Sternomediastinitis following median sternotomy remains one of the most severe infectious complications of cardiac surgery, being associated with prolonged hospitalization, the need for repeated surgical interventions, and high mortality. The clinical significance of this problem has increased with the growing number of open-heart procedures and the rising proportion of patients with comorbidities, including diabetes mellitus, obesity, chronic kidney disease, and chronic obstructive pulmonary disease, which impair tissue repair and increase the risk of deep infection of the sternum and mediastinal structures. This narrative review summarizes data on risk factors, microbiological profiles, diagnostic approaches, and contemporary treatment strategies for postoperative sternomediastinitis based on Russian- and English-language publications from 2015 to 2025. Among the predictors of this complication, disorders of carbohydrate metabolism and obesity are discussed most consistently, along with intraoperative factors such as operative duration, repeat sternotomy, blood loss volume, and inadequate sternal fixation during osteosynthesis. The etiology is most commonly dominated by Gram-positive cocci, primarily Staphylococcus aureus (including methicillin-resistant strains, MRSA) and coagulase-negative staphylococci; however, the contribution of Gram-negative and polymicrobial flora has increased, necessitating broad empirical antimicrobial coverage followed by de-escalation based on culture results. Diagnosis requires an integrated approach combining clinical assessment, dynamic monitoring of inflammatory biomarkers, and imaging. Computed tomography serves as the principal modality for confirming deep infection and planning surgical intervention, whereas positron emission tomography/computed tomography is particularly useful in chronic or recurrent cases and in diagnostically challenging situations. Treatment is regarded as a multidisciplinary task and includes early initiation of antimicrobial therapy, radical surgical debridement with removal of necrotic tissue and infected material, and the use of vacuum-assisted (negative pressure) wound therapy for local infection control and preparation for reconstruction. Chest wall reconstruction may involve primary or delayed sternal refixation, flap reconstruction, and rigid fixation using titanium systems, which improves stability and may reduce the risk of recurrence. Future perspectives include the standardization of diagnostic and therapeutic algorithms, evaluation of novel biomarkers and antibacterial coatings, further development of fixation technologies, and the integration of hybrid imaging techniques and machine learning methods for early detection of this complication.

Cardiovascular diseases (CVD) represent a leading cause of mortality in most industrialized countries. Community-acquired pneumonia significantly worsens the clinical course of CVD and increases the risk of cardiovascular death. Streptococcus pneumoniae (pneumococcus) is one of the most common etiological pathogens of community-acquired bacterial pneumonia. It may cause direct myocardial injury through hematogenous dissemination, as well as exert indirect deleterious effects on the cardiovascular system via the induced inflammatory response and the action of bacterial toxins, the most important of which is pneumolysin. Myocardial and vascular wall injury, along with platelet activation, may substantially contribute to the decompensation of heart failure, as well as to the development of myocardial infarction, stroke, and cardiac arrhythmias in patients with pneumonia. Most cardiovascular complications (CVC) occur during the early acute phase of pneumonia; however, some may also develop in the delayed period, creating conditions for the long-term persistence of an increased risk of cardiovascular death for several years after the infection. The risk of CVC in patients with pneumonia may be reduced by the use of aspirin and statins, as well as effective antibiotic therapy; however, these approaches do not completely eliminate the risk. Vaccination against pneumococcal infection is the most effective method for the prevention of CVC associated with S. pneumoniae. Currently, several types of pneumococcal vaccines are available, with conjugate vaccines being the most advanced, providing sustained immunity against the most prevalent pneumococcal serotypes after a single administration. Vaccination against S. pneumoniae is recommended across a wide spectrum of CVD, including pulmonary hypertension, chronic heart failure, myocarditis, and dilated cardiomyopathy. Broad implementation of pneumococcal vaccination in patients at high cardiovascular risk may significantly reduce both the incidence of cardiovascular complications and overall mortality in this population.

Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as the most common cause of chronic liver disease worldwide, affecting an estimated 25% of the global population. Up to 80% of individuals with hepatic steatosis remain asymptomatic and may show no biochemical abnormalities, meaning that MASLD is frequently silent until complications occur, which makes early diagnosis challenging. Lifestyle modification, including dietary changes, regular physical activity, and sustained weight reduction, is the cornerstone of MASLD management. At present, however, there is still no universally standardized pharmacological treatment for MASLD all over the world, and management continues to rely primarily on lifestyle modification. The amino acids and B-group vitamin complex is expected to be effective in treating the early stage of steatohepatosis and steatohepatitis, reducing aminotransferases levels and decreasing liver fat cell accumulation. This article is published in the journal Consilium Medicum in Russian with the permission of the copyright holders. The original article: Murane N, Sprudza KL, Ivanova J, Zalizko P. Complex of Amino Acids, Choline, and B-Group Vitamins for the Improvement of Early-Stage Metabolic Dysfunction-Associated Steatotic Liver Disease. Health. 2025;17:1252-71. DOI: 10.4236/health.2025.1710083 is distributed under the terms of the Creative Commons Attribution 4.0 International License (CC BY 4.0).

