卷 69, 编号 8 (2024)

Lung cancer is a tumor lesion that is widespread among the population worldwide, accounting for 12.4% of the total number of new cases of malignant tumors. Lung tumors are the leader in the structure of mortality in patients with cancer. According to the World Health Organization, the incidence of lung malignancies is steadily increasing worldwide and will reach 35 million cases per year by 2050, which is 77% higher than the data for 2022.

In the early stages, lung cancer does not have specific clinical symptoms, which makes it difficult to diagnose and leads to late detection, which is noted in more than 70% of patients with this lesion. Thus, lung cancer is a global medical, social, clinical and epidemiological problem worldwide.

With the discovery of extracellular nanovesicles (exosomes), scientists began to develop new approaches in the diagnosis and treatment of lung cancer. It was found that exosomes obtained from tumor cells have a powerful effect on the tumor microenvironment, antitumor immunoregulatory activity, tumor progression and metastasis. In addition, more and more studies are providing various therapies for lung tumors with the loading of drugs, proteins and microRNAs targeting specific antigens into exosomes.

The authors analyzed the data available in the literature on the role of extracellular nanovesicles containing lipids, surface and internal proteins, microRNAs and other compounds in carcinogenesis, as well as on the possibilities of using exosomes as new prognostic biomarkers in the minimally invasive diagnosis of lung cancer.

BACKGROUND: Venous thrombosis is associated with hereditary and acquired conditions characterized by increased activation of the coagulation activity of the hemostatic system in blood vessels. Idiopathic venous thrombosis can often occur in childhood and can also be associated with certain genetic variants of hereditary predisposition.

AIM: To analyze the association of 8 genetic variants (F2 20210 G>A, F5 1691 G>A, F7 10976 G>A, F13 G>T, FGB G455A, ITGA2 807 C>T, ITGB3 1565 T>C, PAI-1-675 5G>4G) with venous thrombosis in children born to mothers with a history of recurrent miscarriage.

MATERIALS AND METHODS: The patient group included 322 children aged 6 to 15 years (average age 8.5 years), who had a history of episodes of venous thrombosis of various locations, born to mothers with a history of recurrent miscarriage. The comparison group included 159 healthy children also aged from 6 to 15 years (average age 8.5 years), who had no history of episodes of venous thrombosis and who were also born to mothers with recurrent miscarriage. Molecular genetic analysis was carried out using real-time polymerase chain reaction with automatic analysis of melting curves.

RESULTS: Based on the results of an analysis of the association of genetic variants with venous thrombosis in children born to mothers with burdened obstetric and gynecological history, a connection with this pathology was established for genetic variants F5 1691 G>A (genotype GA+AA; odds ratio 3.70, 95% confidence interval 1.33–10.33, p <0.0072) and ITGB3 1565 T>C (CC genotype; odds ratio 2.26, 95% confidence interval 1.02–5.00, p <0.0370).

CONCLUSION: Thus, we established an association of 2 genetic variants (Leiden mutation and ITGB3 1565 T>C) with venous thrombosis in children born to mothers with recurrent miscarriage. Based on our study, we can recommend molecular genetic testing of these variants as markers of hereditary predisposition to thrombosis.

BACKGROUND: The development of myocardial infarction is accompanied by an inflammatory reaction involving various immune cells that influence the monocyte response. An adequate inflammatory response has to ensure healing of the necrotic area in myocardium to approach the maximum possible restoration of left ventricular function, which directly affects the prognosis of patients with acute myocardial infarction. Patients with type 2 diabetes mellitus are a special group of patients with chronic low-grade inflammation and a high risk of complications. The features of changes in inflammatory response indicators and, above all, the monocyte response in patients with diabetes mellitus during the development of myocardial infarction have not been sufficiently studied.

AIM: To evaluate the dynamics of inflammatory response indicators in myocardial infarction in patients with type 2 diabetes mellitus.

MATERIALS AND METHODS: The study included 121 patients with myocardial infarction and type 2 diabetes mellitus. In addition to the standard study, the number of cells of different leukocyte subpopulations was evaluated on days 1, 3, 5 and 12 using flow cytometry with the CytoDiff® panel. Nonparametric methods of statistical analysis were used (STATISTICA 10). Quantitative data are presented as Median (Q25; Q75). Wilcoxon test was used to compare related groups, Spearman coefficient (R) was calculated to assess correlation dependencies. Differences were considered significant at p <0.05.

RESULTS: In patients with acute myocardial infarction and type 2 diabetes mellitus, the inflammatory reaction in the early stages was characterized by the development of neutrophilia: on 1^st day — up to 7310 (5304; 10,018) cells/μl, with subsequent normalization of their number by day 12: 4343 (3564; 5496) cells/μl, p <0.001. There was also a lower count of CD16(–) T-lymphocytes and natural killer cells on day 1: 1373 (1007; 1815) cells/μl, with their subsequent increase up to 1571 (1180; 1915) cells/μl, p=0.004. The development of a biphasic monocytic response with proinflammatory phase lasting up to 5 days was observed: on the 5^th day of myocardial infarction, the values of the CD16(–) monocytes reached a maximum in the peripheral blood and amounted to 692 (514; 791) cells/μl, decreasing to 505 (405; 626) cells/μl, p <0.001, by day 12. CD16(+) monocytes count on day 5 was 61 (40; 75) cells/μl with a further decrease in their number to 45 (30; 77) cells/μl (p=0,012) by the 12^th day. A direct correlation was revealed between neutrophils and CD16(–) monocytes on the 1st and 12^th days of myocardial infarction (R=0.650, R=0.573, respectively; p <0.05). Similar correlation was found between CD16(–) and CD16(+) monocytes determined on day 3 and the number of platelets determined on day 1 (R=0.632 and R=0.735, respectively; p <0.05), as well as between B-lymphocytes on day 3 and the percentage of CD16(+) monocytes on day 5 (R=0.786, p <0.05).

CONCLUSION: In patients with type 2 diabetes mellitus, a biphasic monocytic response is observed in acute myocardial infarction with signs of pronounced proinflammatory phase. The revealed correlations between the monocytes and other leukocyte subpopulations count, as well as platelets, indicate the presence of mutual influences between cells and complex regulation of the inflammatory response in myocardial infarction.

BACKGROUND: Screening and identification of antierythrocyte antibodies before transfusion of erythrocyte-containing components contributes to the most accurate selection of donor blood components compatible for the recipient, which reduces the risk of posttransfusion reactions and complications.

CLINICAL CASE DESCRIPTION: Female patient X., age 62, was admitted to the hematology department with a diagnosis of “Iron deficiency anemia, unspecified”. Autoantibodies and antierythrocytic antibodies of the Rhesus system were identified — anti-e antibodies. Conducting a test for individual compatibility of blood components is difficult: the incompatibility of blood components in an indirect antiglobulin test is due to the presence of autoantibodies.

CONCLUSION: An integral part of specialized medical care is blood transfusion, which is based on the immunohematological compatibility of the donor and recipient. At the same time, the safety of transfusion of donated blood and its components is the most important principle of providing transfusion care in medical organizations. Screening of antierythrocyte alloantibodies is a mandatory pretransfusion test. However, the antibody identification process is difficult in the presence of thermal autoimmune antibodies in the plasma under study. To confirm the presence of autoantibodies in the test sample, a direct antiglobulin test (DAGT) is necessary. The standard way to “get rid” of autoimmune antibodies is to use the absorption–elution method, however, the complexity of the technique limits its use in immunohematology laboratories in routine practice.