Introduction. Comorbid conditions in chronic obstructive pulmonary disease (COPD) can significantly worsen quality of life and prognosis, contribute to frequent exacerbations, and increase the risk of hospitalization.

   Aim. To study the effect of comorbid conditions on cardiac performance in patients with COPD exacerbation.

   Materials and methods. The study included 103 patients with COPD exacerbation, divided into two groups. The first group consisted of 36 patients without comorbid conditions, the second group – 67 patients with comorbidities. The control group included 25 persons without COPD. Repeated studies were conducted after 3–6 and 9–12 months. Lung function was assessed using spirometry before and after the bronchodilatory test, bodyplethysmography, and measuring the lung diffusion capacity using the CO single breath technique. The severity of dyspnea was assessed using the mMRC scale and quality of life using the CAT questionnaire. NT-proBNP levels were determined in blood plasma using immunochromatography. The structural and functional state of the heart was assessed using echocardiography with a 5 ms sector sensor at a frequency of 1.5–4.6 MHz with an assessment of global longitudinal strain of the ventricles using speckle tracking.

   Results. In both groups of patients during an exacerbation of COPD, we diagnosed changes in cardiac performance with a decrease in systolic and diastolic functions of both ventricles, which were most pronounced in the group of COPD patients with a comorbid background. According to the correlation analysis, these disorders are closely associated with the degree of bronchial obstruction and impaired diffusion lung capacity, associated with an increase in NT-proBNP levels. In the group without a comorbid background, partial correction of a number of echocardiographic indices was noted 3–6 months after the exacerbation.

   Conclusion. COPD exacerbations lead to significant changes in cardiac function, the severity of which significantly depends on the presence of comorbidity. The results of the analysis confirm the need for active cardiac monitoring in patients with COPD as a basis for improving clinical outcomes and reducing the burden of comorbid conditions.

   Introduction. Chronic obstructive pulmonary disease (COPD) is frequently associated with cardiovascular dysfunction. Heart rate variability (HRV) analysis serves as an additional criterion for evaluating the functional status of COPD patients, reflecting the integrated state of autonomic regulation.

   Aim. To assess HRV parameters in elderly COPD patients undergoing inpatient treatment under middle-mountain climatotherapy conditions before and after a standardized therapeutic course.

   Materials and methods. Thirty-three patients (median age 67.5 years; IQR 62.08; 73.98) with COPD exacerbation received 14 days of standard therapy at a climatic health resort located at 1,342 m above sea level. HRV was assessed on admission and after 10 days using the “Varicard 2.51” system during an orthostatic test.

   Results. On admission, all patients exhibited reduced heart rate variability and diminished total autonomic regulatory effect on circulation. This pattern persisted in the majority (n = 24) after treatment, and postural responses remained blunted. However, in 9 patients (27.3 %), treatment resulted in increased HRV indices (MxDMn, CV), enhanced parasympathetic activity (RMSSD, pNN50), greater total autonomic modulation (SDNN), and reduced regulatory strain (stress index, SI). Their autonomic status shifted from a state of overstrain (PARS [Index of Regulatory System Activity] = 7.0 points) to
functional tension (PARS = 4.5 points), characteristic of adaptive–compensatory processes. In contrast, 24 patients (72.7 %) developed rigid heart rhythm with further HRV deterioration post-treatment.

   Conclusion. Positive HRV dynamics following therapy were observed in only 27.3 % of patients; no significant improvement occurred in the remaining 72.7 %. This lack of response is likely due to incomplete acclimatization, influenced by individual functional capacities and specific adaptive reactions. Therefore, extending the duration of inpatient stays in middle-mountain settings appears necessary to achieve full physiological adaptation in COPD patients. Identifying predictors of heightened sensitivity to high-altitude climatotherapy may provide deeper insights into COPD pathophysiology and personalized therapeutic approaches.

   Aim. To evaluate the three-year dynamics in the frequency and severity of chronic obstructive pulmonary disease (COPD) exacerbations depending on the presence or absence of a prior SARS-CoV-2 infection (COVID-19).

   Materials and methods. The study was controlled prospective (2021–2024). The patients (n = 232) with verified chronic obstructive pulmonary disease (COPD) were examined. Patients divided into two groups: Group 1 (n = 172) – patients with COPD who had COVID-19; Group 2 (n=60) - patients with COPD without a COVID-19 history. The control points were initial examination (K0), examination after 1 year (K1), 2 years (K2) and 3 years (K3). Information collected on the presence, severity and number of exacerbations over the previous year (NEY), the time interval between exacerbations (tmonth), and cases of hospitalization for COPD exacerbation.

