- Belgrade '18
- Vienna '18
- ESCRS Player
- On Demand
- ESCRS YO's
First Author: A.Kirienko RUSSIA
Co Author(s): E. Markelova
Back to previous
To carry out extended research of a local cytokine profile in case of primary open-angle glaucoma.
State budget educational institution of higher professional education Pacific state medical university, Vladivostok city, Russia
Patients with primary open-angle glaucoma (POAG) of I-III stages (72 persons) have been surveyed, where 46 persons had I-II stages, 26 persons had III stage, together with almost healthy people of control group (30 persons) at the age of 30-70 years. Definition of cytokines (IL-1 ?, IL-6, IL-17, IL-2, IL-4, TGF?1, TGF?2, TGF?3) has been made by the ELISA method with application of specific reagents R&D Diagnostics Inc. (USA). For definition of reliability of distinctions nonparametric statistics was used (Mann-Whitney-Wilcoxon test, ?2).
It was found that the content of IL-1 ?, IL-2, IL-4, TGF?1 and TGF?3 in the general group of patients with POAG did not differ from values in control group. Statistically significant (? <0,01-0,05) augmentation of IL-6, IL-17, TGF?2 quantity in the lacrimal fluid of patients with POAG was defined. After allocation of the surveyed depending on POAG stage, certain laws were revealed. On early (I-II) glaucoma stages augmentation of IL-1 ?, IL-17 was revealed. Patients with a far gone stage of glaucoma were found an increase in both proinflammatory (IL-1 ?, IL-6), and anti-inflammatory (IL-4, TGF?2) cytokines. At the same time, deficiency of TGF?1 and TGF?3 was revealed at III stage of POAG. Level of IL-2 was within norm for the patients of all groups.
Increase of mainly proinflammatory cytokines (IL-1 ?, IL-6, IL-17) and TGF?2 in tears at POAG was revealed. Augmentation IL-17 for more than 11,44 pg/ml (?2=5,32 I st. of freedom, ? <0,0001) reflects involving of cellular mechanisms in glaucomatic pathogeny and can serve as an additional marker of an early stage of POAG Intensity of glaucomatic process is linked with: deficiency of local production of TGF?1 (?2=3,9 at I st. of freedom, ? <0,04), TGF?3 (?2=3,21 at I st. of freedom, ?=0,046) and local hyperproduction of TGF?2 (?2=5,32 at I st. of freedom, ? <0,0001). It shows infringement of protective inhibiting influences of TGF?, directed on control of proinflammatory hyperergoc reactions for patients with POAG.