Purpose: to study the concentration of vascular endothelial growth factor (VEGF A) in the tear fluid (TF) of patients with primary open-angle glaucoma after non-penetrating deep sclerectomy (NPDS) at different stages of the perioperative period and to perform immunohistochemical identification of the lymphatic structures of filtering blebs in groups differing in the hypotensive effect of the surgery.Material and methods. 12 months after surgery, POAG patients were divided into 2 groups. Group 1 was composed of patients who experienced a hypotensive effect after NPDS (n = 23; mean age 63.7 ± 4.4 years), while group 2 had no such effect of NPDS (n = 21, mean age 64.3 ± 3.9 years). The concentration of VEGF A (121 and 165) in TF was determined by ELISA method (VEGF-ELISA-Best, Vector Best, Russia). Immunohistochemical examination of conjunctival and subconjunctival tissue samples was performed 12 to 18 months after NPDS in 12 POAG patients and 8 patients aged 62.36 ± 6,31 with no glaucoma, which served as a control group.Results. Significant differences in the concentration of VEGF A (121 and 165) in TF were found in two groups 2 weeks and 2 months after the surgery. Excessive scarring of filtering blebs was accompanied by an initially low level of VEGF A, its moderate increase 2 weeks after surgery and significant suppression 2 months after surgery, which was significantly different from group 1 (a twofold VEGF A increase has been established toward the second month after surgery). From 5 to 7 vessels with lymphatic character were found in tissue samples of group 1. Podoplanin was found in individual cells and sphere-like formations, which may represent reduced lymphatic vessels.Conclusion. The study showed an important role of VEGF A in conjunctival lymphangiogenesis. Suppression of conjunctival lymphangiogenesis and subsequent “hypotensive failure” of glaucoma surgery in some patients who underwent anti-inflammatory and antifibrosis therapy requires optimization, the development of new treatment methods aimed at activating prolymphangiogenic factors.
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