   Results. At point K1 NEY differed significantly between the groups (p = 0.037). In Group 1, the number of individuals with frequent exacerbations was significantly higher than in Group 2 (p = 0.008). In Group 1 at point K1, the risk of identifying the COPD phenotype with frequent exacerbations was 4.71 times higher than in Group 2, and the risk of developing exacerbations leading to hospitalization was 7.33 times higher. Correlation did not found between the severity of COVID-19 and the studied indicators. At point K2 in Group 1, episodes of COPD exacerbations observed less frequently. Indicator tmonth remained significantly shorter in Group 1. The level NEY did not reach the pre-COVID baseline at point K3. Indicator tmonth remained consistently shorter in Group 1 than in Group 2 (p = 0.014).

   Conclusion. In COPD patients, regardless of the initial severity of COVID-19, SARS-CoV-2 infection is associated with a sustained increase in exacerbation frequency and shortened intervals between exacerbations over a three-year period – primarily driven by an increased prevalence of the "frequent exacerbator" phenotype.

   Introduction. Post-COVID syndrome (PCS) leads to multiorgan dysfunction, the primary pathophysiological basis of which is considered to be endothelial dysfunction – a state of imbalance among vasoactive and angiogenic mediators.

   Aim. To evaluate the clinical relevance of endothelin-1 (EDN1) and angiotensin-2 (ANG-2) levels in PCS patients in relation to the timing of enrollment in rehabilitation treatment.

   Materials and methods. The study included 190 patients diagnosed with PCS and 30 healthy controls with no prior history of COVID-19. Assessments encompassed clinical, functional, and laboratory evaluations, including enzyme-linked immunosorbent assay (ELISA) for serum levels of ANG-2, EDN1, bactericidal/permeability-increasing protein (BPI), and C-reactive protein (CRP). Pulmonary function was assessed by spirometry. Physical performance was measured using the 6-minute step test (6MST), dyspnea severity via the Baseline Dyspnea Index (BDI). Fatigue was assessed using the Fatigue Assessment Scale (FAS), and health-related quality of life by the SF-36 questionnaire.

   Results. Patients were stratified into four groups based on PCS duration: Group I (<6 months), Group II (6–12 months), Group III (12–24 months), and Group IV (>24 months). Cardiovascular comorbidities predominated in Groups I and II, whereas bronchial asthma and chronic bronchitis were more common in Groups III and IV. Notably, 11.5 % of patients developed respiratory diseases de novo after COVID-19. ANG-2 levels were elevated across all PCS groups compared to controls. EDN1 concentrations were highest in Group I (52.3 [33.3; 62.5] pg/mL) versus controls (44.4 [39.81; 47.22] pg/mL) and showed a progressive decline with longer PCS duration: Group II – 39.4 [26.4; 50.0] pg/mL; Group III – 23.2 [16.0; 40.7] pg/mL; Group IV – 18.7 [16.5; 21.7] pg/mL. FAS and SF-36 scores revealed persistent chronic fatigue and reduced quality of life – both physical and mental – among PCS patients.

   Conclusion. For up to two years following acute COVID-19, patients exhibit signs of unresolved low-grade inflammation and impaired endothelial vasomotor function, which underlie persistent PCS symptoms, including chronic fatigue and diminished quality of life.

   Introduction. Post-infectious asthenic syndrome (PAS) and cognitive impairments are well-documented consequences of COVID-19 in adults; however, their characteristics in children remain insufficiently studied.

   Aim. To characterize the features of asthenic syndrome and neurocognitive status in children following SARS-CoV-2 infection.

   Materials and methods. A prospective single-center study included 209 children with confirmed COVID-19. Assessment was performed through medical record review, the Multidimensional Fatigue Inventory (MFI-20), and 6-month dynamic follow-up. Neurocognitive testing (assessing memory, attention, and executive function) was conducted in 46 children with PAS (main group) and compared with 12 apparently healthy children (control group).

   Results. PAS was diagnosed in 31.6 % (n = 66) of children, with a median duration of 2 months. The predominant symptoms were generalized physical weakness (69.7 %) and increased mental fatigue (36.4 %). Statistical analysis revealed no significant association between the severity of acute COVID-19 and subsequent PAS development. Neurocognitive evaluation demonstrated significantly lower scores (p < 0.05) in motor-auditory and visual-auditory-motor memory domains in the main group compared to controls.

