Pub Date : 2022-07-19DOI: 10.17650/1818-8338-2022-16-1-k654
E. Konstantinova, E. A. Koroleva, A. G. Popova, E. Popov, D. A. Anichkov, A. Svet, A. Nesterov, M. Gilyarov
Objective. To study the prevalence of depressive disorders using Zung Self-rating Depression Scale (SDS) in patients with acute coronary syndrome (ACS) in the daily work of the Regional Vascular Center in various gender and social subgroups and to compare their severity with the life quality level.Materials and Methods. The survey included 116 (57 female and 59 male) patients, admitted to Regional Vascular Center with ACS from March to November 2020 (Group 1), and 49 patients hospitalized with other cardiological pathology (Group 2), who made up a comparison group comparable in gender, age, presence of diabetes mellitus, heart attack and stroke in anamnesis.Results. In Group I the score on SDS was higher or equal to 50 (depression) in 18 % of cases: 15 % female and 3 % male patients (p <0.05). The average score on SDS was notably higher in women than in men (p <0.05). In Group 2 depression was detected in 27 % of cases, without gender differences. The average level of depression was higher in older age groups, both in men and women, in patients with ACS and without ACS. A negative correlation was established for the indicators of SDS and SF-36: in Group 1 r = –0.62, p <0.05, in Group 2 r = –0.76, p <0.05. In Group 1 indicators of health physical component (SF-36) among women were: physical functioning 50, role functioning 34, general health 51, in men: 80, 58 and 63 respectively (p <0.05). In Group 2 these indicators significantly differed only in physical functioning: 60 female and 72 male. In Group 1 depression was observed in 2 % of working and in 30 % of non-working patients (p <0.05); in Group 2: 0 and 34 % respectively. In Groups 1 and 2 depression was found in 10 and 5 % among married, in 31 and 43 % among unmarried patients (p <0.05). In Group 1 depression was detected in 31 % among patients with diabetes, in 12 % – without diabetes (p <0.05). The other analyzed diseases did not have a significant effect on the de pression score.Conclusions. The presence of ACS was associated with depressive disorders in women. At the same time, the severity of depressive disorders was inversely correlated with the quality of life. In women with ACS, the physical component and the psychological component of health on the quality of life scale are significantly lower in comparison with men. In addition, the absence of work and marriage negatively affected the prevalence of depressive disorders among all examined patients. And the presence of diabetes mellitus was associated with a higher level of depression among patients with ACS. It is necessary to develop and implement specialized rehabilitation programs for the following subgroups of patients with ACS and depression – unemployed and unmarried women, with a low level of quality of life, elderly patients, patients with diabetes mellitus.
{"title":"Depressive disorders and quality of live in patients with acute coronary syndrome in real clinical practice","authors":"E. Konstantinova, E. A. Koroleva, A. G. Popova, E. Popov, D. A. Anichkov, A. Svet, A. Nesterov, M. Gilyarov","doi":"10.17650/1818-8338-2022-16-1-k654","DOIUrl":"https://doi.org/10.17650/1818-8338-2022-16-1-k654","url":null,"abstract":"Objective. To study the prevalence of depressive disorders using Zung Self-rating Depression Scale (SDS) in patients with acute coronary syndrome (ACS) in the daily work of the Regional Vascular Center in various gender and social subgroups and to compare their severity with the life quality level.Materials and Methods. The survey included 116 (57 female and 59 male) patients, admitted to Regional Vascular Center with ACS from March to November 2020 (Group 1), and 49 patients hospitalized with other cardiological pathology (Group 2), who made up a comparison group comparable in gender, age, presence of diabetes mellitus, heart attack and stroke in anamnesis.Results. In Group I the score on SDS was higher or equal to 50 (depression) in 18 % of cases: 15 % female and 3 % male patients (p <0.05). The average score on SDS was notably higher in women than in men (p <0.05). In Group 2 depression was detected in 27 % of cases, without gender differences. The average level of depression was higher in older age groups, both in men and women, in patients with ACS and without ACS. A negative correlation was established for the indicators of SDS and SF-36: in Group 1 r = –0.62, p <0.05, in Group 2 r = –0.76, p <0.05. In Group 1 indicators of health physical component (SF-36) among women were: physical functioning 50, role functioning 34, general health 51, in men: 80, 58 and 63 respectively (p <0.05). In Group 2 these indicators significantly differed only in physical functioning: 60 female and 72 male. In Group 1 depression was observed in 2 % of working and in 30 % of non-working patients (p <0.05); in Group 2: 0 and 34 % respectively. In Groups 1 and 2 depression was found in 10 and 5 % among married, in 31 and 43 % among unmarried patients (p <0.05). In Group 1 depression was detected in 31 % among patients with diabetes, in 12 % – without diabetes (p <0.05). The other analyzed diseases did not have a significant effect on the de pression score.Conclusions. The presence of ACS was associated with depressive disorders in women. At the same time, the severity of depressive disorders was inversely correlated with the quality of life. In women with ACS, the physical component and the psychological component of health on the quality of life scale are significantly lower in comparison with men. In addition, the absence of work and marriage negatively affected the prevalence of depressive disorders among all examined patients. And the presence of diabetes mellitus was associated with a higher level of depression among patients with ACS. It is necessary to develop and implement specialized rehabilitation programs for the following subgroups of patients with ACS and depression – unemployed and unmarried women, with a low level of quality of life, elderly patients, patients with diabetes mellitus.","PeriodicalId":82998,"journal":{"name":"The Clinician","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48002345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-07-19DOI: 10.17650/1818-8338-2022-16-1-k653
V. Gusev, D. A. Medvedev, O. Lvova, N. Shamalov, O. Kovtun
Stroke in young patients is a disease based on a number of known specific non-modifiable factors (extracranial artery dissection, thrombophilia, open oval hole, etc.) and modifiable factors (alcohol abuse, drug use, smoking, etc.), in combination leading to the development of pathology. Smoking is a generally recognized modifiable risk factor for stroke, which is directly proportional to the number of tobacco-containing products smoked. Quitting smoking is the basis of prevention, an integral part of the treatment and rehabilitation of stroke patients. If it is impossible to completely give up smoking combustible cigarettes, it is advisable to switch to alternative smokeless products. This article presents the results of current studies on the comparative assessment of the risk of stroke in young people when using combustible cigarettes and smokeless analogues.
