Cryptogenic stroke (CS) is defined as a subtype of stroke associated with a heterogeneous group of pathogenetic mechanisms that remained undetermined in the course of advanced diagnostic research. One third or fourth of the ischemic strokes is cryptogenic. Paradoxical embolism is considered the important cause of cryptogenic stroke and transient ischaemic attack (TIA) in young patients. It may occur via the following: patent foramen ovale (PFO), atrial septal defect (ASD), and pulmonary arteriovenous malformation (PAVM). When interviewing patients with suspected paradoxical embolism to obtain their health history, a practitioner should consider factors associated with Valsalva maneuvers, deep vein thrombosis/PE or predisposing conditions or situations, as well as symptoms of hereditary hemorrhagic telangiectasia (telangiectasia of the skin and mucous membranes, hemorrhagic syndrome) and pulmonary arteriovenous malformations (PAVMs) (shortness of breath, hemoptysis). If paradoxical embolism is suspected, it is necessary to conduct a stepwise diagnostic search, including transcranial Doppler ultrasound with bubble test, contrast-enhanced transesophageal echocardiography, and CT angiopulmonography. Diagnosis of relevant clinical conditions involves a search of atrial tachyarrhythmias, deep vein thrombosis, and thrombophilia. As the pathogenetic role of ASD and PAVMs in the development of embolic cryptogenic stroke is beyond doubt, the clinical significance of PFO should be determined taking into account several factors, including the presence of deep vein thrombosis/PE, the severity of the right-left shunt, the presence of ASD, the RoPE score, and detection of thrombophilia. The secondary prevention techniques of ischemic stroke or TIA with underlying PFO should be selected on a case-by-case basis, depending on the clinical significance of the anomaly, comorbid pathology, life expectancy of the patient: endovascular occlusion, anticoagulant or antiplatelet therapy. The secondary prevention with underlying ASD and LAVM includes surgical techniques such as endovascular occlusion or open surgery followed by monitoring of their effectiveness.

Ménière’s disease (MD) is an idiopathic inner ear disease, which is characterized by noise in the ears, periodic attacks of vertigo and the development of sensorineural hearing loss. MD is characterized by endolymphatic hydrops – an increase in the volume of endolymph that fills the membered labyrinth of the inner ear. Currently highlighted subtypes MD. The first subtype meets most often and is characterized by classical manifestations of MD. The second subtype is characterized by the development of sensorineural hearing loss, to which only after a long time are joined by the episodes of dizziness. The third subtype of MD includes family cases of the disease. The fourth and fifth subtypes of MD is observed in patients with migraine and autoimmune diseases. The diagnosis of definite MD is based on the 2 or more spontaneous episodes of vertigo with each lasting 20 minutes to 12 hours, low-to medium-frequency sensorineural hearing loss in one ear, fluctuating aural symptoms (fullness, hearing, tinnitus) located in the affected ear, and lack of data for other reasons for dizziness. There are no effective treatment for auditory disorders MD, therapy is aimed at preventing dizziness attacks. The first line of MD’s therapy includes a dietary salt restriction, the use of betahistine and diuretics. Betahistine (Betaserc) is usually used in a daily dose of 48 mg for 3–6 months to reduce the frequency of vertigo. For long-term treatment, it is convenient to use a betahistine modified-released (Betaserc Long) 48 mg, taken once a day. With the ineffectiveness of conservative therapy, other methods of therapy are possible: intratympanic administration of corticosteroids or gentamicin, labyrinthectomy or vestibular neurectomy. Unfortunately, many patients suffering from BM mistakenly makes a diagnosis of cerebrovascular disease, vertebrobasilar insufficiency, cervical osteochondrosis. Diagnostic errors are usually caused by the fact that the patients with MD are not conducted audiometry, vestibular tests, and the signs of cerebral microangiopathy identified when MRI brain are mistakenly regarded as confirmation of vascular dizziness genesis.

