The dissertation is dedicated to the study of the pathogenesis of diabetic retinopathy combined with metabolic syndrome and the identification of the pathogenetic role of cellular and humoral immunity.
The research tasks included determining hormonal, lipid, carbohydrate spectrum parameters in serum, cellular and humoral immunity indicators, inflammation markers, and studying cytokine dysfunction, as well as exploring correlation links between the studied parameters in diabetic retinopathy in the context of metabolic syndrome.
The object of the study was metabolic and immune disorders in patients with diabetic retinopathy in the context of metabolic syndrome.
The subject of the study is markers of lipid and carbohydrate metabolism disorders, systemic inflammation, immune status in diabetic retinopathy in the context of metabolic syndrome, and the interrelation between the investigated parameters.
Methods employed: biochemical, immunoassay, immunological, statistical.
For the examination, 130 patients were selected from the Ophthalmology Department of Lviv Regional Clinical Hospital and the Transfusion Department at LKLSMD from 2019 to 2020. Patients were selected based on clinical data, aged 35-65 years (mean age 46.0 ± 2.0 years), with a gender ratio of men/women = 1/1. Among them, 70 patients had verified diabetic retinopathy, decompensated type II diabetes, in the context of metabolic syndrome - Group 1, while the other 60 patients had verified diabetic retinopathy, compensated type II diabetes, in the context of metabolic syndrome - Group 2. The obtained laboratory parameters were compared with a control group consisting of 40 practically healthy individuals of both genders aged 35 to 65 years without comorbidities, who were donors at the Transfusion Department of the Municipal Clinical Emergency Hospital in Lviv.
Comprehensive changes in hematological and immune status parameters were identified. In the group of insulin-independent patients, a statistically significant increase in eosinophil levels was observed compared to the normal range and the level in the insulin-dependent group (5.5±0.2% vs. 3.2±0.2% and 2.7±0.1%, respectively). The absolute lymphocyte count (ALC) in insulin-independent patients exceeded the normal level by 1.4 times and was lower by 1.5 times compared to the level in insulin-dependent patients (p<0.05). The absolute neutrophil count (ANC) in insulin-independent patients was 1.6 times lower than in the insulin-dependent group (p<0.05). The absolute monocyte count (AMC) in the insulin-independent group was 1.6 times lower than in the insulin-dependent group (p<0.05).
In the insulin-dependent patient group, activation of T-lymphocytes (CD3+) was observed (1.3 times higher than in the control group). The level of T-helper cells in both groups of patients was 1.2 times lower than the normal range. The content of T-suppressor cells in patients with compensated diabetes was 1.5 times higher than normal and 1.3 times lower than in the insulin-dependent patient group. The level of activated T-lymphocytes in both groups of patients exceeded the control group by 2.8 times. The absolute number of B-lymphocytes in the insulin-independent patient group was 1.5 times higher than the control group and 1.2 times lower than the insulin-dependent patient group. The content of activated B-lymphocytes in the insulin-independent patient group was 2.8 times higher than the normal level and 1.5 times lower than in the insulin-dependent patient group. The level of NK cells in patients with compensated type II diabetes exceeded the normal range by threefold and was 1.5 times lower than in the group of patients with decompensated type II diabetes.
