The role of anxiety disorders in the onset and progression of cardiovascular diseases, the relationship between them, and effective treatment strategies for comorbid patients have been discussed with our experts:

Olga D. Ostroumova, Dr. Sci. (Med.), Professor, Head of the Department of Therapy and Polymorbid Pathology named after Academician M.S. Vovsi, Russian Medical Academy of Continuous Professional Education of the Ministry of Health of the Russian Federation, Chair of the RSC Working Group on Cardioneurology, Member of the Presidium of the Moscow Society of Cardiology, Chairman of the Moscow Regional Branch of the Russian Scientific Medical Society of Internal Medicine (RNMOT).

Vladimir A. Parfenov, Dr. Sci. (Med.), Professor, Head of the Department of Nervous Diseases, Institute of Clinical Medicine, Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University).

Endothelial dysfunction is a universal mechanism of injury, not specifically associated with any one nosology. It is characterized by insufficient production of vasodilators, prothrombotic and proinflammatory cell activation, and pathologically increased endothelial permeability. It is clinically heterogeneous, with regional variability in the expression of various pro- and anticoagulant factors. Essentially, all processes represent a continuum of genetic, epigenetic, transcriptomic, proteomic, metabolic, morphological, and functional changes. In 2023, a new concept for the pathogenesis of endothelial dysfunction as a systemic process was developed, enabling the prediction, prevention, and management of a number of diseases. Ten stages of endothelial damage and three degrees of severity are distinguished: mild, moderate, and severe. Mild endothelial dysfunction is characterized by reduced nitric oxide (NO) production and a noncritical decrease in ATP levels, coupled with increased energy consumption to adapt to increasing hypoxia. Clinically, this degree is most often associated with asthenic manifestations. Moderate/ severe ED is associated with progressive neurotransmitter imbalance, adhesion cell activation, microthrombosis, hypoxia, and neuroinflammation. The most pronounced clinical characteristics are secondary headache, cognitive, and anxiety-depressive disorders. Severe ED leads to endothelial cell death. Endothelial loss itself does not lead to thrombosis, but disruption of the parietal membrane integrity can affect blood rheology. Delayed neurological and systemic complications arise at this stage. Understanding the staging of damage is crucial for the development of individualized therapeutic interventions, from lifestyle modification to targeted therapy, with the search for a universal endothelial protector.

Introduction. Delirium’s incidence ranges from 15% to 80% and associated with prolonged intensive care unit (ICU) stay, increased overall hospital length of stay, and higher mortality. In a previously published article we noted a trend toward a reduction in the incidence of delirium with the use of VR. The results of the subsequent study allowed for a more comprehensive assessment of the impact of VR on the incidence, severity and duration of delirium.

Aim. To evaluate the effect of virtual reality on the incidence, severity, and duration of delirium in patients with acute stroke admitted to the ICU.

Materials and methods. A randomized controlled trial was conducted at Veresaev City Clinical Hospital, Moscow. Patients with acute stroke admitted to the ICU who met the inclusion criteria (n = 219) were randomized into two groups. In Group 1, delirium prevention was performed according to the ABCDEF bundle. In Group 2, VR stimulation using dedicated headsets was administered in addition to the ABCDEF bundle. The severity of delirium was assessed using the DRS-R-98 scale.

Results. Delirium developed in 27 patients (23.9%) in the standard therapy group and in 10.4% of patients in the VR group; the difference was statistically significant. Delirium was more severe in the control group compared to the VR group (p < 0.05). The median duration of delirium was 48 hours in Group 1 and 24 hours in Group 2, indicating the effectiveness of VR in reducing delirium duration. VR was well tolerated, and all patients in Group 2 completed the full course of VR sessions.

Conclusions. Virtual reality may be considered an additional non-pharmacological tool for delirium prevention in patients with acute stroke.

Introduction. Ischemic stroke, characterized by combined motor and cognitive impairments and accompanied by an increase in the global burden and needs for rehabilitation, requires early, structured and dosed kinesiotherapy at the inpatient stage, with an assessment of its effectiveness using validated functional, cognitive and patient-oriented scales.

Aim. To assess the dynamics of functional independence, cognitive status, and stroke-specific quality of life in patients of both sexes undergoing early kinesiotherapy in an inpatient setting.