Dipyridamole has been on the pharmaceutical market since 1959 and, as a pyrimidyl-pyrimidine compound, has a variety of mechanisms of action. The very first action of dipyridamole was its antianginal effect. In subsequent years, attention was drawn to the antiplatelet properties of dipyridamole, which are related to inhibition of platelet phosphodiesterase as well as to blocking adenosine transport. Another important property of dipyridamole is its effect on the deformability of red blood cells, thereby improving microcirculation. Dipyridamole affects changes in the dynamics of platelet activity and vascular reactivity and causes improvement of cerebral perfusion. Due to its pronounced antiplatelet properties, the drug has been widely studied for the prevention of ischemic strokes and transient ischemic attacks, both as monotherapy and in combination with other drugs. Unlike other platelet antiaggregants, dipyridamole does not have a damaging effect on mucous membranes. Its antiplatelet effect is not accompanied with inhibition of cyclooxygenase activity and reduction of prostacyclin synthesis. In the treatment of cerebral circulation disorders, dipyridamole can be used to control the antithrombotic effect by selecting the optimal dose of the drug. Dipyridamole has antioxidant properties, enhances NO-mediated pathways, has indirect anti-inflammatory effects via adenosine and prostaglandin-2 as well as direct anti-inflammatory effects and several other effects. Dipyridamole is considered a safe drug based on decades of clinical experience. Its side effects are usually limited and transient. Given the diverse effects of dipyridamole, it can be used for a wide range of pathologies other than thrombosis prevention. Data on the efficacy and safety of dipyridamole in various diseases of the neurological spectrum are presented.

Introduction. The present study analyzed the possibility of using neuropsychological tests to assess postoperative cognitive dysfunction. New data were obtained: in the postoperative period, hippocampal memory impairments predominate in patients, which makes it expedient to use methods for diagnosing primary modal-nonspecific memory disorders in patients who are to undergo neurosurgical intervention on the spinal cord.

The aim of the study to evaluate the influence of surgery with anesthesia on the cognitive functions of middle-age patients.

Materials and methods. The study included 20 middle-aged patients. All patients had to undergo spinal surgery. Patients received total intravenous anesthesia with propofol induction (4–12 mg/kg/hr). Cognitive functions before and after the operation were made with the use of the MoCA, TMT A and B, FCSRT, state-trait anxiety inventory test (STAI).

Results. The development of POCD was noted in 15% of cases. The patients showed a decrease in the FCSRT prompt index (1st day = 87 ± 9.0; 2nd day = 83 ± 15; p = 0,0005), while the overall severity of cognitive impairments (total score of MoCA) did not change significantly (standard deviation according to MoCA: 24.25 ± 2.86 on day 1 and 24 ± 3.24 on the second day, p = 0.61). The RT level decreased by day 2: 44.65 ± 7.4 versus 41.1 ± 8.2 (p = 0.001). Correlation analysis did not show the relationship between the age of patients, education level, comorbidity and development of POCD; however, the duration of anesthesia was associated with a decrease in MoCA scores (Pearson’s correlation coefficient r = –0.44; p = 0.050).

Conclusion. Thus, our study shows that the study of hippocampal memory impairments is important in patients with POCD. These data differ from the data of researchers presented earlier, where the most important clinical manifestations of POCD are considered to be a decrease in attention and speed of mental processes. Of course, the small sample size dictates the need for additional research.

Currently, cognitive impairment is a determining factor in the decline in adaptation in the elderly. Damage to the cerebral vessels is one of the most common causes of the development of cognitive deficits. Patients with severe cognitive impairments are not easily treatable, require outside help, and have significant limitations in daily activities. In most cases, this stage is preceded by a period of mild cognitive impairment. As a rule, mild cognitive impairments often remain undiagnosed, since they do not cause restrictions in daily activities for a long time and are detected only thanks to highly specific neuropsychological tests. But it is precisely the timely diagnosis and treatment of cognitive impairment without dementia, that make it possible to achieve longterm remission of the disease, to delay the onset of pronounced cognitive deficit. Among the correction methods, non-drug methods and pharmacological therapy are distinguished. Of no small importance is the impact on vascular risk factors such as arterial hypertension, diabetes mellitus, hyperlipidemia, smoking, alcohol abuse, etc. Nutrition planning, dosed exercise and cognitive training are the most common non-pharmacological strategies for correcting cognitive impairment. Pharmacological treatment includes anticholinesterase and neurometabolic drugs, as well as drugs aimed at correcting risk factors. A growing number of researchers agree that complex therapy, including lifestyle modification and the use of pharmacotherapy, is preferable. The article discusses the most commonly used methods of treating non-demented cognitive impairments, presents the results of large randomized clinical trials devoted to this problem, presents our own experience of both exclusively non-drug effects on patients and the use of complex treatment using a neurometabolic drug.

Introduction. Kinesitherapy (KT) – one of the leading areas of patient care with chronic nonspecific (musculoskeletal pain) low back pain. For chronic lumbar pain, a standard KT is commonly used, that includes group sessions with a medical specialist. Often not taking into account the individual characteristics of patients, their attitude to KT, does not use a backpain education program in combination with KT (extended KT). Physical activity and hypodynamia are compared in patients with chronic nonspecificlow back pain in standard KT and extended KT.