{"title":"The role of smoking in the development of strokes at a young age","authors":"V. Gusev, D. A. Medvedev, O. Lvova, N. Shamalov, O. Kovtun","doi":"10.17650/1818-8338-2022-16-1-k653","DOIUrl":"https://doi.org/10.17650/1818-8338-2022-16-1-k653","url":null,"abstract":"Stroke in young patients is a disease based on a number of known specific non-modifiable factors (extracranial artery dissection, thrombophilia, open oval hole, etc.) and modifiable factors (alcohol abuse, drug use, smoking, etc.), in combination leading to the development of pathology. Smoking is a generally recognized modifiable risk factor for stroke, which is directly proportional to the number of tobacco-containing products smoked. Quitting smoking is the basis of prevention, an integral part of the treatment and rehabilitation of stroke patients. If it is impossible to completely give up smoking combustible cigarettes, it is advisable to switch to alternative smokeless products. This article presents the results of current studies on the comparative assessment of the risk of stroke in young people when using combustible cigarettes and smokeless analogues.","PeriodicalId":82998,"journal":{"name":"The Clinician","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49259291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-07-19DOI: 10.17650/1818-8338-2022-16-1-k660
A. O. Sorokina, N. Demin, O. Dobrovolskaya, N. Toroptsova
Aim. To determine the frequency of sarcopenia (SP) and to identify factors associated with the muscle mass in women with systemic sclerosis (SSc).Materials and methods. The study included 64 women with SSc aged 40–70 years. Questionnaires, clinical, instrumental, laboratory examinations and absorptiometry. Linear regression analysis was performed to identify factors associat ed with appendicular muscle mass (AMM).Results. Probable SP was detected in 35 (54.7 %), and confirmed SP – 17 (26.5 %) women with SSc. The frequency of SP did not differ depending on the form of the disease. Univariate linear analysis revealed the relationship between the AMM and BMI, nutritional status; mid-upper arm, waist, hip and calf circumferences, skin Rodnan score, cumulative dose of glucocorticoids (GC) and BMD of the proximal hip. Multivariate linear analysis confirmed the presence of associations between the AMM index and BMI (b = 0.65; p <0.001), the Rodnan skin score (b = –0.19; p = 0.047), the cumulative dose of GC (b = –0.22; p = 0.021).Conclusion. The study demonstrated that more than a quarter of patients with SSc had a confirmed SP. Although age is the main risk factor for SP in the general population, in our study it did not differ between patients with low and normal AMM. The cumulative dose of GC and the Rodnan skin score were negatively, and BMI was positively associated with the value of AMМ.