Materials and methods. A total of 60 patients (29 women, 31 men) were examined at the Kyrgyz Research Institute of Balneology and Rehabilitation Treatment, average age 65.68 ± 10.34 years. Rehabilitation was initiated at an early stage and included verticalization, passive and active exercises, as well as therapy based on the Bobath concept. The Barthel Index, the Mini-Mental State Examination (MMSE), and the Stroke-Specific Quality of Life (SS-QOL) questionnaire were assessed at admission and at discharge after 20 days.

Results. During the inpatient rehabilitation stage, patients with ischemic stroke demonstrated statistically significant improvements in functional and cognitive status, as well as in several quality-of-life indicators. According to the Barthel Index, the level of functional independence increased significantly from 54.83 ± 22.62 to 99.25 ± 20.95 points (p < 0.05); similar dynamics were observed in women (from 53.45 ± 23.05 to 98.27 ± 22.64) and men (from 56.12 ± 22.13 to 100.16 ± 19.19; p < 0.05). Cognitive status assessed by the MMSE also improved significantly: the mean score increased from 26.55 ± 3.47 to 29.38 ± 1.42 points (p < 0.05), with comparable changes in women (26.93 ± 3.14 to 29.38 ± 1.45) and men (26.19 ± 3.72 to 29.39 ± 1.38; p < 0.05). According to the SS-QOL questionnaire, statistically significant improvements were observed in the domains of “family role,” “mobility,” “mood,” “self-care,” “social role,” and “upper limb function” (p < 0.05). Several domains (energy, speech, thinking, vision, personality traits, and productivity) demonstrated positive trends without reaching statistical significance (p > 0.05). Overall, the findings indicate substantial recovery of functional independence, cognitive function, and key components of quality of life during the early rehabilitation period, with no clinically significant gender differences.

Conclusion. Early kinesiotherapy initiated in the acute phase of ischemic stroke and implemented through a stepwise program of mobilization and function-oriented exercises is associated with clinically significant improvements in functional independence and cognitive status. It also provides a statistically significant increase in stroke-specific quality of life, predominantly in domains related to mobility, self-care, upper limb function, emotional well-being, and social participation.

Introduction. The treatment of patients with chronic migraine (CM) and medication overuse headache (MOH) is an actual problem in neurology. Predictors of treatment effectiveness for CM and MOH have been poorly studied.

Aim. To study the prognostic factors of therapeutic response in CM.

Materials and methods. 54 patients (11 men, 43 women) with CM aged 18 to 50 years (average age 39 years), with or without MOH received preventive treatment for 12 months with evaluation of results every 2 months. Patients kept a headache diary. The questionnaire took place during each visit and included assessments using the VAS (Visual Analog Scale), SF-36 (SF-36 Health Status Survey), MIDAS (Migraine Disability Assessment), MSQ v2.1 (Migraine Specific Quality of Life Questionnaire version 2.1), Morisky – Green Medication Adherence Scale, Sleep Quality Questionnaire, CSI-A (Central Sensitization Inventory), LDQ (Leeds Dependence Questionnaire), HIT-6 (Headache Impact Test-6), HADS (Hospital Anxiety and Depression Scale).

Results. The baseline monthly migraine frequency was associated with the MSQ v2.1 (restrictive function: β = -0.17, preventive function: β = -0.14, emotional function: β = -0.06, p < 0.001), SF-36 (PH: β = -0.37, MH: β = -0.02, p < 0.001), LDQ (β = 0.5, p < 0.001), HIT-6 (β = 0.47, p < 0.001), CSI-A (β = 0.19, p < 0.001) scores. The baseline MIDAS score was associated with the results of the LDQ (β = 6.1, р < 0.001), CSI-A (β = 2, р < 0.001), HIT-6 (β = 3.46, р < 0.001), НАDS-A (β = 4.5, р < 0.001), HADS-D (β = 2.82, р = 0.014), SF-36 (PH: β = -3.4, MH: β = -2, р < 0.001), MSQ v2.1 (restrictive function: β = -1.66, preventive function: β = -1.77, emotional function: β = -0.9, p < 0.001) and Sleep Quality Questionnaire (β = -4.5, р < 0.001). However, these factors were not associated with the dynamics of reduction in the frequency of headaches and MIDAS. On the background of preventive therapy headache frequency decreased by 2 episodes per month (β = -2.15, p < 0.001), and the MIDAS score decreased by almost 9 points (β = -8.95, p < 0.001). MOH was not a significant predictor of migraine dynamics (p = 0.072) and severity on the MIDAS scale (p = 0.24).