Aim of study is to assess the effectiveness of the standard and extended KT in the enhancement of physical activity.

Materials and methods. 71 patients were observed (17 men and 54 women, average age 55.09 ± 13 years) with chronic nonspecific low back pain. Patients received non-steroidal anti-inflammatory drugs (NSAIDs) as painkillers. 34 patients received a standard KT, 37 patients – an extended KT. Patients were asked to complete the Numeric Pain Rating Scale (NPRS), the Oswestry Low Back Pain Disability Questionnaire, and the International Physical Activity Questionnaire (IPAQ) at baseline, after 7 days and 90 days.

Results and discussion. In the extended KT group, physical activity increased from 11 (7–16) points to 16 (13–19) points after 7 days (p = 0.001) and up to 23 (15–26) points after 3 months (p = 0.0002). There has been a statistically significant decrease in the proportion of patients with hypodynamy (p = 0.0015). There is no statistically significant increase in physical activity in the standard therapy group. The use of NSAIDs in non-specific low back pain is discussed, the effectiveness of the use of dexketoprofen (Dexalgin) during lumbar pain is noted.

Conclusion. In the case of nonspecific low back pain, the extended KTimprovesphysical activity and reduce hypodynamy.

Chronic pain continues to remain one of the urgent problems of modern medicine. From 15 to 25% of the adult population suffers from chronic pain. Medical treatment includes the appointment of non-steroidal anti-inflammatory drugs (NSAIDs) and muscle relaxants. The greatestform for the appointment of NSAIDs is the topical form. According to the recommendations of International and National societies for the treatment of pain syndrome, osteoarthritis (OA) therapy are recommended to start with topical NSAIDs, as drugs with less systemic adverse side effects (NSAIDs).Topical NSAIDs have proven analgesic and antiinflammatory efficacy in the treatment of diseases of the musculoskeletal system, musculoskeletal pain, but have a low risk of developing systemic NSAIDs in comparison with oral forms, which expands the possibilities of their appointment in patients with comorbid pathology (diseases of the gastrointestinal tract, cardiovascular risks).Among NSAIDs, diclofenac is the "gold standard" of analgesia. After topical application, diclofenac penetrates through the skin and further into the deeper underlying tissues while maintaining sufficient concentration to provide a therapeutic effect. The topical form of diclofenac – diclofenac diethylamine 2%, when used correctly, can cause an analgesic effect comparable to the oral form. This topical form has a high clinical efficacy in the treatment of acute musculoskeletal pain (sprains), the course of therapy takes 1 week, for chronic pain syndromes (knee OA or hand) the course of therapy is from 2 to less than 6 weeks. The clinical efficacy of diclofenac diethylamine monotherapy is comparable to that for complex therapy in combination with oral forms of NSAIDs, while having good tolerability.

Back and neck pain is widespread in the population. Preferably, patients of working age are sick, which leads to serious economic losses. The transition of pain from acute to chronic increases financial costs, so effective treatment of back pain is an important medical, social and economic problem. Musculoskeletal pain (MSP) prevails among all types of back pain. The source of the MSP can be various structures of the musculoskeletal system: bones, joints, muscles, fascia, tendons, ligaments, intervertebral discs. The provoking factors for the development of the MSP are static and dynamic overloads arising from physical work, long stay in a fixed posture, unprepared movements, hypothermia, vibrations. The leading diagnostic method for the MSP is a physical research of a patient which includes a detailed collection of complaints and anamnesis, inspection in statics and dynamics, carrying out global and special tests, neuroorthopedic and neurological research. In most cases, the analysis of the results obtained allows you to set a clinical diagnosis without appointing additional research methods. Two cases of acute MSP with different localization, clinical manifestations and flow are offered to the discussion. In the first case, the process was localized in the muscles of the law back. In the second patient, the muscular tonic syndrome developed in the muscles of the neck and shoulder belt and was supported by functional blockades of the vertebral motor segments. For the treatment of both patients, NSAID, muscle relaxant, glucocorticoid, as well as non-drug therapy methods were used. For local injection therapy, a drug group of glucocorticoids was used, having a sodium phosphate and betamethazone dipropionate as part of the sodium betamethasone. The combination of two betamethazone salts provides both the rapid and prolonged effect of the drug, which makes it reasonable to use it with acute musculoskeletal pain.