   Conclusion. Previous COVID-19 infection in children is associated with a distinct post-infectious asthenic syndrome characterized by physical weakness, reduced tolerance to physical and mental exertion, excessive fatigue, impaired mnemonic functions, emotional lability, headache, dizziness, and specific memory deficits. These findings underscore the necessity for long-term monitoring and the development of targeted rehabilitation programs for pediatric patients recovering from COVID-19.

   Introduction. According to current clinical guidelines, glucocorticosteroids are recommended for children with chronic adenoiditis combined with allergic rhinitis. However, their prolonged use increases the risk of adverse effects and may negatively impact the child’s immune status. Therefore, it is clinically relevant to evaluate the dynamics of disease symptoms when replacing glucocorticosteroids with antihistamines.

   Aim. To assess the feasibility of optimizing pharmacotherapy for chronic adenoiditis associated with allergic rhinitis in pediatric practice.

    Materials and methods. Two groups of children aged 6–15 years with diagnosed adenoid hypertrophy and allergic rhinitis were formed at the Amur Regional Children’s Clinical Hospital (Blagoveshchensk). The control group (n = 15) received standard therapy with intranasal mometasone furoate spray–1 dose (50 µg) per nostril once daily (total 100 µg/day)–for 1 to 3 months. In the main group (n = 12), mometasone was discontinued and oral desloratadine was administered once daily at 2.5 mg (for children 6–11 years) or 5 mg (for children ≥12 years). Symptom monitoring (rhinorrhea, nasal congestion, breathing difficulty) was performed by patients and their parents at follow-up visits on days 7, 14, 21, and 28 using three criteria: "complete symptom resolution", "improvement", or "no change".

   Results. By the end of the second week, the proportion of patients with complete symptom resolution in the desloratadine group was 40% higher than in the control group (χ² = 14.25, p = 0.00016); by the third week, the difference increased to 42 % (χ² = 18.11, p = 0.00002); and by the fourth week, it reached 43 % (χ² = 26.10, p < 0.00001). Endoscopic nasopharyngeal examination on day 28 confirmed therapeutic efficacy, revealing positive dynamics in nearly all patients in the main group.

   Conclusion. The study demonstrates that pharmacotherapy for chronic adenoiditis associated with allergic rhinitis in children can be optimized by incorporating the histamine H1-receptor antagonist desloratadine into the treatment regimen while omitting topical glucocorticosteroids. Larger-scale studies with increased sample sizes are warranted to confirm these findings and establish robust statistical conclusions.

   Introduction. Researchers are increasingly focused on the balance of cytokines that regulate the types of immune-inflammatory responses predominant in patients with asthma.

   Aim. To assess the levels of Th2, Th1, and Th17 cytokines in blood and their interrelationships in asthma patients according to disease severity and level of asthma control.

   Materials and methods. Serum concentrations of interleukin (IL)-4, IL-13, interferon (IFN)γ, IL-2, IL-6, IL-17A, IL-17F, and IL-22 were measured in 144 asthma patients of varying severity. Lung function was evaluated by spirometry and bodyplethysmography.

   Results. Patients with intermittent asthma (Group 1) exhibited elevated serum levels of both Th2 (IL-4, IL-13) and Th1/Th17 cytokines (IFNγ, IL-2, IL-17F, IL-6). In patients with mild persistent asthma (Group 2), IL-4 levels were low, while IFNγ was elevated. In patients with moderate-to-severe uncontrolled asthma during exacerbation (Group 3), Th17 cytokines – IL-17F and IL-22 – were significantly increased. In Group 1, FEV1/FVC ratio positively correlated with IL-6 (Rs = 0.44; p = 0.037), and bronchodilator response (ΔFEV1) negatively correlated with IL-17A (Rs = – 0.76; p = 0.009). In Group 2, IL-17A showed a strong inverse correlation with residual volume/total lung capacity ratio (RV/TLC) (Rs = –0.66; p = 0.0015). In Group 3, expiratory airway resistance (Raw ex) correlated positively with IL-17A (Rs = 0.50; p = 0.031); IL-17F correlated negatively with TLC (Rs = –0.52; p = 0.008) and FVC (Rs = –0.56; p = 0.003). Among uncontrolled moderate-to-severe asthma patients (Group 3), IL-17F negatively correlated with Asthma Control Test (ACT) score (Rs = –0.70; p = 0.014), indicating worse asthma control; IL-17A negatively correlated with FEV1/FVC (Rs = –0.64; p = 0.011); and IL-2 negatively correlated with both FEV1/FVC (Rs = –0.54; p = 0.026) and forced expiratory flow at 50% FVC (FEF50) (Rs = –0.43; p = 0.043).

