Genetic heterogeneity of primary open-angle glaucoma, and
concentration changes of various inflammation and immune response
mediators in the blood, aqueous humor or tissues, indicate the
involvement of different genetic mechanisms and immune system
activity in the pathogenesis of POAG.
The aim of study was to determine the interdependent clinical,
genetic and biochemical findings in POAG-HTG patients.
Distribution of genetic polymorphisms for TNF-α -308 G/A and -
863 C/A in DNA samples was examined using PCR-RFLP, the
concentrations of circulating TNF-α and HSP 70 in a plasma and
concentration of sFas and sFasL in the aqueous humor were measured
by commercial ELISA tests. Their association with quantitative
clinical parameters was examined.
This study included 357 subjects: 81 POAG-HTG, 35 PEXG, 77
with senile cataract and 164 healthy subjects age-sex matched.
Furthermore, 35 samples of aqueous humor of POAG-HTG patients ,
24 PEXG and 29 with senile cataract were treated.
The results showed that serum concentration of TNF-α was
significantly higher in patients with glaucoma. Genotypes GG TNF-α
(-308) and CC TNF-α (-863) were significantly higher in POAGHTG.
No significant association between TNF-α (-308) G/A and
TNF-α (-863) C/A polymorphism and investigated clinical parameters
was found in POAG-HTG. HSP 70 concentration significantly affects
MD, RNFL Avg, Sup and Inf in POAG-HTG patients. There is a
significant negative correlation between Fas concentration and RNFL
Inf, and negative correlation of FasL with MD and RNFL Avg in
POAG-HTG.
The study concluded that serum TNF-α is a powerful cytokine
with potent significant role in the pathogenesis of glaucoma and
glaucoma neuropathy. HSP 70, sFas and sFasL play a role in
pathogenesis of POAG and may be indicators of the development and
progression of glaucoma neuropathy. It has been shown that TNF-α (-
863) A allelic polymorphism has a protective role in the pathogenesis
of POAG