Dizziness is one of the most frequent complaints of patients in daily clinical practice. The prevalence of vertigo increases significantly in older patients. In most cases, vertigo is caused by pathology of the peripheral vestibular system: benign paroxysmal positional vertigo, vestibular neuronitis, Meniere’s disease. Episodes of recurrent vestibular vertigo without hearing loss can be associated with vestibular migraine, a diagnosis of which remains low in our country. Modern treatment regimens have been developed for patients with various causes of vertigo and unsteadiness. High effectiveness is achieved with a comprehensive approach to the management of patients with vertigo, which includes vestibular exercises, psychological training, and medications that help to reduce the severity and frequency of vertigo attacks and improve vestibular compensation. Many studies have shown high efficacy of the low-dose combination drug cinnarizine 20 mg + dimenhydrinate 40 mg for the treatment of peripheral and central vertigo, which is well tolerated and does not delay vestibular compensation. The efficacy of the low-dose combination drug cinnarizine + dimenhydrinate and betahistine dihydrochloride was compared in the treatment of patients with unilateral vestibular neuronitis, Meniere’s disease, and other diseases of the peripheral and central vestibular system. Studies have shown no less efficacy of the combined drug cinnarizine + dimenhydrinate in the treatment of Meniere’s disease than of betahistine, a more pronounced improvement in vestibular function in the treatment of vestibular neuronitis with the combined drug than with betahistine. For patients with peripheral vestibulopathy of various etiologies, treatment with the combination drug was more effective than therapy with betahistine.

Trigeminal autonomic cephalalgias (TACs) are rare but are the most intense primary headaches that severely limit patients’ ability to work and be socially active. This article reviews the modern classification of TACs, based on the International Classification of Headache Disorders-3, and the key differences between TAC types, as well as the pathophysiological mechanisms – the role of the trigeminovascular system, autonomic nervous system, hypothalamus and vagus nerve – and their relation to circadian rhythms. The sleep disturbances that can occur in patients with TACs, exacerbating the course of the disease, and the role of melatonin, hypothalamus and suprachiasmatic nucleus in these conditions are also discussed. In addition, current therapies for cluster headache are described, which include acute therapy and prophylactic therapy, with recommendations regarding the timing of prophylactic therapy discontinuation. The review also includes the available data on melatonin as well as new therapies such as CGRP monoclonal antibodies and neuromodulation, which includes the two most promising techniques: non-invasive vagus nerve stimulation and sphenopalatine ganglion microstimulation. Furthermore, the authors present the clinical case of a patient with chronic cluster headache, which was significantly reduced in frequency and intensity when melatonin was added to the therapy.

Drug-induced parkinsonism (DIP) is one of the most frequent extrapyramidal disorders that develops against the background of prescribing a large number of medications. Initially, DIP was described as an adverse drug reactions (ADRs) against the background of the use of antipsychotic drugs, but later recognized as ADRs of a number of other drugs, including prokinetics, antidepressants, calcium channel blockers and antiepileptic drugs. The relative risk of developing LIP on the background of taking typical antipsychotics increased by 2.92 times compared to patients who do not take these drugs. The risk of developing DIP in patients receiving flunarizine is increased by 2.75-4.07 times. The risk of DIP with the use of antidepressants is increased by 2.14 times, among the drugs of this group with an increased risk of DIP, the use of selective serotonin reuptake inhibitors is most often associated with DIP (relative risk 1.24). Among other antidepressants, there is evidence of the development of DIP against the background of the use of duloxetine, mirtazapine, amitriptyll clomipramine, venlafaxine, trazodone. Among anticonvulsants, DIP can rarely develop against the background of the appointment of valproic acid, gabapentin, pregabalin, carbamazepine, oxcarbazepine. The risk of DIP in patients receiving metoclopramide is extremely low (0.06%), but it is 2.16 times higher compared to people who do not take this drug. Among drugs from other groups, DIP can occur against the background of the use of lithium carbonate, tacrolimus, cyclosporine, amiodarone, captopril, amphotericin B. If DIP develops, it is necessary, if possible, to reduce the dose or cancel the inducer drug, or replace it with another drug with minimal risk of DIP. Symptoms of DIP most often regress within a few weeks or months after dose reduction or withdrawal of the drug inducer. If the symptoms persist longer, it is necessary to exclude the presence of Parkinson’s disease or dementia with with Lewy bodies.

Introduction. Carpal tunnel syndrome (CTS) is a neurological disease associated with tunnel mononeuropathies. There are various proven treatment regimens for patients with the use of conservative and surgical methods of treatment. Studies devoted to a comparative analysis of the effectiveness of methods of conservative therapy in patients with CTS are not enough to choose a treatment strategy.

Purpose of the study. To study the therapeutic efficacy of wearing a wrist orthosis with and without the use of NSAIDs in the treatment of patients with CTS.

