Sporadic PHP-Ib cases typically differ from familial PHP-Ib cases in the nature of the GNAS epigenetic defects they exhibit, yet evaluation of many cases with these PHP forms indicates that the divergence in the epigenetic features do not directly translate into differences in clinical presentation. The age of onset and the severity of hypocalcemia and hyperphosphatemia that result from PTH resistance appear to be similar in sporadic and familial cases [62]. As explained above, Gsα expression is also predominantly maternal in the pituitary somatotrophs [43]; however, growth hormone deficiency and short stature are not typical clinical features of PHP-Ib. It is possible that the epigenetic defects do not affect Gsα expression in this tissue, thereby allowing unimpaired GHRH signaling. This could suggest that the mechanisms underlying Gsα imprinting are different between the pituitary and the proximal tubule. Alternatively, GHRH resistance may be present in patients with PHP-Ib, but it may be too mild to become clinically manifest. This is similar to the TSH resistance in PHP-Ib, which can be absent in many PHP-Ib patients, is milder than in PHP-Ia, and
