["Vitamin resistant" osteomalacia due to a defect in hepatic hydroxylation of vitamin D; reversible secondary-pseudo-hypoparathyroidism due to calcium administration]. / Ostéomalacie "vitamino-résistante" par défaut d'hydroxylation hépatique de la vitamine D; pseudo-hypoparathyroïdisme secondaire réversible par administration de calcium.

The authors report a case of vitamin resistant osteomalacia in an adult due to an apparently acquired absence of hepatic hydroxylation of vitamin D. This case was also of interest as the osteomalacia caused a state of type II pseudo-hypoparathyroidism which proved reversible on calcium drip. Thus a defect of hepatic hydroxylation of vitamin D may be a cause of vitamin resistant osteomalacia in the adult apart from the forms already described related to defect of renal hydroxylation of vitamin D. Hypocalcemia may be responsible for hypoparathyroidism due to the coexistence of a rise of circulating immuno-reactive PTH and an increase in urinary cyclic AMP. Normalisation of the calcemia permitted in this case, restoral of the efficacy of endogenous PTH.

Reduced bone growth in rats treated with anticonvulsant drugs: a type II pseudohypoparathyroidism?

The effect of anticonvulsant drugs on bone growth and calcium metabolism was studied in Wistar strain rats. Animals were treated for 40-48 days with diphenylhydantoin (DPH) or sodium valproate (SV), or were thyroparathyroidectomized (TPTX) and maintained with thyroxine supplements. Bone growth, measured radiographically as increase in bone length, was reduced by up to 12% in the drug-treated and TPTX groups. Plasma iPTH concentrations were raised twofold- to threefold by DPH and SV. Total plasma calcium was not significantly altered in the DPH-treated rats but was elevated by SV treatment. Similarly, elevated iPTH and normal calcium values were also found in carbamazepine-treated and diazepam-treated rats in a separate experiment. Plasma alkaline phosphatase was reduced by high doses of the drugs. These results imply that anticonvulsant drugs induce end-organ resistance to PTH (a feature of pseudohypoparathyroidism), which may be responsible for some of the skeletal and dental abnormalities found in patients treated with anticonvulsants.