Background. Benign prostatic hyperplasia (BPH) is one of the most common disorders in middle-aged and older men. In the past 10 years, there has been an upward trend in BPH incidence in younger subjects, emphasizing the need for more careful diagnosis by urologists and adequate pharmacotherapy to alleviate the lower urinary tract symptoms (LUTS) and prevent the need for surgical intervention. Recently, combination therapy (α1-blocker and phytotherapeutic agent) has been increasingly used in the management of LUTS due to its positive clinical outcomes and ability to enhance patient quality of life. Aim. To evaluate the clinical efficacy of the combination of ProstOptima and α1-blocker (tamsulosin) in the treatment of BPH-related mild to moderate LUTS. Materials and methods. The study included 76 males with BPH and mild-to-moderate LUTS. The patients were randomized into two groups of 38 subjects each. Group 1 (n=38) received standard therapy with tamsulosin 0.4 mg QD for 2 months, Group 2 (n=38) received combination therapy with tamsulosin 0.4 mg QD and ProstOptima 1 capsule QD with food. Therapy was continued for 2 months. Follow-up examinations were performed 1 and 2 months after the start of treatment. Results. After 2 months of treatment, combination therapy (tamsulosin + ProstOptima) showed a statistically significant superiority over monotherapy, with better trends in key indicators and a more pronounced improvement in the International Prostate Symptom Score (IPSS) and the Quality of Life (QoL) scale. Conclusion. Combination therapy with tamsulosin and ProstOptima demonstrated high efficacy and safety in the treatment of BPH-related LUTS, as evidenced by objective urodynamic parameters and quality-of-life questionnaire data.

Macrophages are a heterogeneous population of immune cells derived primarily from bone marrow monocytes and embryonic yolk sac erythromyeloid progenitors, capable of altering their phenotype and functions depending on the microenvironment. This article presents a review of current knowledge on the origin, structure, and function of dermal macrophages, including historical data from the first observations by I.A.E. Goeze (1777), confirmed by W.F. von Gleichen-Russwurm, the term "Fresszellen" by K. Klaus, and the phagocytic theory of I.I. Mechnikov (1882–1884) to the M1/M2 dichotomy of Mills et al. (early 2000s). This paper summarizes literature data on the human monocyte-macrophage system in both normal and pathological conditions, taking into account the heterogeneity of classical monocytes as precursors of tissue macrophages, non-classical monocytes for endothelial homeostasis, intermediate and organ-specific macrophages (Langerhans cells in the epidermis, microglia in the central nervous system, and Kupffer cells in the liver). Data are presented on various macrophage phenotypes, from proinflammatory M1 with glycolytic metabolism and inducible nitric oxide synthase to reparative M2 with mitochondrial respiration and arginase-1, and their involvement in immune surveillance, skin protection, regeneration, angiogenesis, and tissue remodeling. The article presents an analysis of the role of macrophages in response to cosmetic procedures: ablative and non-ablative lasers 10600 and 1550 nm, microneedle RF, SMAS-lifting, injections of polylactic acid, calcium hydroxyapatite, the role of Langerhans cells in response to external stimuli of ultraviolet radiation, cosmetics, etc., the role of macrophages in the development of fibrosis M1-initiation, M2a-proliferation, M2c-resolution, SPP1+ with CXCL4 from platelets, PRP-hypothesis, regulation of the adipocyte population in dermal-associated adipose tissue dWAT, elimination of biomaterials. Attention is paid to resident dermal macrophages located perivascularly and perineurally in the papillary and reticular layers, their ability to proliferate in situ to maintain homeostasis, the synthesis of collagenase enzymes, elastase, hyaluronidase and cytokines that regulate the functions of dermal and epidermal cells.

Non-alcoholic fatty liver disease (NAFLD) and cholelithiasis (CL) are widespread diseases worldwide. The combination of NAFLD and CL is a common clinical situation. CL and NAFLD have common risk factors and are closely associated with such concomitant diseases as obesity, dyslipidemia, and carbohydrate metabolism disorders. Numerous studies in different populations have shown that NAFLD is an independent risk factor for CL, and CL is an independent risk factor for NAFLD. Insulin resistance is now being considered as a key link between NAFLD and the development of cholesterol cholelithiasis. In addition, changes in the expression of transcription factors, including hepatic X-receptor, farnesoid X-receptor, and membrane bile acid receptors, play an important role. It leads to increased lipogenesis in the liver and to bile cholesterol supersaturation, contributing to the development of gallstones and fatty liver. An equally important role in the pathogenesis of both diseases is played by gallbladder dysfunction, which serves as an important link between the liver and the intestine within the hepatic-gallbladder-intestinal axis and supports the metabolic homeostasis of cholesterol, triglycerides, and bile acids. It is supported by evidence that cholecystectomy increases the risk of NAFLD, contributes to insulin resistance, and promotes fat accumulation in the liver. The choice of drug therapy in patients with a combination of NAFLD and CL is based on knowledge of the general pathophysiological processes typical of both diseases. Drugs should comply with the principles of multipurpose monotherapy, targeting as many therapeutic targets as possible, and their combination should potentiate each other’s pharmacological effects. The treatment of patients with a combination of NAFLD and CL is primarily based on weight loss through exercise and a Mediterranean diet, enhanced by psyllium-containing agents and butyric acid, a key mediator of the Mediterranean diet’s positive effects. The drug of choice in patients with a combination of NAFLD and CL is ursodeoxycholic acid, exerting a pathogenetic effect on both diseases.

