Abstract
The problem with PHP is that it is almost certainly a heterogeneous condition encompassing a number of defects within the PTH receptor-adenylate cyclase complex. The clinical manifestations of PTH resistance are amplified and extended by a number of associated abnormalities. These include a low intracellular calcium concentration, secondary hyperparathyroidism, reduced production of 1,25-(OH)2D and perhaps the secretion of an abnormal PTH peptide. Almost every aspect of PTH function seems involved and this makes PHP a fascinating condition in which to test current views of the role of PTH in the integration of the calcium homoeostatic system.
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