   Conclusion. Disease progression in asthma is associated with a shift in endotype, driven by regulatory cytokines that orchestrate airway inflammation. This shift correlates with declining bronchial patency, poor asthma control, and the emergence of distinct phenotypic features of endogenous inflammation.

   Introduction. Bitter taste receptors TAS2R31 can be expressed on respiratory epithelium, leukocytes, bronchial smooth muscles, and are capable of mediating relaxation of smooth muscle cells. Nevertheless, data on the relationship of TAS2R31 single nucleotide variants (SNVs) with asthma, as well as with various phenotypic features of the disease, are currently lacking.

   Aim. To analyze the spectrum of TAS2R31 SNVs in patients with asthma and practically healthy volunteers and to evaluate their possible relationship with the presence of the disease, smoking, lung function parameters and the level of asthma control.

   Materials and methods. The study included 119 patients with persistent asthma (main group, 40 % males, 48.5 ± 1.51 years) and 72 practically healthy volunteers (control group, 58% males, 38.2 ± 1.15 years). Detection and genotyping of TAS2R31 SNVs were performed within the amplified 839 bp gene fragment by Sanger sequencing. Lung function was assessed by standard spirometry, and asthma control was determined using the ACT questionnaire.

   Results. In total, five SNVs were identified in the combined sample of patients and controls: rs10845295 (p.Arg35Trp), rs12370363 (p.Ala141=), rs10743938 (p.Leu162Met), rs10845293 (p.Ala227Val), and rs10772423 (p.Val240Ile). The association with asthma was tested for rs12370363 and rs10743938, whereas associations with smoking, asthma control and lung function were analyzed for rs10845295, rs12370363 and rs10743938. SNV rs10743938 was significantly associated with the presence of asthma (OR 1.95 95% CI (1.11-3.43), p = 0.02 in the log-additive model after adjusting for gender, age, and smoking status). The same SNV was associated with smoking among asthma patients (OR 1.9 95 % CI (1.02-3.75), p = 0.04 in the log-additive model after adjusting for gender and age). No significant associations were found between the studied SNVs with lung function parameters or asthma control.

   Conclusion. In the examined samples, the spectrum of common TAS2R31 SNVs was relatively limited and only partially overlapped with the extensive list of common variants reported in public genetic databases. The present study revealed an association of the rs10743938 A allele with asthma and smoking among asthma patients, suggesting a potential role for TAS2R31 variations in the development of genetic predisposition to the disease and smoking in the presence of asthma.

   Introduction. COVID-19 is associated with a high risk of cardiovascular complications, including acute myocardial infarction (AMI), even in young patients who may exhibit minimal traditional risk factors. Timely identification of individuals at high risk for AMI remains a clinical challenge, necessitating the development of novel prognostic models based on pathophysiologically relevant biomarkers.

   Aim. To develop a prognostic model for AMI risk in young patients with confirmed COVID-19 based on the expression levels of TNF-related apoptosis-inducing ligand (TRAIL) and transforming growth factor beta 1 (TGFβ1).

   Materials and methods. The study included 52 patients with moderate COVID-19, divided into two groups: the main group (n = 28) with AMI developed during hospitalization, and the comparison group (n = 24) without AMI. Peripheral blood samples were collected within the first 72 hours of admission. TRAIL (using APC-conjugated monoclonal antibodies) and TGFβ1 (using PE-conjugated monoclonal antibodies) expression on peripheral blood monocytes was assessed by flow cytometry on a BD FACS Canto II (USA).

   Results. In the main group, TRAIL expression (58.7% [52.1; 64.3]) and TGFβ1 expression (17.8 % [15.2; 21.4]) were significantly higher than in the comparison group (14.2 % [10.8; 18.6] and 4.5 % [3.1; 6.2], respectively; p < 0.001). Using discriminant analysis, a mathematical prognostic index (PI) for AMI was developed: PI = –13.197 + 0.355 × TRAIL + 0.276 × TGFβ1. A cutoff value of 12.90 was established: PI ≥ 12.90 indicates high risk of AMI; PI < 12.90 indicates low risk of AMI.