{"title":"The frequency of sarcopenia and factors affecting appendicular muscle mass in patients with systemic sclerosis","authors":"A. O. Sorokina, N. Demin, O. Dobrovolskaya, N. Toroptsova","doi":"10.17650/1818-8338-2022-16-1-k660","DOIUrl":"https://doi.org/10.17650/1818-8338-2022-16-1-k660","url":null,"abstract":"Aim. To determine the frequency of sarcopenia (SP) and to identify factors associated with the muscle mass in women with systemic sclerosis (SSc).Materials and methods. The study included 64 women with SSc aged 40–70 years. Questionnaires, clinical, instrumental, laboratory examinations and absorptiometry. Linear regression analysis was performed to identify factors associat ed with appendicular muscle mass (AMM).Results. Probable SP was detected in 35 (54.7 %), and confirmed SP – 17 (26.5 %) women with SSc. The frequency of SP did not differ depending on the form of the disease. Univariate linear analysis revealed the relationship between the AMM and BMI, nutritional status; mid-upper arm, waist, hip and calf circumferences, skin Rodnan score, cumulative dose of glucocorticoids (GC) and BMD of the proximal hip. Multivariate linear analysis confirmed the presence of associations between the AMM index and BMI (b = 0.65; p <0.001), the Rodnan skin score (b = –0.19; p = 0.047), the cumulative dose of GC (b = –0.22; p = 0.021).Conclusion. The study demonstrated that more than a quarter of patients with SSc had a confirmed SP. Although age is the main risk factor for SP in the general population, in our study it did not differ between patients with low and normal AMM. The cumulative dose of GC and the Rodnan skin score were negatively, and BMI was positively associated with the value of AMМ.","PeriodicalId":82998,"journal":{"name":"The Clinician","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43951803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-07-19DOI: 10.17650/1818-8338-2022-16-1-k643
A. M. Alieva, I. Baykova, K. Voronkova, N. Teplova, L. M. Shnakhova, R. Valiev, D. A. Elmurzaeva, A. M. Rakhaev, M. R. Kalova, I. Nikitin
Introduction. Currently, the search and study of new biological markers that can help early diagnosis of heart failure, serve as a laboratory tool for assessing the effectiveness of therapy, be a predictive marker of possible adverse clinical outcomes and a significant criterion for risk stratification is very relevant. While cardiospecific markers, including natriuretic peptides, their precursors, and highly sensitive troponins, are widely used in clinical practice, the need to use other markers does not have sufficient evidence. aspect of a biological marker of heart failure.Gamma-glutamyl transpeptidase is an enzyme localized on the outer side of cell membranes and involved in the metabolism of glutathione and cysteine. This enzyme is a dimeric glycoprotein (68 kDa), consisting of 2 subunits – a large and a small (46 and 22 kDa). Gamma-glutamyl transpeptidase is encoded by a multigene family consisting of at least 7 different genes located on chromosome 22; however, only 1 of these genes is involved in the formation of a functional enzyme. Gamma-glutamyl transpeptidase was found in all cells except erythrocytes. There is a significant variability in enzyme activity, which is especially high in tissues with a secretory and absorptive function, such as the kidneys, biliary tract, intestines, and epididymis.Purpose of the review is to present an overview of current publications devoted to the study of γ-glutamyl transpeptidase in the aspect of a biological marker of heart failure.Materials and methods. The analysis of literature sources (foreign and domestic articles) was carried out in the databases: PubMed, RSCI, MedLine, Google Scholar, Science Direct. The search was performed according to the following keywords: biological markers, heart failure, γ-glutamyl transpeptidase, biological markers, heart failure, γ-glutamyl transpeptidase.Results. In addition to its clinical use as a test for liver disease, biliary tract disease, and alcohol abuse, γ-glutamyl transpeptidase is of great interest because of its association with cardiovascular disease, diabetes, metabolic syndrome, and cancer. In the literature available to us, we found a small number of works devoted to the study of γ-glutamyl transpeptidase in patients with heart failure. In the review, we have presented data from experimental and clinical studies indicating a clear link between γ-glutamyl transpeptidase and heart failure. The pathogenetic mechanism of the possible relationship between γ-glutamyl transpeptidase and heart failure is not completely clear. The localization of this enzyme in tissues with a transport function has led to the assumption that it is involved in the transport of amino acids through the γ-glutamyl cycle.Conclusion. Further deeper understanding of the structure and function of the enzyme is needed, as well as future clinical studies to determine the diagnostic, prognostic and possibly therapeutic significance of this biological marker.
{"title":"Gamma-glutamyl transpeptidase is a promising biological marker of heart failure","authors":"A. M. Alieva, I. Baykova, K. Voronkova, N. Teplova, L. M. Shnakhova, R. Valiev, D. A. Elmurzaeva, A. M. Rakhaev, M. R. Kalova, I. Nikitin","doi":"10.17650/1818-8338-2022-16-1-k643","DOIUrl":"https://doi.org/10.17650/1818-8338-2022-16-1-k643","url":null,"abstract":"Introduction. Currently, the search and study of new biological markers that can help early diagnosis of heart failure, serve as a laboratory tool for assessing the effectiveness of therapy, be a predictive marker of possible adverse clinical outcomes and a significant criterion for risk stratification is very relevant. While cardiospecific markers, including natriuretic peptides, their precursors, and highly sensitive troponins, are widely used in clinical practice, the need to use other markers does not have sufficient evidence. aspect of a biological marker of heart failure.Gamma-glutamyl transpeptidase is an enzyme localized on the outer side of cell membranes and involved in the metabolism of glutathione and cysteine. This enzyme is a dimeric glycoprotein (68 kDa), consisting of 2 subunits – a large and a small (46 and 22 kDa). Gamma-glutamyl transpeptidase is encoded by a multigene family consisting of at least 7 different genes located on chromosome 22; however, only 1 of these genes is involved in the formation of a functional enzyme. Gamma-glutamyl transpeptidase was found in all cells except erythrocytes. There is a significant variability in enzyme activity, which is especially high in tissues with a secretory and absorptive function, such as the kidneys, biliary tract, intestines, and epididymis.Purpose of the review is to present an overview of current publications devoted to the study of γ-glutamyl transpeptidase in the aspect of a biological marker of heart failure.Materials and methods. The analysis of literature sources (foreign and domestic articles) was carried out in the