Conclusion. The duration of preventive treatment under the control of a specialist is the main predictor of a positive therapeutic response in CM and MOH.

Alzheimer’s disease (AD) is rarely diagnosed in our country, which is largely due to the poor awareness of doctors about its symptoms and clinical forms. The logopenic variant of primary progressive aphasia (lvPPA) represents a rare presentation of AD and is characterized by isolated language impairment in the early stages. A clinical case of a 70-year-old patient with lvPPA due to AD is presented. Despite the prevailance of speech impairment in her clinical picture, for long she was observed for cerebrovascular disease. Signs of severe brain atrophy according to MRI data and a significant decrease in the beta-amyloid content in the cerebrospinal fluid made it possible to diagnose AD as the cause of lvPPA. Timely diagnosis of lvPPA is difficult due to its clinical similarity to other forms of lvPPA. A hallmark of PPA is word-finding difficulty during speech production, resulting in slowed speech. Comprehension of spoken language, grammatical structure, and articulation remain preserved. This language deficit is associated with dysfunction of the “phonological loop”. Clinical, instrumental, and pathomorphological characteristics of different PPA variants are described to provide a more systematized view on lvPPA. Early diagnosis of lvPPA is important both for the timely prescription of available symptomatic treatments, implementation of non-pharmacological therapy, and for defining indications for pathogenetic therapy aimed at preventing progression of AD.

Introduction. The concept of mild cognitive impairment (MCI) serves as a useful diagnosis for clinicians, enabling careful monitoring and extensive potential for therapeutic interventions. The phenotypic classification of MCI allows to identify the probable cause of MCI and predict its development.

Aim. To evaluate the effect of a 12-week (3-month) therapy course with Picamilon® Ginkgo on restoration of cognitive functions in patients with the non-amnestic MCI phenotype.

Materials and methods. The treatment group included 21 patients receiving Picamilon® Ginkgo as part of combination therapy. The comparison group included 25 patients receiving only stable combination therapy aimed to manage vascular risks. Cognitive impairment was diagnosed and assessed at baseline and at 12 weeks (3 months) of stable therapy using the MoCA test to determine total MoCA sores (MoCA-Total), MoCA-MIS, and MoCA domain-specific index scores: executive function, attention, and visual-constructive skills.

Results. After treatment, the mean MoCA-total score was significantly higher in the group of patients who additionally received Picamilon® Ginkgo as compared to the patients receiving vascular risk reduction therapy alone (26.8 ± 1.1 versus 25.3 ± 1.3 points, p < 0.05). Among patients randomized to Picamilon® Ginkgo group, 47.6% returned back to normal cognitive function (MoCA-total ≥26 points) scores versus 20.0% of patients in the comparison group (χ² = 3.962, p < 0.05).

Conclusion. The combination agent Picamilon® Ginkgo is an effective, safe, and promising treatment for vascular cognitive impairment, including the potential for reversion to normal cognitive function.

Cognitive impairment can develop in various neurological, psychiatric, and somatic diseases and encompass a spectrum of neuropsychological changes from mild cognitive impairment to dementia. The clinical picture is determined by the underlying disease causing the cognitive impairment and its severity, manifesting as a deterioration in cognitive functions (attention, memory, speech, praxis, gnosis, and executive functions) compared to baseline. Examination of patients with cognitive impairment includes collecting complaints and anamnesis, a physical examination with neurological status, a neuropsychological examination with an assessment of cognitive functions, neuroimaging, laboratory, and instrumental diagnostic methods. The most common differential diagnoses include asthenic syndrome (chronic fatigue syndrome), anxiety and depressive disorders, fatigue syndrome after a viral illness, and chronic cerebral ischemia. To illustrate the diagnostic process, this article presents three clinical cases. The combination drug Vinpotropile has demonstrated efficacy and safety in achieving this goal. Treatment of mild cognitive impairment should be aimed at both reducing their severity and preventing the potential development of dementia. Non-pharmacological treatments play a significant role in therapy.

