No abstract

Search for new informative markers and methods of prognosis prediction glaucomatous optic neuropathy (GON) in primary open-angle glaucoma (POAG) is an urgent task. We have established efficiency surgical treatment of POAG, but the progression of GON is observed in 10–15 % patients. It is known that the main mechanism of GON is apoptotic death retinal ganglion cells, a marker of which is recognized as tumour necrosis factor-α (TNFα), Fas-ligand (FasL) and a soluble form of the Fas-receptor (sFas/APO-1). The aim of the study: to find out the possibility of using apoptosis factors (TNFα, FasL and sFas/APO-1) to predict postoperative progression of GON at POAG. Methods. 69 patients (69 eyes) with POAG stage I–III were examined, who underwent trabeculectomy with implantation of an Ex-Press shunt. In intraocular fluid (IOF) markers of apoptosis was determined by the method enzyme-linked immunosorbent assay. Repeated ophthalmological examination was performed in 1 year. The control group consisted of 25 patients who were operated on about phacoemulsification of cataracts. For statistical and regression analysis used software package GLZ (Statistica 10, StatSoft, Inc. USA) and module of analysis of operational characteristics of regression models – ROC-diagrams (MedCalc 18.9.1, MedCalc Software, Belgium). Results. Multivariate regression analysis showed that the progression of GON determine the content in IOF of TNFα and sFas/Apo-1 before surgery and intraocular pressure after three months. Based on these indicators, it is calculated satisfactory model of GON progression prediction with 95.4 % accuracy. One-factor logistic regression analysis proved the influence of the content of TNFα, FasL and sFas/Apo-1 for the presence or absence of progression of GON during the year after operations: direct dependence took place for TNFα and FasL and inverse – for sFas/Apo-1. The critical limits of the content in the IOF markers are calculated apoptosis, in which the progression of GON is unmistakably predicted during year after surgery. Conclusions. The obtained results prove the significant influence of the studied markers apoptosis on the progression of GON after surgery. Direct pathogenetic influence belongs to TNFα and FasL.

Glaucoma is regarded as a heterogeneous group of diseases with a specific change in biomechanics of the anterior and posterior chambers of the eye, resulting in the increased production and decreased outflow of the aqueous humor. Progressive degeneration of retinal ganglion cells, microglia, astrocytes, Mueller cells leads to chronic damage, thinning of the neuroretinal layer and narrowing of visual field. In this study we investigated primary open-angle glaucoma (POAG). According to many American Optometric Association studies, POAG is the most common type of glaucoma (accounting for up to 72–96 % of cases) characterized by asymptomatic course with gradual decrease in peripheral vision. The reason for this abnormal condition is the optic nerve damage, inefficiency of eye drainage system with fluid accumulation and increased intraocular pressure. Investigation of POAG occurrence and progression becomes more and more relevant each year. Epidemiological studies for the past 50 years showed progressive increase in the incidence of glaucoma. In 5 % of cases, glaucoma is a monogenic disease with Mendelian inheritance. A significant proportion of cases POAG are genetically determined and have a clear hereditary predisposition, which according to various estimates determines from 20 to 60 %. NOS3 gene polymorphism is of considerable scientific interest due to its influence on the development of endothelial dysfunction. Of great scientific interest is determination of the relationship between the rs1799983 and rs2070744 polymorphisms with the development and progression of POAG. Literature review was performed in following database of scientific literature: Web of Science, Google Scholar, PubMed, Scopus etc. Keywords: prevalence of glaucoma, glaucoma epidemiology, gene polymorphism, NOS3 gene, endothelial dysfunction.