databases: PubMed, RSCI, MedLine, Google Scholar, Science Direct. The search was performed according to the following keywords: biological markers, heart failure, γ-glutamyl transpeptidase, biological markers, heart failure, γ-glutamyl transpeptidase.Results. In addition to its clinical use as a test for liver disease, biliary tract disease, and alcohol abuse, γ-glutamyl transpeptidase is of great interest because of its association with cardiovascular disease, diabetes, metabolic syndrome, and cancer. In the literature available to us, we found a small number of works devoted to the study of γ-glutamyl transpeptidase in patients with heart failure. In the review, we have presented data from experimental and clinical studies indicating a clear link between γ-glutamyl transpeptidase and heart failure. The pathogenetic mechanism of the possible relationship between γ-glutamyl transpeptidase and heart failure is not completely clear. The localization of this enzyme in tissues with a transport function has led to the assumption that it is involved in the transport of amino acids through the γ-glutamyl cycle.Conclusion. Further deeper understanding of the structure and function of the enzyme is needed, as well as future clinical studies to determine the diagnostic, prognostic and possibly therapeutic significance of this biological marker.","PeriodicalId":82998,"journal":{"name":"The Clinician","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44493846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-07-19DOI: 10.17650/1818-8338-2022-16-1-k657
N. Shostak, N. G. Pravduk, M. O. Anischenko, M. S. Dzhauari
Osteoarthritis (OA) is a multifactorial disease that can be caused by genetic factors, obesity, joint microtrauma, and excessive physical exercises. The key features of OA include gradual loss of articular cartilage, bone tissue remodeling, development of osteophytes, and subchondral sclerosis. The pathogenesis of OA is based on the loss of glycosaminoglycans, collagen disorganization, and inflammation mediated by a cytokine cascade. OA is a complex disease affecting not only cartilage, but also intraarticular and periarticular tissues. Together, these changes compromise joint function and cause chronic pain. Considerable attention has beer recently paid to OA phenotyping in order to introduce a tailored approach into patient management. Phenotypes are applicable to the three most common peripheral OA locations: gonarthrosis, coxarthrosis, and hand OA. An international group of experts of primary care has developed algorithms for OA patient management, including diagnostic criteria, treatment options, and criteria for referring the patient to a specialist (rheumatologist). Current guidelines recommend non-drug therapy, pharmacotherapy, and surgery. There is a growing interest in phytopharmaceuticals, a heterogeneous group of molecules with a high capacity of suppressing inflammation, oxidative stress, and pain, as well as improving joint function. Mucosate® in capsules (DIAMED-pharma, Russia) is one of currently available complex products with phytocompounds. It contains the NEM® complex (natural eggshell membrane), Harpagophytum root extract, glucosamine sulfate, chondroitin sulfate, and manganese sulfate monohydrate.
{"title":"Osteoarthritis: management strategies depending on the location of lesions","authors":"N. Shostak, N. G. Pravduk, M. O. Anischenko, M. S. Dzhauari","doi":"10.17650/1818-8338-2022-16-1-k657","DOIUrl":"https://doi.org/10.17650/1818-8338-2022-16-1-k657","url":null,"abstract":"Osteoarthritis (OA) is a multifactorial disease that can be caused by genetic factors, obesity, joint microtrauma, and excessive physical exercises. The key features of OA include gradual loss of articular cartilage, bone tissue remodeling, development of osteophytes, and subchondral sclerosis. The pathogenesis of OA is based on the loss of glycosaminoglycans, collagen disorganization, and inflammation mediated by a cytokine cascade. OA is a complex disease affecting not only cartilage, but also intraarticular and periarticular tissues. Together, these changes compromise joint function and cause chronic pain. Considerable attention has beer recently paid to OA phenotyping in order to introduce a tailored approach into patient management. Phenotypes are applicable to the three most common peripheral OA locations: gonarthrosis, coxarthrosis, and hand OA. An international group of experts of primary care has developed algorithms for OA patient management, including diagnostic criteria, treatment options, and criteria for referring the patient to a specialist (rheumatologist). Current guidelines recommend non-drug therapy, pharmacotherapy, and surgery. There is a growing interest in phytopharmaceuticals, a heterogeneous group of molecules with a high capacity of suppressing inflammation, oxidative stress, and pain, as well as improving joint function. Mucosate® in capsules (DIAMED-pharma, Russia) is one of currently available complex products with phytocompounds. It contains the NEM® complex (natural eggshell membrane), Harpagophytum root extract, glucosamine sulfate, chondroitin sulfate, and manganese sulfate monohydrate. ","PeriodicalId":82998,"journal":{"name":"The Clinician","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43038064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-03-05DOI: 10.17650/1818-8338-2021-15-1-4-k652
N. Shostak, N. Pravdyuk, V. Timofeev, D. V. Abeldyaev
Pain syndrome in the shoulder occurs in every 5th adult and is the 2nd most frequent reason for seeking primary medical care among all musculoskeletal disorders. Group of local causes of pain syndrome in the shoulder area. The starting point for differential search is patient’s age. For persons younger than 40, the most common causes are joint instability (dislocations / subluxations), as well as mild damage of the rotator cuff muscles due to injury. Patients older than 40 have an increased risk of severe chronic disorders of the above-mentioned muscles, adhesive capsulitis, and osteoarthritis of the shoulder joint. Treatment of shoulder joint and soft tissue pathology is nosological in nature and has to be justified by pathogenesis. Chondroreparants are a new class of pharmaceuticals based on hyaluronic acid modified by low molecular weight compounds using solid-phase stabilization. During physical stabilization (mechanosynthesis) of hyaluronic acid, chemical crosslinkers are not used, which leads to high tolerability and safety. Modified hyaluronic acid in Hyalrepair formulas has a number of structural features leading to its slower biodegradation in the tissues. Chondroreparant Hyalrepair-10 consists of hyaluronic acid, ascorbyl phosphate, zinc, cysteine, and glutathione; Hyalrepair- 2 consists of hyaluronic acid, ascorbyl phosphate, L-proline, L-lysine, and glycine. Use of intra-joint and periarticular injection of hyaluronic acid can be an effective approach in combination pathogenesis-directed therapy of the shoulder and soft tissues.