Materials and methods. The study involved 40 patients (the average age of the participants was 32.8 ± 4.3 years) with a primary diagnosis of CTS, who were admitted to the neurological department of of the St Petersburg State Budgetary Healthcare Institution “Elizavetinskaya Hospital”, the Department of Medical Rehabilitation of St. Petersburg State Budgetary Healthcare Institution “St. Luke’s Clinical Hospital” in the period from 2017 to 2021. Patients were randomized into two comparable groups for complex conservative treatment and observation for 2 months of the dynamics of neurological symptoms, pain scale, QuickDASH questionnaire and neurophysiological parameters. The first group of patients received NSAIDs (Nimesil), 1 sachet (100 mg of nimesulide) twice a day after meals for 4 weeks, and the second group – NSAIDs with the imposition of a wrist orthosis for 4 weeks.

Results. The study involved 40 patients. The average age of the participants was 32.8 ± 4.3 years (range from 20 to 48 years). Neurophysiological indicators in the studied groups at the screening stage were comparable: distal latency of the M-response (DLMO), ms; the amplitude of the negative peak of the M-response, mV; sensory latency (SL), ms and sensory impulse conduction velocity (SSPI), m / s: 5.7, 5.3, 3.5 and 31.8 in the first group and 5.4, 5.5, 3.8 and 32.4 in the second group (p > 0.05 when comparing the corresponding parameters). After the course of treatment, significant changes in the analyzed parameters were revealed (p < 0.05).

Conclusions. In patients who received nimesulide and wore a wrist brace, the effectiveness of treatment was higher.

Patients with COVID-19 may develop various neurological disorders of the central and peripheral nervous systems. It is known that diabetes mellitus (DM) type 1 or 2, cardiovascular diseases, obesity, old age and old age, male gender are risk factors for a severe course and complications of COVID-19. Currently, the COVID-19 pandemic is ongoing, and patients with the listed risk factors are recommended to follow a regime of social restriction or self-isolation. Outpatient treatment is most appropriate for this category of patients. Patients with diabetes who have undergone COVID-19 are at risk of developing or progressing diabetic polyneuropathy (DPN). It seems relevant to develop the principles of effective treatment of patients with DM and DPN in outpatient settings. Glycemic level correction, diet, weight normalization, therapy of combined cardiovascular diseases, an increase of physical activity, sleep normalization, maintenance of normal psychological state are the main principles of treatment of patients with DM and DPN in COVID-19 pandemic conditions. Pathogenetic therapy of DPN continues to be discussed, in our country the preparations of B vitamins, alpha-lipoic acid are widely used. B-group vitamin preparations can be used in the form of tablets or solutions for intramuscular injections. The effectiveness of B vitamins (B1, B6, B12) in the treatment of a severe course of COVID- 19, prevention of complications of COVID-19, especially in elderly patients and with diabetes is discussed.

Polyneuropathies are diseases of the peripheral nervous system with lesions of motor, sensory or autonomic fibers which are encountered by attending physicians of almost all specialties in outpatient and clinical settings. To date, more than 100 different causes of polyneuropathies have been identified. Metabolic and toxic polyneuropathies are the most common in the group of secondary polyneuropathies. Diabetic, alcoholic, uremic, and drug-induced polyneuropathies take the leading place among these diseases. The main forms of diabetic polyneuropathy are presented. The main clinical form is distal symmetrical polyneuropathy. Clinical symptoms depend on the type of fibers involved in the pathological process - thin or thick. There is an assessment scale in points to determine the severity of diabetic polyneuropathy, which helps in clarifying the diagnosis and prognosis of the disease. The next most frequent among metabolic polyneuropathies is uremic polyneuropathy as the most frequent complication in patients suffering from chronic renal insufficiency. Risk factors of uremic polyneuropathy development, clinical picture, the course of the disease are described. Within the framework of toxic polyneuropathies, the main place is given to alcoholic polyneuropathies, chemotherapy-induced, and drug-induced. For each of these categories, clinical forms and pathophysiology of development are described. For all polyneuropathies, the main diagnostic aspects are presented. The main therapeutic approaches are shown. A separate place is given to the use of alpha-lipoic acid.