Chronic nonspecific (musculoskeletal) low back pain (CNLBP) is one of the most common causes of temporary disability and decreased quality of life. Risk factors for CNLDP include heavy physical labor, excessive flexion and extension, frequent bending, heavy lifting, a sedentary lifestyle, and exposure to vibration. Chronic low back pain is facilitated not only by pathological changes (damage to the intervertebral disc, facet joint, sacroiliac joint, muscles, and ligaments), but also by inadequate treatment of acute pain, excessive limitation of physical activity, a “pain-prone” personality type, and anxiety and depressive disorders (social and psychological factors of pain). The diagnosis of CNLBP is based on a clinical examination and the absence of signs of dangerous disease (“red flags”), radiculopathy, and spinal stenosis. In chronic lower back pain, it is recommended to inform the patient about the favorable prognosis of the disease and its risk factors, the need to avoid excessive static and physical stress, incorrect positions and postures, and the advisability of maintaining physical, social, and professional activity. A multimodal approach is most effective in chronic lower back pain, which, as non-drug methods, should include an educational program, therapeutic physical exercises, manual therapy, and, for some patients, psychological therapy methods. Non-steroidal anti-inflammatory drugs (NSAIDs) are most often used to reduce pain in chronic lower back pain. The efficacy and safety of etoricoxib (Arcoxia) as an NSAID and local administration of Diprospan for lesions of the lumbar facet joints and lumbosacral articulation are discussed. To prevent low back pain, therapeutic exercises and an educational program on avoiding excessive static and physical stress, incorrect positions and postures are recommended.

Introduction. Limb compression-ischemic neuropathies are typically characterized by pain and sensory loss. However, in cubital tunnel syndrome (CuTS), pain syndrome is relatively uncommon and develops at later stages of the disease, warranting further investigation.

Aim. To determine the frequency and causes of pain syndrome in patients with CuTS before and after surgical decompression, depending on sex, age, and comorbid disorders.

Materials and methods. The study included patients with compression-ischemic neuropathy of the ulnar nerve (CuTS, n = 42), of whom a subset (n = 15) had pain syndrome. Clinical and neurophysiological examinations were performed, utilizing diagnostic scales and questionnaires before decompressive surgery and at 12–24 months postoperatively.

Results. All patients showed positive dynamics in the recovery of lost functions after surgical treatment, both in the group with pain syndrome and the group without pain (according to the Symptom Severity Scale, p = 0.002 and p = 0.013, respectively, and the Functional Status Scale of the Boston Questionnaire, p < 0.001 and p = 0.013, respectively). A correlation was established between the severity of pain syndrome (assessed by the Numerical Rating Scale), the presence of comorbid emotional disorders (p < 0.001), and sleep disturbances (p < 0.001) in CuTS. A significant decrease in quality of life was demonstrated in patients with pain syndrome (p < 0.001). A negative impact of increased anxiety, depression, and sleep disturbances on the development, severity, and duration of neuropathic pain syndrome was identified.

Conclusion. Increased anxiety, depression, and sleep disorders are associated with the presence of pain in CuTS. Therefore, they require timely diagnosis and adequate correction, which holds significant medical and social importance for the rehabilitation of this patient category.

Anxiety disorders are among the most common forms of mental illness in the modern world, and one of the most significant is generalized anxiety disorder. This disorder is characterized by long-term, persistent, and severe anxiety about various issues, as well as numerous distressing sensations in the body, fatigue, sleep disturbances, and pain symptoms. Numerous studies have shown that untreated generalized anxiety disorder significantly reduces patients’ quality of life, increases the risk of disability, and negatively impacts the course of a number of socially and clinically significant somatic diseases. Despite the large number of developed diagnostic and therapeutic methods, managing patients with this disorder in real-world clinical practice remains a challenging task, requiring the clinician to select differentiated therapeutic interventions. According to current data, lifestyle modification recommendations, psychotherapeutic interventions (primarily cognitive behavioral therapy), and psychopharmacotherapy can be effective in treating generalized anxiety disorder. Monoamine reuptake inhibitors are the first-line psychopharmacotherapy for generalized anxiety disorder, and benzodiazepine tranquilizers have the most pronounced rapid anti-anxiety effect. However, both classes of medications are not without side effects and drawbacks, limiting their universal use in all patients with generalized anxiety disorder. This article concludes with two case reports demonstrating how the non-benzodiazepine anxiolytic original etifoxine may be a useful treatment option for generalized anxiety disorder, depending on the clinical situation, either as monotherapy or as an adjunct to a serotonin-norepinephrine reuptake inhibitor.

