[Tertiary hyperparathyroidism induced by the treatment of hypophosphatemic osteomalacia].
Tertiary hyperparathyroidism developed after a 30-year treatment of low phosphorus osteomalacia with phosphorus supplementation. Parathormone stimulation by exogenous phosphorus would result from sequestration of calcium leading to low plasma levels of both ionized and total calcium. In this case, decreased calcium level was favoured by renal failure. Addition of calcitriol (1.25 hydroxyvitamin D3) to the phosphorus supplementation could avoid secondary hyperparathyroidism in patients with low phosphorus osteomalacia by increasing intestinal absorption of phosphorus and inhibiting, though not totally, parathyroid stimulation. Tertiary hyperparathyroidism is thus a potential complication of long-term phosphorus supplementation in vitamin D-resistant osteomalacia. Parathormone and phosphorus should be measured regularly in order to diagnose induced hyperparathyroidism early since this state is reversible with calcitriol and reduced doses of phosphorus.
Vedere
V
V
Service de Rhumatologie, Hôpital Bretonneau, CHU, Tours.
Goupille
P
P
Valat
J P
JP
Lecomte
P
P
D000328:Adult; D006801:Humans; D006961:Hyperparathyroidism / Q000139:chemically induced*; D008297:Male; D010018:Osteomalacia / Q000097:blood* / Q000188:drug therapy*; D010758:Phosphorus / Q000008:administration & dosage / Q000097:blood* / Q000627:therapeutic use*
D010758:Phosphorus
Hyperparathyroïdie tertiaire induite par le traitement d'une ostéomalacie hypophosphorémique.