The need to review the guidelines for the management of patients with multiple sclerosis using multiple sclerosis disease modifying drugs has become acute enough since the beginning of 2020 following the outbreak of the COVID-19 pandemic caused by a novel coronavirus SARS-CoV-2. Immunosuppressive drugs were also specifically addressed, as it is during administration of these drugs that the more severe course of COVID-19 disease was expected. Both the Russian and foreign teams published results of their research works. This article presents a retrospective analysis of the incidence rates of COVID-19 in patients with multiple sclerosis after selective immunosuppressive therapy with alemtuzumab and a clinical case when a patient was infected with coronavirus in the first days following the last infusion of the therapy course without clinical manifestations of the infectious disease. The author discusses the mechanisms underlying such a favourable outcome due to the CD52 lymphocyte depletion leading to the reduction of risks of developing hyperimmune reactions that underlie severe complications of COVID-19, and analyses previously published works of our foreign colleagues on the same theme. The review of the accumulated works and personal experience suggest that it is the CD52 lymphocyte depletion that makes it possible to avoid the cytokine storm and, as a result, the more severe course of COVID-19. Amidst the COVID-19 pandemic, during the prescription of multiple sclerosis disease modifying drugs, it should be borne in mind that patients should have access to all types of modern therapy and that the benefits should outweigh the sum of possible risks.

The article presents modern recommendations for the use of systemic administration of glucocorticoids. It is indicated that there is a clear tendency to minimize the doses and timing of the appointment of systemic glucocorticoids in rheumatoid arthritis, and in seronegative spondyloarthropathies (ankylosing spondylitis, psoriatic arthritis), in accordance with both foreign and domestic recommendations, systemic therapy with glucocorticoids is not carried out. It is emphasized that at the present stage, the role of local administration of glucocorticoids will increase as an effective way to reduce the activity of arthritis in any nosologically form. The mechanisms of action of locally administered glucocorticoids leading to anti-inflammatory and analgesic effects are described. The comparative characteristics of locally administered glucocorticoids with different duration of action according to their effectiveness and safety are presented. Predictors of the effectiveness of local therapy with glucocorticoids are described. The data on the evaluation of the duration of the anti-inflammatory and analgesic effects of various local glucocorticoids, including in comparison with the intra-articular administration of hyaluronic acid preparations, which showed the advantages of betamethasone over triamcinolone acetate, are presented. The differences in the crystal structure of betamethasone and triamcinolone acetate are described. It is indicated that the 2.5-fold smaller size of betamethasone crystals compared to triamcinolone acetate crystals and the absence of betamethasone crystals makes it possible to use betamethasone in the treatment of inflammatory processes in periarticular tissues, as well as in crystalline arthritis (gout, pseudogout). The data on the safety of the use of intra-articular injection of glucocorticoids are presented. It is indicated that the registration in the Russian Federation of a new form of betamethasone in pre-filled syringes makes it even more possible to avoid infectious complications of this type of therapy. Rare cases of complications of local therapy with glucocorticoids are described.

Introduction. To date, there is no consensus regarding the gender characteristics of the course of gout. There is little data on the possible difference between men and women in response to uric acid-lowering therapy.

Aim. To compare the clinical characteristics of the course of gout and evaluate the differences in response to urate-lowering therapy (ULT) with allopurinol and febuxostat in men and women.

Material and methods. The retrospective cohort study included 279 men and 83 women diagnosed with gout (ACR/EULAR, 2015). The comparative analysis of the clinical characteristics of gout, as well as responses to the intake of xanthioxidase (XO) inhibitors in representatives of different sexes, was carried out. We compared the gender characteristics of obtaining a positive response to ULT, defined as achieving a target serum uric acid (sUA) level of < 360 μmol / l within 6 months of treatment, while taking allopurinol and febuxostat.

Results. By the age at which the onset of gout took place, women were older than men, the duration of the disease in them was shorter. Men showed a shorter duration of the first attack of arthritis. Chronic arthritis was diagnosed in 56% of men and 35% of women (p < 0.05). The process involved the joints of both the lower and upper extremities. However, more often the joints of the lower extremities were affected in men, and in the upper extremities in women. Tophus were detected in 35% of patients, of whom 30.3% were men, 4.7% were women (p < 0.05). Allopurinol was prescribed to 216 men and 54 women, and febuxostat was prescribed to 63 men and 29 women. After six months, the proportion of women who achieved the target sUA was 57.5% and 65.8%, the proportion of men – 60.4% and 76.2% for allopurinol and febuxostat, respectively.

Conclusion. The clinical manifestations of gout in men and women differ. Due to the pronounced increase in the level of uric acid, men develop more severe joint damage due to the tendency to chronicity. However, the study did not reveal gender differences in the response to XO inhibitors, which indicates that there is no need to choose therapy depending on the patient’s gender.