{"title":"Pathology of the shoulder joint and soft tissues: clinical variants, current capabilities of pathogenesis-directed therapy","authors":"N. Shostak, N. Pravdyuk, V. Timofeev, D. V. Abeldyaev","doi":"10.17650/1818-8338-2021-15-1-4-k652","DOIUrl":"https://doi.org/10.17650/1818-8338-2021-15-1-4-k652","url":null,"abstract":"Pain syndrome in the shoulder occurs in every 5th adult and is the 2nd most frequent reason for seeking primary medical care among all musculoskeletal disorders. Group of local causes of pain syndrome in the shoulder area. The starting point for differential search is patient’s age. For persons younger than 40, the most common causes are joint instability (dislocations / subluxations), as well as mild damage of the rotator cuff muscles due to injury. Patients older than 40 have an increased risk of severe chronic disorders of the above-mentioned muscles, adhesive capsulitis, and osteoarthritis of the shoulder joint. Treatment of shoulder joint and soft tissue pathology is nosological in nature and has to be justified by pathogenesis. Chondroreparants are a new class of pharmaceuticals based on hyaluronic acid modified by low molecular weight compounds using solid-phase stabilization. During physical stabilization (mechanosynthesis) of hyaluronic acid, chemical crosslinkers are not used, which leads to high tolerability and safety. Modified hyaluronic acid in Hyalrepair formulas has a number of structural features leading to its slower biodegradation in the tissues. Chondroreparant Hyalrepair-10 consists of hyaluronic acid, ascorbyl phosphate, zinc, cysteine, and glutathione; Hyalrepair- 2 consists of hyaluronic acid, ascorbyl phosphate, L-proline, L-lysine, and glycine. Use of intra-joint and periarticular injection of hyaluronic acid can be an effective approach in combination pathogenesis-directed therapy of the shoulder and soft tissues.","PeriodicalId":82998,"journal":{"name":"The Clinician","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44728028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-03-05DOI: 10.17650/1818-8338-2021-15-1-4-k650
N. Shostak, A. Klimenko, N. Demidova, A. Kondrashov, D. Y. Andryashkina, Yu. M. Saakyan, G. Varaksin, A. Y. Tarantina
The new coronavirus infection (COVID-19) is associated with a wide spectrum of various clinical manifestations including involvement of the musculoskeletal system which can persist for a long time after the infection. Supposedly, pathogenesis of musculoskeletal manifestations of COVID-19 is primarily caused by systemic inflammation accompanied by cytokine hyperexpression (interferon γ, interleukins 1β, 6, 8, 17, tumor necrosis factor α), as well as hypoxia leading to overproduction of inflammatory cytokines, activation of bone reabsorption by osteoclasts and subsequent decrease of mineral bone density and osteonecrosis in some cases. Additionally, some drugs prescribed to patients with COVID-19 (some antiviral drugs and glucocorticoids) should also be taken into account as they can lead to development of musculoskeletal pathology. In the acute period of COVID-19, myalgias are common, but in rare cases myositis with proximal muscular weakness and increased levels of creatine phosphokinase, lactate dehydrogenase can occur. Arthralgias in the acute period of COVID-19 are rarer than myalgias. In the studies of clinical manifestation of COVID-19, frequency of arthralgias and myalgias in the acute period is between 15.5 and 50 %. After COVID-19, frequency of arthralgias and myalgias gradually decreases, however there are cases of long-term joint and muscle pains, as well as post-viral arthritis, development of arthritis in the context of various autoimmune disorders. Myalgias and arthralgias during COVID-19 usually regress spontaneously and in most patients do not require prescription of antipain medications, but in some cases pain management is necessary. Use of non-steroid anti-inflammatory drugs and vitamin D during COVID-19 is a safe and effective method of pain management, including myalgia and arthralgia. Rehabilitation programs play an important role in improvement of functional state and patient recovery after moderate and severe COVID-19.