   Conclusion. The proposed prognostic model based on TRAIL and TGFβ1 expression levels on peripheral blood monocytes is a highly informative tool for assessing AMI risk in young patients with COVID-19. Implementation of this algorithm enables early initiation of preventive and therapeutic interventions aimed at reducing fatal cardiovascular complications and improving clinical outcomes.

   Aim. To determine the diagnostic significance of laboratory blood parameters in predicting the duration of inpatient treatment for community-acquired pneumonia (CAP) caused by Klebsiella pneumoniae.

   Materials and methods. Study design: single-center, continuous, retrospective case series study; study subjects: 52 patients (all HIV-negative), 55.8 % (29/52) male and 44.2 % (23/52) female, diagnosed with CAP caused by K. pneumoniae; study duration: from 2016 to 2022; primary endpoint: recovery and discharge of the patient from hospital; Description of methods: analysis of paired contingency tables – Pearson's criteria (χ²), (without Yates's correction for continuity) for df = 1, logistic regression (simple and multiple).

   Results. Statistically significant threshold values predictive of hospitalization exceeding 10 days were identified as follows: lymphocyte count ≤ 2.01 × 109/L, monocyte count ≤ 0.68 × 109/L (lower values associated with increased risk), and erythrocyte sedimentation rate (ESR) ≥ 52 mm/h (higher values associated with increased risk).

   Conclusion. The prognosis for the duration of hospitalization longer than 10 days during treatment for CAP caused by K. pneumoniae can be determined with a high degree of probability using three laboratory parameters of a complete blood count or a combination of them (lymphocyte, monocyte, and ESR levels).

   Introduction. Despite well-documented adverse effects of COVID-19 on gestation and perinatal outcomes, the criteria for placental insufficiency (PI) development in this patient population remain incompletely understood, and existing data are fragmented.

   Aim. To determine the prognostic value of CD68 and tumor necrosis factor receptor 1 (TNFR1) expression on peripheral blood monocytes for predicting placental insufficiency in pregnant women with COVID- 19.

   Materials and methods. A total of 114 pregnant women were enrolled and divided into three groups: the main group (n = 37) – moderate-severe COVID-19 with PI; the comparison group (n = 42) – moderate-severe COVID-19 without PI; and the control group (n = 35) – healthy pregnant women without COVID-19 or PI. CD68 and TNFR1 expression on peripheral blood monocytes was assessed by flow cytometry.

   Results. Pregnant women in the main group demonstrated significantly higher CD68 and TNFR1 expression on monocytes compared to both the comparison and control groups (p < 0.001). Threshold values of CD68 ≥ 25.0 % and TNFR1 ≥ 79.0 % were identified as predictive markers for PI development in the third trimester among patients with COVID-19.

   Conclusion. The strong association between these immunological markers and PI supports their use as additional diagnostic criteria for evaluating the risk of placental dysfunction in pregnant women infected with SARS-CoV-2.

   Introduction. Exacerbation of bronchial asthma during pregnancy in the context of acute-phase reactivation of chronic viral infection in women is frequently associated with the development of cerebral and cardiac pathology in their offspring.

   Aim. To provide an echocardiographic characterization of cardiac structure and function in full-term newborns of mothers who experienced exacerbation of bronchial asthma associated with reactivation of chronic cytomeg-alovirus (CMV) infection during pregnancy.

   Materials and methods. Echocardiography was performed in 42 newborns of mothers with uncomplicated pregnancies (control group) and in 68 newborns with cerebral ischemia whose intrauterine development was complicated by mild bronchial asthma exacerbation associated with CMV reactivation in the second trimester of gestation (main group). The main group was subdivided into two subgroups: 36 newborns with grade I cerebral ischemia (subgroup 1) and 32 with grade II cerebral ischemia (subgroup 2).

   Results. Compared with the control group, newborns in subgroup 1 had significantly lower Apgar scores at 1 minute (p < 0.001) and 5 minutes (p < 0.001), as well as lower birth weight (p < 0.01). However, no significant differences were found in echocardiographic parameters: end-diastolic dimension (EDD, p > 0.05), end-systolic dimension (ESD, p > 0.05), stroke volume (SV, p > 0.05), ejection fraction (EF, p > 0.05), or fractional shortening (FS, p > 0.05). In contrast, newborns in subgroup 2 showed significantly lower Apgar scores at 1 and 5 minutes (p < 0.001) and reduced birth weight compared with both the control group (p < 0.01) and subgroup 1 (p < 0.001). Echocardiographically, subgroup 2 exhibited significantly decreased EDD (p < 0.01), ESD (p < 0.01), SV (p < 0.05), EF (p < 0.01), and FS (p < 0.001) compared to subgroup 1.