Introduction. Osteoporosis is a common complication of rheumatoid arthritis. Its development is associated with the mechanisms underlying in the progression of autoimmune inflammatory diseases and therapeutic approaches used for them. The study of risk factors for osteoporosis can contribute to the clarification of its pathogenesis components, as well as the development of new methods for prevention, diagnosis and treatment of this condition.

Aim. To study the role of anamnestic, clinical and laboratory factors for secondary osteoporosis in women with rheumatoid arthritis.

Materials and methods. 102 women with rheumatoid arthritis were enrolled in our study. Exclusion criterias were type 2 diabetes mellitus, hepatic cirrhosis, hepatocarcinoma and level of alanine aminotransferase ≥ than 3 upper limit ofnormal. The cumulative dose, duration and daily dose of glucocorticoids (GC) were determined by patient intake. All patients undergone standard clinical and immunological examination. Serum fetuin-A, 25-hydroxycalciferol, C-telopeptide of collagen I type, N-terminal propeptide of collagen I type levels were determined using ELISA. X-ray of afflicted joints and dual-energy x-ray absorptiometry were performed. Statistical analysis was performed using conventional methods. Forced data entry was used to perform multiple logistic regression. Hereinafter data is presented as odds ratio (OR) and 95% confirmation intervals (CI).

Results. OR for osteoporosis were higher in women of age ≥ 58.5 years (OR 1,07 (1.02–1.12)), body mass index (BMI) ≤ 27 kg/m2 (OR 1.1 (1.01–1.2)), cumulative dose of GC ≥ 7.6 g (OR 1.09 (1.02–1.17), serum fetuin-A levels ≤ 660 μg/ml (OR 1,05 (1,01–1,09) and if the duration of GC intake is more than 3 months (hereinafter if dose of glucocorticoids is ≥ 5 mg for prednisolone daily) (OR 12.3 (4.12–36.5). Adjusted OR for osteoporosis were higher in women of age ≥ 58.5 years old (adjOR 1.08 (1.01–1.16), serum fetuin-A levels ≤ 660 μg/ml (adjOR 1.08 (1.01–1.15) andif the duration of GC intake is ≥ than 3 months (adjOR 12.1 (1.44–102.3).

Conclusions. Women with RA of ≥ than 58.5 years old, duration of GCs intake more than 3 months and serum fetuin-A levels ≤ than 660 μg/ml had higher odds for osteoporosis.These are independent factors for osteoporosis in women with rheumatoid arthritis, whichshould be used in patient’s management.

The problem of comorbid infections in rheumatology seems to be very relevant in connection with the active introduction into clinical practice of innovative disease-modifying anti-rheumatic drugs (DMARDs), the so-called targeted DMARDs (tDMARDs), as well as genetically engineered biological drugs (biologics), the action of which is directed at specific links in the pathogenesis of immuno-inflammatory rheumatic diseases. With the accumulation of global clinical experience, the association of the use of these drugs with an increasing risk of developing comorbid infections of various nature and localization has become clearly traced. The real way out of this situation seems to be the creation, improvement and introduction into clinical practice of various vaccines. At the same time, a number of anti-rheumatic drugs may have a certain negative effect on the immunogenicity of some vaccines, which may lead to a decrease in the preventive effectiveness of the latter. This review presents the latest data on the effect of various anti-rheumatic drugs on the immunogenicity of vaccines against influenza, pneumococcal and herpes virus infections, viral hepatitis B, yellow fever and COVID-19 used in rheumatological patients. It has been shown that the anti-B-cell drug ritux imab has a significant negative effect on the immunogenicity of vaccines, which increases with a shortening of the time between immunization and the use of the drug. Methotrexate also negatively affects the immunogenicity of most vaccines, but to a lesser extent. Abatacept probably reduces the immunogenicity of vaccines, although studies were performed in the absence of adequate control groups. Tumor necrosis factor inhibitors-α and tDMARDs (janus kinase inhibitors) reduce the absolute values of antibody concentrations for many vaccines, but apparently do not have a significant effect on the frequency of patients who have achieved seroprotection. Inhibitors of interleukin (IL) -6, IL-12 / IL-23 and IL-17 practically do not affect the immunogenicity of vaccines. The accumulated data on the effect of the above drugs on the immunogenicity of the vaccine against SARS-CoV-2, apparently, are similar to those obtained in studies on vaccination against other infections in patients with immuno-inflammatory rheu matic diseases. Further clinical studies are needed to assess the effect of immunosuppressive therapy on the vaccine response and to develop methods for its optimization.

