Types include: ;Type 1a (OMIM ) : Has a characteristic phenotypic appearance (Albright's hereditary osteodystrophy), including short fourth and fifth metacarpals and a rounded facies. It is most likely an autosomal dominant disorder. It is also associated with thyroid stimulating hormone resistance. Caused by GNAS1 mutation. ; Type 1b (OMIM ) : Lacks the physical appearance of type 1a, but is biochemically similar. It is associated with a methylation defect in the A/B exon of GNAS1, caused by STX16 disruption. ; Type 2 (OMIM ) : Also lacks the physical appearance of type 1a. Since the genetic defect in type 2 is further down the signalling pathway than in type 1, there is a normal cAMP response to PTH stimulation despite the inherent abnormality in calcium regulation. The specific gene is not identified. While biochemically similar, type 1 and 2 disease may be distinguished by the differing urinary excretion of cyclic AMP in response to exogenous PTH. Some sources also refer to a "type 1c" (OMIM ). The phenotype is the same as in type 1a, but red blood cells show normal Gs activity. As it is also caused by a GNAS mutation, it is not clear whether it should be considered an entity separate from Ia.
causes of Hyperphosphatemia
causes of Hypercalcaemia
causes of Chronic kidney disease
causes of Nephrotic syndrome
causes of Osteitis fibrosa cystica
risks of Peritonitis
complications of Hypophosphatemia
medical cause of Hyperphosphatemia