Abstract

Diabetic retinopathy (DR) is the most significant and common cause of visual impairment in diabetes patients. The aim of the study was to enhance the understanding of the pathogenesis of DR associated with metabolic syndrome (MS) and elucidate the role of cellular and humoral immunity factors. The study included 130 patients. Group 1 comprised 70 patients diagnosed with DR and insulin-dependent type 2 diabetes against the background of MS. Group 2 included 60 patients diagnosed with DR and non-insulin-dependent type 2 diabetes associated with MS. The immunological analysis focused on evaluating subpopulations of blood lymphocytes using flow cytometry; systemic inflammation markers, such as CRP, specific IgA, IgM, and IgG, cytokines measured by ELISA. Significant changes in immune status were observed in patients with DR associated with MS, depending on diabetes compensation. In Group 1 patients with DR, more pronounced alterations in the T-cell immunity pathway were observed, including T-cell immunodeficiency accompanied by the activation of killer and B-cell immunity, compared to non-insulin-dependent patients. Both groups exhibited type IV hypersensitivity reactions. Elevated CRP level was detected only in insulin-dependent patients with DR. An analysis of the immune parameters indicated predominant activation of the specific humoral immunity pathway, suggesting chronicity of the condition. Non-insulin-dependent patients showed significant activation of mucosal humoral defenses and early humoral protective mechanisms. The data revealed more pronounced changes in specific humoral immunity markers, such as immunoglobulins, compared to systemic inflammation markers like CRP.

Abstract

A dangerous combination of two diseases that have reached pandemic proportions, COVID-19 and type 2 diabetes, have unique features of the comorbid course. Intense inflammation, hypercoagulation, dysglycemia, and immune and renal dysfunction are underlying processes in the pathogenesis of the combination of these diseases. Our study aimed to compare groups of hospitalized patients with moderate to severe coronavirus disease with and without diabetes, paying particular attention to renal function and examining the relationships between markers of renal dysfunction, inflammation, and thrombosis in these patient groups. In total, 79 patients aged 24 to 73 with moderate to severe coronavirus disease were examined. Patients were divided into 2 groups: 1st – without diabetes; 2nd – with diabetes. The clinical picture, laboratory results (additionally determined cystatin C level) and instrumental studies were compared. Correlation analysis was conducted in groups. The group of patients with type 2 diabetes mellitus had significantly lower oxygen saturation upon admission to the hospital. A significantly higher concentration of glucose in blood serum (11.3 (8.1; 16.5) mmol/l 5.2 (4.4; 6.6) mmol/l, P<0.01) and a lower creatinine level (106.0 (87.3; 123.0) mcmol/l vs. 129.5 (104.8; 167.3) mcmol/l, P<0.05) were observed in the 2nd group while there were no differences in urea and cystatin C levels. By means of correlation matrices, it was established that inflammation, hypercoagulation, dysglycemia, and impaired kidney function are underlying causes of the coronavirus disease pathogenesis in group 1 of patients. At the same time, inflammation and hypercoagulation are the causes in the group of patients with a combined course of type 2 diabetes mellitus. Although the combined course of coronavirus disease and type 2 diabetes mellitus is prognostically more severe, we found a significantly lower creatinine level in the group of patients with type 2 diabetes.

Abstract

УДК 616.12-005.4:616-008.9+616-056.5+616.379.-008.64+616.12-008.331.1-092:612.15]-074

For many years, and to this day, cardiovascular disease has been and remains the leading cause of death worldwide. Cardiovascular diseases mainly affect people in countries with middle and low living standards.

The aim of the study was to find out the peculiarities of lipid, carbohydrate, and hormonal changes in patients with coronary heart disease against the background of metabolic syndrome.

Materials and methods: 120 patients with verified coronary heart disease were examined, including 60 patients with coronary heart disease without metabolic syndrome and 60 patients with coronary heart disease with metabolic syndrome. The control group consisted of 30 practically healthy individuals of appropriate age and sex. The content of HbA1c, glucositol C-peptide, triacylglycerols, total cholesterol, leptin, HDL-cholesterol, and LDL-cholesterol in blood serum was determined by modern methods.

Results: The analysis of the results of laboratory tests of patients' blood revealed more pronounced changes in carbohydrate and lipid metabolism in patients with coronary artery disease against the background of metabolic syndrome, which indicates the severity of the clinical course in such patients. The results obtained indicate that in coronary heart disease with metabolic syndrome, there are more pronounced dysmetabolic changes: hyperleptinemia, glucosemia, elevated HbA1c, and decreased C-peptide content. Studies have shown that obesity is accompanied by high levels of leptin, which exacerbates insulin resistance and is a trigger for the development of coronary heart disease.