   Conclusion. Newborns with grade II cerebral ischemia and an antenatal history of mild maternal bronchial asthma exacerbated by CMV reactivation in the second trimester demonstrate significantly greater cardiovascular burden in the early neonatal period compared to those with grade I ischemia under similar antenatal conditions. This is likely due to the adverse impact of antenatal hypoxia on fetal cardiac organogenesis and histogenesis.

   Introduction. Lynch syndrome is one of the most common hereditary cancer syndromes, characterized by early-onset development of multiple malignancies, particularly colorectal cancer. It is caused by germline mutations in DNA mismatch repair (MMR) genes.

   Aim. To present a rare case of Lynch syndrome to familiarize clinicians with current diagnostic approaches.

   Materials and methods. A clinical case from the authors’ practice is described.

   Results. The patient, born in 1984, presented with two primary tumors of the colon. Given the early age of onset and multiplicity of tumors, Lynch syndrome was clinically suspected. Molecular genetic testing for microsatellite instability (MSI) was performed, revealing a pathogenic heterozygous germline duplication in the MLH1 gene: NM_000249.4 c.1921dup
(p.Leu641Profs*4). The diagnosis was confirmed as Lynch syndrome, and an individualized surveillance program was established.

   Conclusion. This case illustrates the diagnostic and therapeutic capabilities available for Lynch syndrome and proposes a structured algorithm for long-term follow-up of both diagnosed patients and their at-risk relatives.

   The complexity of the pathogenesis of bronchial asthma (BA) has been caused by the influence of the environmental, genetic and epigenetic factors that interact with each other and contribute to the development and exacerbation of this pathology. In recent years researchers have focused on the neurogenic component of the BA pathogenesis. The ankyrin receptor TRPA1(the transient receptor potential cation channel subfamily A member 1) is expressed in the sensory C-fibers of the lungs and activated by the cold, cigarette smoke, allergens and number of chemicals that are the triggers of BA. It triggers the influx of Ca²⁺ into sensory neurons and activates the cascades responsible for the expression of the brain-derived neurotrophic factor (BDNF) gene. BDNF is involved in airway remodeling, enhances airway innervation and exacerbates airway hyperreactivity, and also maintains sensory hypersensitivity through a feedback loop. BDNF gene polymorphisms confer susceptibility to BA, with carriers of TRPA1 gene polymorphisms more sensitive to epigenetic modifications and may have strong BDNF expression in response to the stimuli. Despite the fact that the epigenetics of TRPA1 and BDNF in BA is under study, the epigenetic changes of TRPA1 and BDNF are well described in neurology, which may be interesting in the context of their interaction in BA, given the role of neuroimmune inflammation in the pathogenesis of this disease. The present review discusses the role and relationship of genetic and epigenetic changes induced by environmental factors initiating BA development, as well as role of TRPA1 and BDNF in this process.

   Аsthma in the elderly is a significant medical and social problem due to its high prevalence, polymorbidity, polypharmacy, and age-related changes in the body's regulatory systems. This review examines current approaches and features of the restorative treatment of аsthma in the elderly. Attention is drawn to the importance of using non-drug methods in the restorative treatment of elderly patients, including physical rehabilitation, breathing exercises, educational programs, and physiotherapy. The main physiotherapeutic methods (inhalation therapy, laser therapy, ultrasound, magnetic therapy, electrotherapy, speleoclimatotherapy, interval hypoxic hyperoxytherapy), their mechanisms of action, and the evidence base for their effectiveness are presented. It is noted that age is not a contraindication for physiotherapy treatment.

   Particular attention is paid to the principles of rehabilitation in elderly patients, which require an individualized, comprehensive, dosed, and safe approach, taking into account age-related characteristics and comorbidities. Insufficient study of the long-term effects and specific application of many methods in geriatrics is noted.

   Further research into the specific application of physiotherapy methods in the elderly, taking into account involutional processes and comorbidities, will enable the development of individualized rehabilitation programs. The need to improve the accessibility and quality of rehabilitation care for this category of patients is emphasized.