Abstract
Purpose: :
In normal tension glaucoma (NTG), glaucomatous optic nerve atrophy occurs without increase of intraocular pressure. Therefore other mechanisms have to be responsible for optic nerve damage in NTG. Hyperhomocysteinemia induces pathologic changes which are similar to that seen in NTG: extra cellular matrix changes, apoptosis of retinal ganglion cells, cell damage due to oxidative stress and hypoxia caused by ocular and systemic vascular dysregulation. Therefore we investigated the hypothesis that homocysteine (Hcy) might be a risk factor in the pathogenesis of NTG.
Methods: :
In order to investigate the role of Hcy in NTG we determined Hcy plasma levels by fluorescence polarization immunoassay in 42 patients with NTG from the Erlangen glaucoma registry and in 42 controls, matched in terms of age, sex, common clinical and lifestyle factors known to influence Hcy levels. In addition plasma levels of vitamin B6 (high-performance liquid chromatographie), vitamin B12 and folate (immunoassay), as major non-genetic determinants of the plasma Hcy level, were measured.
Results: :
No significant difference regarding Hcy levels (NTG:10.95 ± 2.65 µmol/l; controls: 11.29 ± 2.76 µmol/l) (p=0.639) was found. There was also no significant difference in plasma levels of vitamin B6 (NTG: 14.45 ± 12.89 ng/ml; controls: 13.57 ± 10.41 ng/ml) (p=0.629), vitamin B12 (NTG: 387.73 ± 282.04 pg/ml; controls: 423.27 ± 188.85 pg/ml) (p=0.052) and folate (NTG: 9.45 ± 3.42 ng/ml; controls: 10.82 ± 4.48 ng/ml) (p=0.181) between both groups.
Conclusions: :
A major role of Hcy in the pathogenesis of NTG seems unlikely. The detailed pathogenesis of NTG still remains unknown and elusive and warrants further and lager-scale studies. Especially a further investigation of the other intermediate products of the Hcy metabolism may be reasonable.
Clinical Trial: :
www.clinicaltrials.gov NCT00494923
Keywords: clinical (human) or epidemiologic studies: risk factor assessment • clinical laboratory testing