The dissertation is dedicated to solving the current task of modern ophthalmology - by studying the condition of the perilimbal tissues of the eye and biochemical blood markers (LOX1, TGFb2 and pNF-H) during the surgical treatment of patients with primary open-angle glaucoma, to determine the risk factor for the development of intraocular pressure decompensation and to optimize the diagnosis of the progression of glaucomatous optic neuropathy after surgical antiglaucoma intervention.
Justification of the choice of research topic. Glaucoma is the main cause of irreversible blindness both worldwide and in Ukraine. It is the second leading cause of blindness worldwide after cataracts, and blindness caused by glaucoma is usually irreversible. According to WHO estimates, 57.5 million people worldwide have primary open-angle glaucoma (POAG), and this number is expected to reach 111.8 million by 2040 (Allison K. et al., 2020; Ricca A. et al., 2020).
Unfortunately, over the past five years, glaucoma has been the leading cause of visual impairment in Ukraine. This negative situation is due to the asymptomatic course of the subclinical and initial stages of the disease and a number of medical and social factors. Primary open-angle glaucoma is the most common type both in the United States of America and in Ukraine (Weinreb R.N. et al., 2016; Rykov S.O. et al., 2019). Primary open-angle glaucoma is a multifactorial chronic neurodegenerative disease characterized by the acquired loss of retinal ganglion cells and subsequent optic nerve atrophy (Serdyuk V.M. et al., 2021). Although the pathogenesis of glaucoma is not fully understood, it is known that the level of intraocular pressure (IOP) is interrelated with the death of retinal ganglion cells (Burton M. J. et al., 2024). Neither significant successes in the surgical treatment of glaucoma, nor the development of new minimally invasive surgical interventions and a significant expansion of the arsenal of medicinal hypotensive agents can stop its constant progress (Rolim-de-Moura C.R. et al., 2022; Bezditko P.A. et al., 2022; Shargorodska I.V., 2003).
The gradual accumulation of data from the world and domestic literature indicates that in patients with POAG, the cellularity of the trabecular meshwork (TM) is reduced, which leads to a decrease in the physiological function of the TM tissue (Keller K.E. et al., 2022; Zavgorodnia N.G., 2022; Tsybulska T.E., 2021). Dysfunction and blockage of this main pathway can lead to increased outflow resistance, increased IOP and, ultimately, to the development of glaucoma (Dietze J, et al., 2024). Previous studies indicate that it is the area of the inner wall of Schlemm's canal in combination with the juxtacanal tissue that is the main site of outflow resistance (Buffault J. et al., 2020; Vit V.V., 2018). Analysis of the literature of recent years indicates that the number of necessary reoperations in glaucoma patients is about 50% (Jia et al., 2022; Ul’yanova N.A. et al., 2019). However, to date, the pathogenetic mechanisms leading to canal overgrowth have not been fully elucidated, and the development and implementation of modern devices (valves) does not solve the problem. The relationship between changes in the state of perilimbal tissues of the eye and failures of surgical antiglaucoma treatment of patients with POAG remains poorly studied to date.
World literature data indicate that increased IOP is the result of cellular and molecular changes in the TM, which are caused by an increase in the level of transforming growth factor (TGF), in particular TGFb2 in the aqueous humor. The expression of which is increased in the TM of patients with POAG, which increases the contractile ability of TM cells, promotes the formation of actin stress fibers, which increases the resistance to fluid outflow and thereby leads to an increase in IOP in the eyes after surgical interventions (Yemanyi F. et al., 2020; Vit V.V., 2018).
Previous studies indicate that another important factor that may affect the strength and elasticity of the TM is lysyl oxidase-1 (LOX1), a major component of fibrillar aggregates of the extracellular matrix (ECM), which is involved in tissue fibrogenesis in glaucoma patients who have undergone anti-glaucomatous surgery (Wagner I. et al., 2022).
