In the present study, there was a significant increase in IOP and AL of the eyeball in patients with PXE than controls and no significant differences were found in LT, ACD, and CC.
Hepsen et al., in a study, proved that CC is steeper in eyes with PXE as compared to normal eyes,  but in the present study, there was no significant change in CC.
PXE (synonym Gronblad-Strandberg syndrome) is a rare, inherited multisystem disorder primarily affecting the skin, eyes, and cardiovascular system.3 It is characterized by progressive calcification and degeneration of elastic fibres.
Recent molecular genetic studies show evidence for a recessive inheritance pattern only.8 PXE has no particular racial patient predilection.
PXE shows an autosomal recessive inheritance pattern.
PXE is a multisystemic disorder involving the skin, cardiovascular system and eyes characterized by fragmentation and calcification of elastic fibrils.
Cultured dermal fibroblasts from PXE patients show signs of chronic oxidative stress in vitro (17).
In the PXE patients, earlier disease onset was observed for homozygous carriers of this allele.
The association of each polymorphism with PXE was measured by the odds ratio (OR) and 95% CI.
Comparison of the allelic frequencies of the detected SPP1 promoter polymorphisms between PXE patients and healthy controls revealed the 4 variants c.-1748A>G, c.-155_156insG, c.-66T>G, and c.244 245insTG to be significantly more frequent in the PXE group (P <0.05 each) (Table 2).
PXE is histologically characterized by progressive calcification of elastic fibers and massive accumulation of proteoglycans in the extracellular matrix (24-26).
Although most PXE patients, as well as the ABCC6-deficient mice, have been shown to have serum calcium and phosphate concentrations within the reference intervals, the authors of several case reports observed important alterations to serum calcium and phosphate in patients with PXE (4, 27, 29, 33).