Conclusions: 1. Leptin resistance is a potential cause of insulin resistance and, consequently, obesity, which ultimately leads to metabolic syndrome and the development of coronary heart disease. The data obtained indicate a greater tendency to obesity in women with coronary heart disease complicated by metabolic syndrome.

1. The data obtained may indicate a latent disorder of carbohydrate metabolism in patients with coronary artery disease without metabolic syndrome.
2. The detected deviations in lipid metabolism indicate the presence of type II dyslipoproteinemia in patients of group 1 and type IV dyslipoproteinemia in patients of group 2.

УДК 616.153.96:616.155.394-097.37:618.19-002]-074

Вступ. Сприятливими факторами для розвитку запального процесу в молочній залозі є лактостаз, наявність патогенної флори, а також зниження імунобіологічної реактивності організму жінки. Запальний процес спричиняє і регулює низка медіаторів. Зокрема, прозапальний інтерлейкін-1β індукує запальну реакцію і гострофазну відповідь, здійснює взаємозв’язок між неспецифічною та специфічною ланками імунітету. Дослідники вважають прокальцитонін найбільш перспективним індикатором септичного процесу, який дозволяє провести диференційну діагностику бактеріального і небактеріального запалення, оцінити тяжкість стану хворого й ефективність протизапальної терапії.

Мета дослідження – оцінити вміст інтерлейкіну-1β та  прокальцитоніну в сироватці крові хворих на лактаційний мастит.

Методи дослідження. Досліджено сироватку крові 97 жінок віком від 18 до 36 років (середній вік – (26±5) років). Контрольну групу становили 30 практично здорових жінок, які лактують. До 1-ї групи ввійшли 30 жінок із лактостазом, до 2-ї ‒ 37 жінок, в яких розвинувся лактаційний мастит. Вміст інтер­лейкіну-1β та прокальцитоніну визначали методом імуноферментного аналізу за допомогою автоматичного аналізатора “STAT FAX 303 plus”.

Результати й обговорення. Вміст інтерлейкіну-1β у сироватці крові жінок 1-ї групи ((6,37±0,46) пг/мл) у 3,5 раза перевищував показник контрольної групи ((1,78±0,11) пг/мл, р<0,05). Середня його концентрація у сироватці крові жінок 2-ї групи становила (8,32±0,38) пг/мл, що в 4,7 раза більше за контрольне значення та перевищувало показник жінок 1-ї групи в 1,3 раза (р<0,05). При розвитку лактостазу вміст прокальцитоніну ((0,07±0,02) нг/мл) був у 3,3 раза більшим за показник контрольної групи ((0,021±0,004) нг/мл, р<0,05). У сироватці крові жінок 2-ї групи він становив (0,81±0,25) нг/мл, що перевищувало величини цього маркера в контрольній і 1-й групах у 38,6 та 11,6 раза відповідно (р<0,05).

Висновки. Встановлена концентрація інтерлейкіну-1β підтверджує участь цього цитокіну в захисній реакції, її можна використовувати для оцінки активності запального процесу при лактостазі й лакта­ційному маститі. Визначення прокальцитоніну як маркера бактеріальної інфекції є доцільним для прогнозу септичного процесу в молочній залозі.

Abstract

Pathogenetic mechanisms of diabetic retinopathy are associated with the toxic effects of hyperglycemia and subsequent activation of stress-sensitive systems. The purpose was to determine the features of immune dysfunction in patients with diabetic retinopathy against the background of metabolic syndrome. Clinical and laboratory examinations of 130 patients with diabetic retinopathy have been carried out (70 insulin-dependent patients – group 1 and 60 insulin-independent patients – group 2). In determining the surveyed individuals’ contents of the lymphocyte populations and subpopulations, the monoclonal antibodies were used to CD3 +, CD4 +, CD8 +, CD19 +, CD23 +, CD25 +, CD56 + in the reaction of indirect immunofluorescence with fluorescein-isothiocyanate labeled antibodies and indices were calculated – the ratio of the lymphocyte populations and subpopulations. The population and subpopulation composition of blood lymphocytes were studied, and the ratio of cellular factors of immunity in patients with diabetic retinopathy was calculated. The immune status of patients with diabetic retinopathy is characterized by more pronounced changes in insulin-dependent patients’ cellular immunity – the activation of nonspecific killer immunity, suppressor potential and humoral immunity than in insulin-independent patients. The results allow the pathogenetic correction of diabetic retinopathy with the immune imbalance.