For a long time, there has been scientific debate about the appropriateness of prescribing drugs to lower the level of uric acid in patients without clinical manifestations of gout. Long-term hyperuricemia is known to be the cause of gout and gouty arthritis. However, an increased level of uric acid is often found in a number of other diseases (metabolic syndrome, kidney disease, cardiovascular disease, psoriasis). Clinical evidence suggests that uric acid-lowering therapy slows the progression of cardiovascular disease and chronic kidney disease. And, if in rheumatological practice this issue still remains a subject of discussion, then the cardiological community by 2019 has clearly defined the indications for starting urate-lowering therapy. The Consensus on the Management of Patients with Hyperuricemia and High Cardiovascular Risk strongly recommends that the practitioner prescribe drugs to control hyperuricemia in hypertensive patients. The need to control the level of uric acid is reflected in the relevant sections of the Clinical Guidelines for the Management of Patients with Arterial Hypertension, 2020. This article provides a review of the literature on the etiology, pathophysiology, pharmacotherapy of hyperuricemia in patients with cardiovascular and rheumatic diseases. A separate section is devoted to scientific studies of the effects of colchicine in advanced therapy for CVD and RD. A clinical case of observation of a patient with newly diagnosed psoriatic arthritis, hyperuricemia, high cardiovascular risk is presented. The peculiarity of this clinical case is the onset of the disease after orthopedic surgery on the knee joints, high comorbidity and poor tolerance of standard basic therapy. The use of colchicine stabilized the patient’s condition. Thus, in clinical practice, it is necessary to take into account the role of hyperuricemia in the pathogenesis of inflammation in cardiovascular pathology. Colchicine may be the drug of choice for patients with hyperuricemia at high cardiovascular risk.

Back pain and insomnia (insomnia) significantly impair the quality of life of patients. Pain contributes to the development of sleep disorders and vice versa, poor quality sleep increases pain. Sleep disorders are widespread in the population, and in chronic pain syndrome, almost 70% of patients suffer from insomnia. The National Sleep Association singles out pain as one of the leading causes of sleep disorders. The article discusses a typical clinical case of the combination and interaction of chronic pain syndrome and insomnia. A patient with acute back pain developed a sleep disorder for which therapy was not carried out. The prescribed standard therapy for back pain, which included a non-steroidal anti-inflammatory drug, muscle relaxant, made it possible to relieve pain in a short time. However, the patient’s insomnia not only persisted, but also progressed, which led to the appearance of symptoms of asthenia in the form of fatigue, irritability, decreased performance, and ultimately significantly reduced the quality of life. In order to normalize sleep, the patient was prescribed a histamine H1 receptor blocker from the ethanolamine group, namely the drug Doxylamine. Follow-up observation for 1 year showed no exacerbation of back pain and sleep disturbances. In the treatment of patients with chronic back pain, it is necessary to pay attention to the presence of sleep disturbances and provide appropriate therapy. Today, three groups of hypnotics are used in clinical practice: melatonin receptor agonists (insufficient effectiveness in acute sleep disorders), benzodiazepines (addictive and addictive), and antihistamines. The modern drug Doxylamin belongs to the group of antihistamine hypnotics, has a good efficacy and safety profile and is included in the domestic recommendations for the treatment of insomnia.

The issue nonsteroidal anti-inflammatory drugs (NSAIDs) use safety is associated with a high frequency of adverse events (AEs) from the gastrointestinal tract and cardiovascular risks. Patients with lower back pain (LBP) and osteoarthritis (OA), as a rule, have comorbid diseases, such as arterial hypertension (AH), coronary heart disease (CHD), gastrointestinal tract (GIT) diseases, which significantly complicates the appointment of NSAIDs. The main guideline in NSAIDs appointment is the selective ability to inhibit cyclooxygenase-1 and -2 (COX). The ratio of the activity of NSAIDs when blocking COX-1/COX-2 allows us to judge their potential toxicity. And, then higher the selectivity of NSAIDs, then lower its toxicity. For example, the ratio of COX-1/COX-2 in meloxicam is 0.33, diclofenac – 2.2, tenoxicam – 15, piroxicam – 33, indomethacin – 107. To the predominantly selective COX-2 NSAIDs include meloxicam, which has little effect on the GIT, the lowest relative risk (RR) of complications from the cardiovascular system (CVS). The therapeutic efficacy of meloxicam is comparable to piroxicam and diclofenac. A number of studies have shown the high efficacy of meloxicam, both with per oral (p/o) administration (7.5–15 mg/d), and with intramuscular (i/m) administration (1.5 ml), and when injected into trigger zones. Both with p/o and the injectable form of meloxicam has minimal GIT AEs and absence local reaction in the injection area. The drug can be recommended both as a combination therapy and prescribed in monotherapy.