The increasing prevalence of prediabetes and metabolic syndrome poses a major public health challenge at both regional and global levels. Diabetic neuropathies are the most common complications of diabetes, contributing to high morbidity, increased mortality, reduced quality of life, and increased healthcare costs. Prediabetes is characterized by glucose levels in the intermediate range – above normoglycemia but below the diagnostic threshold for diabetes. Adults worldwide may have impaired glucose tolerance and impaired fasting glucose, yet most are unaware of prediabetes. Over the past decades, there has been considerable debate about whether prediabetes and metabolic syndrome are associated with peripheral polyneuropathy. This review and the accompanying case report examine current data confirming the increased risk of distal polyneuropathy in individuals with prediabetes and metabolic syndrome. Diagnosis and assessment of the severity of peripheral polyneuropathy in individuals with prediabetes and metabolic syndrome are primarily based on clinical assessments of neuropathy and electrophysiological studies. The data presented should help raise awareness and translate current knowledge about peripheral neuropathies in people with prediabetes and metabolic syndrome into clinical practice. The current recommendation that over-weight or obese adults be screened for prediabetes and metabolic syndrome and offered or referred preventive interventions should ultimately lead to the prevention of peripheral neuropathy. Treatment includes lifestyle modification, pharmacotherapy aimed at pathogenesis, symptomatic treatment of neuropathic pain and prevention of complications.

Introduction. Effectiveness and safety of satralizumab in the treatment of neuromyelitis optica spectrum disorders (NMOSD) have been demonstrated in randomized clinical trials and continue to be evaluated in the real clinical practice (RCP).

Aim. To analyze the experience of satralizumab administration in Russian patients with NMOSD in the RCP.

Materials and methods. The study was a multicenter retrospective. Analyzed data were taken from outpatient charts/medical records. Baseline clinical and demographic characteristics of patients with results on efficacy and safety of satralizumab treatment were assessed.

Results. Data of 71 patients with ages ranging from 12 to 69 years at the start of satralizumab treatment were analyzed. 100% of patients had NMOSD with antibodies to aquaporin-4. At baseline 18.3% of patients were with highly active NMOSD by exacerbation frequency, 69% had previous relapse preventive treatment, 41% received low-dose glucocorticoids. The annualized relapse rate (ARR) during previous 2 years before treatment was 1.26. The median duration of satralizumab therapy was 15 [12; 24.5] months. 58 (82%) patients were relapse-free and included 9 (16%) persons with highly active NMOSD. The ARR decreased to 0.11 over 2 years of therapy (p < 0.001). In 8 (62%) of 13 patients with relapses first attack developed before 6 months of treatment and in 6 (46.2%) cases – during the “clustered period”, 11 (84.6%) patients did not receive low doses glucocorticoids or they were discontinued before 6 months of satralizumab therapy. Adverse events were reported in 19 (26.8%) patients. The neutropenia was the most common. 27 (84.4%) of 32 patients switched from rituximab to satralizumab were relapse-free with a favorable safety.

Conclusions. The analysis of the experience on the satralizumab administration in the RCP demonstrated efficacy and favorable safety profile in Russian patients with NMOSD with antibodies to aquaporin-4 aged 12 years and older.

GM1 gangliosidosis is a rare autosomal recessive hereditary disorder caused by mutations in the GLB1 gene. The deficient activity of the enzyme β-galactosidase leads to the pathological accumulation of GM1 ganglioside, primarily in the cells of the central nervous system and visceral organs, resulting in progressive neurodegeneration and systemic symptoms. The clinical presentation is highly heterogeneous and can include neurological deterioration, epilepsy, skeletal abnormalities, facial dysmorphism, organomegaly, and ophthalmological manifestations. This clinical polymorphism, along with the variable age of onset and the differing degrees of neurological and systemic involvement, is attributed to the specific mutations and their impact on the residual enzyme activity. Based on this, three types of GM1 gangliosidosis are distinguished: the infantile, juvenile, and late-onset forms. This article reviews current knowledge on the etiology, biochemical defects, pathogenesis, and clinical manifestations of GM1 gangliosidosis. It also analyzes novel potential therapeutic approaches for patients, with insights from animal model studies. While no effective cure for GM1 gangliosidosis currently exists, several strategies show significant promise. The most advanced therapeutic approaches include enzyme replacement therapy, substrate reduction therapy, chaperone therapy, hematopoietic stem cell transplantation, and gene therapy using adeno-associated viral vectors, some of which have already progressed to clinical trials.