{"title":"Musculoskeletal manifectations of the new coronavirus infection: focus on arthralgia and myalgia","authors":"N. Shostak, A. Klimenko, N. Demidova, A. Kondrashov, D. Y. Andryashkina, Yu. M. Saakyan, G. Varaksin, A. Y. Tarantina","doi":"10.17650/1818-8338-2021-15-1-4-k650","DOIUrl":"https://doi.org/10.17650/1818-8338-2021-15-1-4-k650","url":null,"abstract":"The new coronavirus infection (COVID-19) is associated with a wide spectrum of various clinical manifestations including involvement of the musculoskeletal system which can persist for a long time after the infection. Supposedly, pathogenesis of musculoskeletal manifestations of COVID-19 is primarily caused by systemic inflammation accompanied by cytokine hyperexpression (interferon γ, interleukins 1β, 6, 8, 17, tumor necrosis factor α), as well as hypoxia leading to overproduction of inflammatory cytokines, activation of bone reabsorption by osteoclasts and subsequent decrease of mineral bone density and osteonecrosis in some cases. Additionally, some drugs prescribed to patients with COVID-19 (some antiviral drugs and glucocorticoids) should also be taken into account as they can lead to development of musculoskeletal pathology. In the acute period of COVID-19, myalgias are common, but in rare cases myositis with proximal muscular weakness and increased levels of creatine phosphokinase, lactate dehydrogenase can occur. Arthralgias in the acute period of COVID-19 are rarer than myalgias. In the studies of clinical manifestation of COVID-19, frequency of arthralgias and myalgias in the acute period is between 15.5 and 50 %. After COVID-19, frequency of arthralgias and myalgias gradually decreases, however there are cases of long-term joint and muscle pains, as well as post-viral arthritis, development of arthritis in the context of various autoimmune disorders. Myalgias and arthralgias during COVID-19 usually regress spontaneously and in most patients do not require prescription of antipain medications, but in some cases pain management is necessary. Use of non-steroid anti-inflammatory drugs and vitamin D during COVID-19 is a safe and effective method of pain management, including myalgia and arthralgia. Rehabilitation programs play an important role in improvement of functional state and patient recovery after moderate and severe COVID-19.","PeriodicalId":82998,"journal":{"name":"The Clinician","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45714544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-03-05DOI: 10.17650/1818-8338-2021-15-1-4-k644
A. M. Alieva, M. A. Batov, K. Voronkova, O. Ettinger, R. Valiev, I. Nikitin
Heart failure (HF) remains a serious problem in Russian and world health care due to the growing morbidity and mortality from complications of heart failure, despite the development and implementation of programs for the early detection and treatment of heart failure in asymptomatic patients. Currently, a large number of new biological markers have been studied that could serve as a laboratory tool for diagnosing and predicting the course of heart failure, but only brain natriuretic peptides have found application in real clinical practice. Renalase is a recently discovered cytokine that is synthesized by the kidneys and released into the blood. To date, seven subtypes of renalase have been found, each of which plays a different physiological role in the human body. Renalase is usually positioned as a signaling molecule that activates cytoprotective intracellular signals, leading to a decrease in blood pressure and protection of the heart muscle. The concentration of renalase freely circulating in the bloodstream of an adult is approximately 3–5 ng / ml. Currently, the level of renalase is determined by the enzyme immunoassay with a detection range of 3.12 to 200 ng / ml, while the minimum detectable concentration of the marker is less than 1.38 ng / ml. The presence of missense polymorphism of renalase is associated with myocardial dysfunction. Data from animal and human studies have shown that renalase plays a key role in the metabolism of catecholamines and in cardioprotective processes. Studies have shown the contribution of renalase to the occurrence of cardiovascular diseases: ischemic heart disease, arterial hypertension, diabetes mellitus, and aortic stenosis. Moreover, detailed protocols of multicenter prospective studies have demonstrated that functional polymorphism of the renalase gene was associated with myocardial hypertrophy in patients with aortic stenosis, hypertension, metabolic syndrome, unstable angina pectoris and stable forms of coronary artery disease, as well as in patients receiving renal replacement therapy. Based on these data and further studies, renalase has been proposed as a predictive biomarker of ischemia in patients with coronary microvascular dysfunction, as well as a predictor of clinically significant progression of chronic kidney disease in patients with cardiovascular diseases.Our review presents data on the role of renalase in heart failure. Further study of the structure and function of renalase, as well as future clinical studies, will allow determining the diagnostic, prognostic and, possibly, therapeutic significance of this biological marker in HF and other cardiovascular diseases.
