The pathogenetic role of 1,25-dihydroxycholecalciferol (1,25-DHCC) deficiency in hypoparathyroidism (HP) will be evaluated. By measurement of serum PTH and urinary cyclic AMP and electrolyte responses to PTH infusion, patients with HP will be divided into hormone-deficient, hormone-ineffective and hormone-resistant groups. In each case, a search will be made for deficiency of 1,25-DHCC by circadian measurements. To determine the cause of 1,25-DHCC deficiency in each group, an attempt will be made to stimulate production of this metabolite by intramuscular PTH injections or by lowering serum phosphate with antacids. One may hypothesize that in hormone-deficient or hormone-ineffective HP, decreased synthesis of 1,25-DHCC may be explained by the absence of these two recognized stimuli, whereas synthesis of 1,25 DHCC may be "primarily" deranged in hormone-resistant HP. Only in the first instance would provision of either one of these stimuli be expected to restore 1,25-DHCC to normal levels.