Asthenic disorder in children and adolescents is a polyetiological condition characterized by a varied clinical picture with the dominant complaint of increased fatigue and rapid exhaustion, both mental and physical, which are persistent and last for a long period of time. It is reported that medical aid appealability rates due to asthenic symptoms achieve up to 64%. The prevalence of asthenic disorder in children and adolescents is extremely difficult to determine, as the numerous clinical symptoms are often viewed within the context of other diseases rather than as a single, hallmark pathology. The development of this condition is driven by challenging-to-differentiate functional and organic disorders that arise secondary to other, diverse pathologies. Dysfunction of the reticular activating system (RAS) is one of the primary mechanisms underlying asthenic syndrome. Severe manifestations of asthenic disorder which result in the significant impairment of daily activities and considerable deterioration of the patient's quality of life for more than 6 months are considered as a separate nosological entity — chronic fatigue syndrome (CFS). Genes regulating the hypothalamic-pituitary-adrenal (HPA) axis that is the body's main way of responding to stress are believed to be involved in the development of CFS. A single component failure can disrupt the entire system and contribute to the development of increased fatigue. Asthenic disorders are one of the common symptoms in patients who have suffered a traumatic brain injury (TBI). N-acetylaspartate (NAA) is seen as one of the markers of nerve tissue damage and repair in traumatic brain injury. Research on the role of NAA in the development of asthenic disorders is of great interest. Brain magnetic resonance spectroscopy (MRS) has found specific neurochemical abnormalities that can potentially be treated with agents targeting metabolic disturbances identified in the central nervous system. The search for new physiological and biochemical markers of asthenic syndrome will expand our understanding of the pathogenesis and treatment options for these disorders.

A comprehensive, multimodal, patient-centered approach to the treatment of osteoarthritis (OA) using non-pharmacological and pharmacological treatments can significantly improve the disease course and outcomes. Pathogenetically based introduction of new drugs and medications into therapy, as well as expanded indications for well-studied and safe medications, allow for an expanded arsenal of medications for the treatment of OA. Extensive experience has been accumulated over more than 30 years using preparations containing bioactive small marine fish concentrate (SMFC). In the Russian Register of Medicines (RLS), injectable SMFCs are included in the clinical-pharmacological group of tissue reparation stimulators of natural origin and are classified as “bone and cartilage metabolism correctors” or “other drugs for the treatment of musculoskeletal diseases”. SMFCs are intended to reduce pain and achieve a structure-modifying effect with long-term use. Intramuscular and intraarticular administration of CMMRs increase bioavailability, reduce the frequency of drug administration, and ensure a rapid onset of effect. Thanks to the high-quality evidence accumulated during clinical trials investigating the safety and efficacy of CMMRs for knee, hip, and small joint OA, as well as nonspecific low back pain (NLP), it became possible to include CMMRs in the Clinical Guidelines for Polyarthrosis (Generalized Osteoarthritis), approved in late 2025 and valid through 2027. This article provides a brief overview of the key clinical studies that served as the rationale for including CMMRs in the clinical guidelines, as well as key materials on a recently registered Russian drug from the CMMR group. A literature search was conducted in eLibrary.ru for the period from 2020 to 2025. The search string included “CMMR” or trade names of drugs present in the abstract, article title, keywords, or full text of the publication, with the requirement that the full text of the article be available on eLibrary.ru. A total of 98 references were identified, including six duplicates in both lists. Analysis of 92 sources revealed that 39 presented clinical trial results, 13 described clinical cases, and 40 contained clinical reviews, meeting resolutions, or expert consensus statements on the use of CMMR.

Introduction. Inadequate dietary calcium intakes and poor vitamin D status are common findings in population living in Russia, which can be a cause of excessive bone mass loss and falls.

Aim. To study the efficacy and safety of different dosage forms of a dietary supplement containing ossein-hydroxyapatite complex (OHC) and vitamin D (CigaPan® OSTEO/CigaPan® OSTEO Forte) and compare their ease of use in postmenopausal women with osteopenia.