{"title":"Renalase – a new instrument in multicomponent heart failure assessment","authors":"A. M. Alieva, M. A. Batov, K. Voronkova, O. Ettinger, R. Valiev, I. Nikitin","doi":"10.17650/1818-8338-2021-15-1-4-k644","DOIUrl":"https://doi.org/10.17650/1818-8338-2021-15-1-4-k644","url":null,"abstract":"Heart failure (HF) remains a serious problem in Russian and world health care due to the growing morbidity and mortality from complications of heart failure, despite the development and implementation of programs for the early detection and treatment of heart failure in asymptomatic patients. Currently, a large number of new biological markers have been studied that could serve as a laboratory tool for diagnosing and predicting the course of heart failure, but only brain natriuretic peptides have found application in real clinical practice. Renalase is a recently discovered cytokine that is synthesized by the kidneys and released into the blood. To date, seven subtypes of renalase have been found, each of which plays a different physiological role in the human body. Renalase is usually positioned as a signaling molecule that activates cytoprotective intracellular signals, leading to a decrease in blood pressure and protection of the heart muscle. The concentration of renalase freely circulating in the bloodstream of an adult is approximately 3–5 ng / ml. Currently, the level of renalase is determined by the enzyme immunoassay with a detection range of 3.12 to 200 ng / ml, while the minimum detectable concentration of the marker is less than 1.38 ng / ml. The presence of missense polymorphism of renalase is associated with myocardial dysfunction. Data from animal and human studies have shown that renalase plays a key role in the metabolism of catecholamines and in cardioprotective processes. Studies have shown the contribution of renalase to the occurrence of cardiovascular diseases: ischemic heart disease, arterial hypertension, diabetes mellitus, and aortic stenosis. Moreover, detailed protocols of multicenter prospective studies have demonstrated that functional polymorphism of the renalase gene was associated with myocardial hypertrophy in patients with aortic stenosis, hypertension, metabolic syndrome, unstable angina pectoris and stable forms of coronary artery disease, as well as in patients receiving renal replacement therapy. Based on these data and further studies, renalase has been proposed as a predictive biomarker of ischemia in patients with coronary microvascular dysfunction, as well as a predictor of clinically significant progression of chronic kidney disease in patients with cardiovascular diseases.Our review presents data on the role of renalase in heart failure. Further study of the structure and function of renalase, as well as future clinical studies, will allow determining the diagnostic, prognostic and, possibly, therapeutic significance of this biological marker in HF and other cardiovascular diseases.","PeriodicalId":82998,"journal":{"name":"The Clinician","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45188028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-03-05DOI: 10.17650/1818-8338-2021-15-1-4-k645
M. Gilyarov, I. Ivanov, E. Konstantinova, N. I. Raschetnova, N. Shostak
Currently, one of the key methods of treating a patient with ST-elevation myocardial infarction is to restore blood flow to the infarct-related artery as quickly, completely and steadily as possible. However, in some cases, it is not possible to achieve adequate myocardial reperfusion, despite the restoration of coronary blood flow. This phenomenon was named no-reflow. Due to the lack of a unified approach to the diagnosis of no-reflow, its occurrence varies widely – from 2 to 44 %. Failure to achieve adequate myocardial perfusion leads to a higher mortality rate – from 7.4 to 30.3 %, as well as to more aggressive remodeling of the myocardium. For a long time, distal embolization in percutaneous coronary intervention was considered one of the leading mechanisms. However, the routine use of protective devices did not show a pronounced effect on the outcome and prognosis, although it is justified in certain clinical situations. Ischemic injury directly plays a significant role due to overload of cardiomyocytes with calcium, cellular edema, necrosis and apoptosis, which is significantly aggravated by myocardial reperfusion and forms obstruction at the level of the microcirculatory bed. More data is being accumulated about immune-mediated injury through activation of cellular immunity, intense inflammation and thrombosis in situ. Despite the success in the animal experiment, the clinical use of certain groups of drugs showed an ambiguous results. According to the latest recommendations European Society of Cardiology / European Association for Cardio-Thoracic Surgery (ESC / EACTS) 2018, GPIIb / IIIa platelet receptor inhibitors are recommended in the case of no-reflow. Besides this, according to the literature nicorandil and sodium nitroprusside, as well as IL-1β antagonists, seem to be promising. As a non-drug therapy, selective intracoronary hypothermia also has shown its effectiveness and safety in a pilot study. To date, it is clear that the no-reflow phenomenon is a manifestation of a complex cascade of reactions, including ischemic, reperfusion and immune-related injury, as well as distal embolization. Considering its significant contribution to the frequency of adverse outcomes and late complications, it seems necessary to introduce unified approaches to the diagnosis, prevention and treatment of no-reflow, which requires high-quality clinical studies.
