Parathyroid hormone and calcium metabolism in generalized scleroderma. Increased PTH level and secondary hyperparathyroidism in patients with aberrant calcifications. Prophylactic treatment of calcinosis

Parathyroid hormone (PTH) in serum and biochemical parameters of calcium metabolism were analysed in 45 patients with systemic sclerosis. Calcification of the skin and subcutaneous tissue was assessed by X-ray examination of the hands. Analyses disclosed secondary hyperparathyroidism (increased PTH in serum, low calcium 'ion' in serum, decreased urinary excretion of calcium and phosphate), in particular in patients with calcinosis (P less than 0.05) as compared to those with no calcinosis. The duration of systemic sclerosis was longer in patients with calcinosis (P less than 0.05). The calcinosis type of systemic sclerosis is characterized by secondary hyperparathyroidism developed during the progression of the disease. A hypothesis is made regarding calcium metabolism in the early no-calcinosis (with increased synthesis of Vitamin D) and late calcinosis types. PTH may stimulate aberrant calcification. The hypothesis implicates that prophylactic treatment with Vitamin D in low dose may prevent calcinosis.