Registered on ClinicalTrials
VLASOVA A.S. 1.4*, MALISHEVSKAYA T.N. 2*, PETROV S.A.1.3*, GUBIN D.G. 5*, PETROV S.YU. 2*, FILIPPOVA Yu.E. 1*
1* West Siberian Institute of Postgraduate Medical Education, Tyumen, Russia;
2* Helmholtz National Medical Research Center of Eye Diseases, Moscow, Russia;
3* Tyumen Scientific Center of the Siberian Branch of the Russian Academy of Sciences, Tyumen, Russia;
4* Regional Ophthalmological Dispensary, Tyumen, Russia;
5* Tyumen State Medical University, Tyumen, Russia
Place of publication:
VESTNIK OPHTHALMOLOGII, 2024, Vol. 140, No. 4
Abstract:
Many key aspects of retinal ganglion cell (RGC) neurodegeneration in glaucoma focus on mitochondrial dysfunction. Understanding the mechanisms and relationships between structural and functional changes in mitochondria would be useful for developing mitochondria-based therapeutic strategies to protect RGCs from glaucomatous neurodegeneration. Study Objective: To determine the severity of mitochondrial dysfunction in patients with primary open-angle glaucoma (POAG) and to evaluate the possibility of stabilizing the glaucomatous process by improving mitochondrial functional activity and their energy-producing function during therapy with Mexidol and Mexidol FORTE 250. Material and Methods: The study included 80 patients with advanced POAG with compensated intraocular pressure and 20 healthy volunteers. The severity of mitochondrial dysfunction was determined by the activity level of mitochondrial enzymes: succinate dehydrogenase (SDH) and α-glycerophosphate dehydrogenase (α-GPDH) in peripheral blood lymphocytes during cytochemical examination and cytomorphodensitometry. Patients of the main group received sequential therapy with Mexidol according to the following regimen: Mexidol solution for intravenous and intramuscular administration 50 mg/ml, 300 mg per day intramuscularly once a day for 14 days, followed by Mexidol FORTE 250 tablets, 1 tablet 3 times a day for 56 days. Stabilization of glaucomatous optic neuropathy during treatment was assessed using a set of perimetric, electrophysiological, structural and topographic methods at 14, 56 and 90 days. Results. During sequential therapy, patients in the study group showed a significant increase in mitochondrial enzyme activity compared to baseline after 14 and 56 days, with a gradual regression by the end of the observation period (after 90 days). This increase was accompanied by an increase in the number of mitochondria and an increase in their optical density during cytomorphodensitometry. Improvement in mitochondrial enzyme activity after 14 and 56 days was accompanied by positive dynamics in the structural and functional parameters of the retina, as measured by static perimetry, optical coherence tomography, and a set of electrophysiological studies. Conclusion. The obtained data can be used to optimize POAG therapy by reducing mitochondrial dysfunction and stabilizing glaucomatous optic neuropathy. Key words: primary open-angle glaucoma, mitochondrial dysfunction, succinate dehydrogenase, α-glycerophosphate dehydrogenase, cytomorphodensitometry, Mexidol.