{"title":"No-reflow phenomenon and reperfusion injury. Mechanisms and treatment","authors":"M. Gilyarov, I. Ivanov, E. Konstantinova, N. I. Raschetnova, N. Shostak","doi":"10.17650/1818-8338-2021-15-1-4-k645","DOIUrl":"https://doi.org/10.17650/1818-8338-2021-15-1-4-k645","url":null,"abstract":"Currently, one of the key methods of treating a patient with ST-elevation myocardial infarction is to restore blood flow to the infarct-related artery as quickly, completely and steadily as possible. However, in some cases, it is not possible to achieve adequate myocardial reperfusion, despite the restoration of coronary blood flow. This phenomenon was named no-reflow. Due to the lack of a unified approach to the diagnosis of no-reflow, its occurrence varies widely – from 2 to 44 %. Failure to achieve adequate myocardial perfusion leads to a higher mortality rate – from 7.4 to 30.3 %, as well as to more aggressive remodeling of the myocardium. For a long time, distal embolization in percutaneous coronary intervention was considered one of the leading mechanisms. However, the routine use of protective devices did not show a pronounced effect on the outcome and prognosis, although it is justified in certain clinical situations. Ischemic injury directly plays a significant role due to overload of cardiomyocytes with calcium, cellular edema, necrosis and apoptosis, which is significantly aggravated by myocardial reperfusion and forms obstruction at the level of the microcirculatory bed. More data is being accumulated about immune-mediated injury through activation of cellular immunity, intense inflammation and thrombosis in situ. Despite the success in the animal experiment, the clinical use of certain groups of drugs showed an ambiguous results. According to the latest recommendations European Society of Cardiology / European Association for Cardio-Thoracic Surgery (ESC / EACTS) 2018, GPIIb / IIIa platelet receptor inhibitors are recommended in the case of no-reflow. Besides this, according to the literature nicorandil and sodium nitroprusside, as well as IL-1β antagonists, seem to be promising. As a non-drug therapy, selective intracoronary hypothermia also has shown its effectiveness and safety in a pilot study. To date, it is clear that the no-reflow phenomenon is a manifestation of a complex cascade of reactions, including ischemic, reperfusion and immune-related injury, as well as distal embolization. Considering its significant contribution to the frequency of adverse outcomes and late complications, it seems necessary to introduce unified approaches to the diagnosis, prevention and treatment of no-reflow, which requires high-quality clinical studies.","PeriodicalId":82998,"journal":{"name":"The Clinician","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45181549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-03-05DOI: 10.17650/1818-8338-2021-15-1-4-k651
N. Chipigina, N. Karpova, N. A. Kashentseva, V. Morits
Infective endocarditis (IE) caused by Gram-negative bacteria is a rare and insufficiently characterized form of endocarditis. The literature review presents data on the frequency, course, risk factors, diagnosis and treatment of both IE caused by the HACEK microorganisms (Haemophilus spр., Aggregatibacter spp., Cardiobacterium hominis, Eikenella corrodens, Kingella) and other Gram-negative bacteria. Gram-negative bacteria are the cause of 3.6–13.6 % IE cases (HACEK microorganisms in 0.8–3 % of IE cases in adults, non-HACEK in 1.8–3.9 %). Patients with IE caused by the HACEK microorganisms are younger, their disease is not associated with previous in-hospital treatment and is subacute with favorable prognosis (intrahospital mortality is 2–3 %). HACEK microorganisms mostly retain sensitivity to many antibiotics. Risk factors of IE caused by HACEK microorganisms are dental interventions, heart disorders, valve prostheses and other implanted cardiac devices. IE caused by non-HACEK Gram-negative bacteria is more common in elderly with concomitant disorders and usually is acute; intrahospital mortality is 13–36.5 %. Risk factors of IE caused by non-HACEK microorganisms are valve prostheses, electrical pacemakers, venous and central catheters, recent in-hospital treatment, Gram-negative bacteremia, decreased immunity, drug abuse, urinary infection, alcoholism, cirrhosis of the liver, removed spleen, consequences of dog and cat bites, working with the soil. Among Gram-negative non-HACEK bacteria causing IE, 28 % have multi-drug resistance (MDR / XDR) against antibiotics. Therefore, Gram-negative bacteria rarely cause IE but during selection of empiric therapy in patients with IE with corresponding risk factors, probability of Gram-negative causative microorganisms in IE etiology should be taken into account.
{"title":"Infective endocarditis caused by gram-negative bacteria","authors":"N. Chipigina, N. Karpova, N. A. Kashentseva, V. Morits","doi":"10.17650/1818-8338-2021-15-1-4-k651","DOIUrl":"https://doi.org/10.17650/1818-8338-2021-15-1-4-k651","url":null,"abstract":"Infective endocarditis (IE) caused by Gram-negative bacteria is a rare and insufficiently characterized form of endocarditis. The literature review presents data on the frequency, course, risk factors, diagnosis and treatment of both IE caused by the HACEK microorganisms (Haemophilus spр., Aggregatibacter spp., Cardiobacterium hominis, Eikenella corrodens, Kingella) and other Gram-negative bacteria. Gram-negative bacteria are the cause of 3.6–13.6 % IE cases (HACEK microorganisms in 0.8–3 % of IE cases in adults, non-HACEK in 1.8–3.9 %). Patients with IE caused by the HACEK microorganisms are younger, their disease is not associated with previous in-hospital treatment and is subacute with favorable prognosis (intrahospital mortality is 2–3 %). HACEK microorganisms mostly retain sensitivity to many antibiotics. Risk factors of IE caused by HACEK microorganisms are dental interventions, heart disorders, valve prostheses and other implanted cardiac devices. IE caused by non-HACEK Gram-negative bacteria is more common in elderly with concomitant disorders and usually is acute; intrahospital mortality is 13–36.5 %. Risk factors of IE caused by non-HACEK microorganisms are valve prostheses, electrical pacemakers, venous and central catheters, recent in-hospital treatment, Gram-negative bacteremia, decreased immunity, drug abuse, urinary infection, alcoholism, cirrhosis of the liver, removed spleen, consequences of dog and cat bites, working with the soil. Among Gram-negative non-HACEK bacteria causing IE, 28 % have multi-drug resistance (MDR / XDR) against antibiotics. Therefore, Gram-negative bacteria rarely cause IE but during selection of empiric therapy in patients with IE with corresponding risk factors, probability of Gram-negative causative microorganisms in IE etiology should be taken into account.","PeriodicalId":82998,"journal":{"name":"The Clinician","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46032780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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