed calcinosis cutis due to primary hyperparathyroidism, an unusual presentation.

Case description
We present the case of a 54-year-old female patient with a past medical history of hypertension, hyperlipidemia, and orbital glioma treated with surgical resection and radiation therapy. She was diagnosed with primary hyperparathyroidism in 2019 after laboratory tests revealed persistent hypercalcemia and elevated parathyroid hormone (PTH) levels. Since her diagnosis, she had been under yearly surveillance without indication for parathyroid surgery. She had discontinued thiazide diuretics at the time, and was not taking lithium, calcium or vitamin A supplements. She had no history of nephrolithiasis, and bone density testing showed osteopenia.

In early 2024, she developed firm, white, nodular skin lesions on her forehead and cheeks. A dermatologic biopsy confirmed calcinosis cutis. Rheumatology evaluated the patient for autoimmune causes; clinical examination and review of systems were unremarkable. Autoimmune serologies for systemic sclerosis, antiphospholipid syndrome, and other connective tissue diseases were negative. Renal function was unremarkable.

Given her long-standing hyperparathyroidism and negative autoimmune workup, metastatic calcinosis cutis secondary to metabolic disturbance was suspected. Nuclear medicine parathyroid imaging showed a mild focus of increased uptake inferior to the right lower thyroid pole, consistent with a parathyroid adenoma or hyperplasia. She subsequently underwent parathyroidectomy, after which postoperative laboratory testing demonstrated normalization of both PTH and calcium levels.

Conclusion
Metastatic calcinosis due to primary hyperparathyroidism is a rare but important diagnosis to recognize. In this case, the absence of autoimmune markers and the presence of longstanding hyperparathyroidism support a metabolic cause. Hypercalcemia increases the calcium-phosphate product, promoting soft tissue calcification. Early diagnosis and parathyroidectomy are crucial to prevent progression and potential complications. This case underscores the need to consider metabolic etiologies in patients with calcinosis cutis and negative autoimmune workup.

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