Despite the development of modern technologies in the field of healthcare and the wide application of modern diagnostic and treatment methods, mortality from ischemic heart disease remains the leading cause of death among diseases. It is known that coronary artery bypass grafting in combination with optimal medical therapy is the gold standard for treating patients with multivessel coronary artery disease. However, for several decades now, percutaneous coronary intervention has proven to be an alternative method of myocardial revascularization for patient with multivessel coronary artery disease and low or intermediate risk. Nevertheless, despite accumulated experience in treating patients with ischemic heart disease, the choice of revascularization method for patients with complex coronary artery disease and high surgical risk (not eligible for CABG) remains debatable. In this review article, the authors described the main factors influencing the choice of myocardial revascularization strategy and demonstrated the results of clinical studies dedicated to studying this issue.

The incidence of benign prostatic hyperplasia is increasing annually, affecting progressively younger age groups. These epidemiological shifts necessitate a deeper investigation into the pathogenesis of the disease to identify its key mechanisms and develop effective pharmacological treatment approaches. Recently, 5α-reductase inhibitors have become particularly relevant for managing lower urinary tract symptoms (LUTS) caused by BPH. Appropriate dosing and duration of therapy with this drug class not only slow disease progression but also effectively prepare patients for surgical intervention, reducing the risks of peri- and postoperative complications. This article explores not only the role of 5α-reductase inhibitors in treating LUTS but also their potential use for managing other conditions, such as prostate cancer chemoprevention or androgenetic alopecia treatment.

Background. Hypersensitivity pneumonitis (HP) is an immune-mediated interstitial lung disease that often progresses to pulmonary fibrosis, negatively affecting patients' quality of life (QOL). Aim. To assess QOL in patients with different HP phenotypes using the K-BILD and EQ-5D-5L questionnaires and identify clinical and functional factors affecting QOL. Materials and methods. The study included 105 HP patients [33 non-fibrotic (nfHP), 72 fibrotic (fHP), 32 with usual interstitial pneumonia (UIP) pattern on high-resolution computed tomography]. QOL, clinical data, respiratory function, echocardiography, dyspnea (mMRC scale), cough (VAS scale, LCQ), 6MWT results, and high-resolution computed tomography changes over 12 months were assessed. Statistical analysis involved nonparametric methods, correlation, linear, and multiple regression. Results. fHP and nfHP patients showed significant differences. fHP patients had a longer disease duration, more severe symptoms, lower lung function, and worse QOL. Those with fHP+UIP had worse lung function and more disease progression but similar QOL to fHP patients without UIP. For K-BILD, cough severity (LCQ), 6MWT distance, and forced vital capacity most affected QOL. For EQ-5D-5L, the 6MWT distance was the key factor. Conclusion. fHP patients experience a more severe disease course than nfHP patients. UIP pattern correlates with a more aggressive clinical progression. K-BILD and EQ-5D-5L are reliable tools for assessing QOL in HP. The greatest influence on QOL is exerted by the severity of cough, forced vital capacity and exercise tolerance.

Acute suppurative pyelonephritis is a severe kidney infection characterized by areas of ischemia and necrosis, making accurate assessment of renal perfusion crucial for diagnosis and treatment. In recent years, modern functional imaging techniques, including perfusion computed tomography (CT perfusion), have been increasingly used to evaluate renal blood flow. This review presents current data on the capabilities of renal CT perfusion in diagnosing and monitoring acute suppurative pyelonephritis, describing the principles of the technique and data post-processing for quantitative hemodynamic measurements. The CT perfusion method helps identify ischemic areas in the affected kidney and provides an objective assessment of perfusion impairment. Clinical studies show that perfusion abnormalities correlate with disease severity and the occurrence of suppurative complications, supporting the use of CT perfusion as an important prognostic tool for selecting optimal conservative or surgical treatment. Several advantages of CT perfusion are highlighted, such as high diagnostic value due to combined morphological and functional assessment, short examination time, and the ability to simultaneously assess both kidneys for comparison. However, the method also has significant limitations: high radiation exposure and the need for intravenous contrast increase the risk of complications (e.g., contrast-induced nephropathy) and restrict its use in patients with renal insufficiency. To mitigate these risks, careful patient selection, minimal necessary doses of radiation and contrast, and adequate hydration are recommended. Thus, renal CT perfusion is a promising adjunct in the diagnosis of acute pyelonephritis, capable of improving the assessment of pathological changes and patient outcomes when used judiciously.