Materials and methods. A total of 28 postmenopausal women with osteopenia were examined. In this study, we assessed the following clinical parameters — VAS back pain scores, skeletal muscle strength and function, and levels of phosphorus-calcium metabolism and bone remodelling markers.

Results. In women receiving the dietary supplement for a 3-month period, back pain was found to significantly decrease according to the VAS from 60 [50; 60] mm to 23 [0; 50] mm (p < 0.05) in the thoracic spine and from 43 [35; 70] mm to 18 [0; 38] mm (p < 0.01) in the lumbar spine. The time needed to complete the time-up-and-go test decreased from 9.5 ± 4.1 sec to 8.3 ± 4.4 sec (p < 0.001). Biochemical test results were within normal reference ranges throughout the observation period. Osteocalcin levels were reported to increase significantly by 11%, whereas collagen type Ia C-terminal telopeptide levels decreased by 15% (p < 0.05). Three patients discontinued the supplement due to gastrointestinal adverse events.

Conclusion. The dietary OHC and vitamin D supplement was safe and well-tolerated, improved skeletal muscle function, and had beneficial effects on bone metabolism. It can be used as an additional source of calcium, phosphorus, and vitamin D in postmenopausal women.

In recent decades, there has been clear progress in rheumatology related to the introduction of genetically engineered biological disease-modifying antirheumatic drugs (bDMARDs) and targeted disease-modifying antirheumatic drugs (tDMARDs) into practice. At the same time, the use of these drugs is associated with an increasing risk of developing infections of a diverse nature and localization, including opportunistic ones, as well as an increased risk of reactivation of latent infection, primarily tuberculosis (TB). In addition, cases of severe infections (pneumonia, sepsis, bacterial arthritis, skin and soft tissue lesions, etc.), including fatal ones, have been reported. To date, the mechanisms underlying the increasing risk of infectious complications associated with the use of b/tDMARDs have not been fully recognized. Within the framework of this narrative (non-systematic) review, modern data on the frequency and localization of major infections in rheumatological patients treated with various b/tDMARDs are presented. The need for wider use of immunization with various vaccines (primarily against influenza and pneumococcal infection) in patients with immuno-inflammatory rheumatic diseases is emphasized. In preparing the review, the authors conducted an exhaustive literature search (mainly in English) in MEDLINE databases (via PubMed) for the following keywords: “biologics/rheumatic diseases AND infection”, “tumor necrosis factor-α antagonists/rheumatic diseases AND infection”, “targeted synthetic disease modifying antirheumatic drugs/rheumatic diseases AND infection” with preferential selection of national and international registers, systematic reviews and meta-analyses. The materials of two major annual international rheumatological forums held under the auspices of the European Alliance of Rheumatology Associations (EULAR) and the American College of Rheumatology (ACR) were also reviewed. After eliminating duplicate materials, 168 relevant sources were selected for further analysis.

This article presents four clinical observations of patients who underwent 14-day personalized rehabilitation activities. All patients complained of upper extremity weakness and pain on shoulder movement. The first patient received various physical rehabilitation treatments which allowed to improve a range of motion: shoulder flexion angle increased from 100° to 110°, abduction angle from 90° to 100°, and scores for the Fugl-Meyer assessment of the upper extremity (FMA-UE) increased from 11 to 14 and for FMA-LE from 15 to 19 points. In the second patient, who received physical rehabilitation combined with kinesio taping and muscle relaxant therapy, pain intensity in the right shoulder joint on VAS reduced from 7 to 5 points; flexion angle increased from 100° to 110°, abduction angle from 80° to 90°; and scores for FMA-UE increased from 7 to 8 and for FMA-LE from 2 to 27. In the third patient, physical rehabilitation care combined with botulinum toxin therapy resulted in a reduction of left shoulder joint pain on the VAS from 8–9 to 4 points, an increase in flexion angle from 60° to 90°, abduction angle from 30° to 45°, and an increase in the FMA-LE scores from 8 to 9 points. In the fourth patient, the combination of physical rehabilitation, botulinum toxin injections, and kinesiology taping allowed to achieve a reduction of left shoulder joint pain on the VAS from 8–9 to 4 points, an increase in flexion angle from 60° to 90°, abduction angle from 30° to 45°, and an increase in the FMA-LE scores from 8 to 9 points. All patients accomplished their treatment goals at the end of the rehabilitation course.