Pseudohypoparathyroidism: The molecular basis for hormone resistance: A retrospective

The basis for prolactin deficiency in pseudohypoparathyroidism remains unexplained. Although additional patients with pseudohypoparathyroidism and prolactin deficiency have been described, prolactin secretion appears to be normal in many patients with pseudohypoparathyroidism. Furthermore, there appears to be no correlation between prolactin deficiency and G unit deficiency in pseudohypoparathyroidism. This should not be surprising since secretion of prolactin appears to be regulated primarily by changes in intracellular calcium rather than in cyclic AMP concentration. The original suggestion of Carlson et al. that an autoimmune process might account for prolactin deficiency (and other abnormalities) in patients with pseudohypoparathyroidism remains a provocative but unsubstantiated hypothesis. Presumably, future studies of this disorder (and particularly of patients with pseudohypoparathyroidism in whom G unit activity is normal) will provide further insights into the molecular mechanisms of hormone resistance.