ABSTRACT. This article presents a clinical observation illustrating the differential diagnosis between the true combination of B12-deficiency pernicious anemia (PA) and autoimmune hemolytic anemia and the phenomenon of “pseudo-hemolysis.” A 71-year-old female patient with verified PA against a background of autoimmune atrophic gastritis and concomitant autoimmune thyroiditis was found to have macrocytic anemia, hyperbilirubinemia, elevated lactate dehydrogenase (LDH), and a positive direct Coombs test (DAT) with negative anti-erythrocyte antibodies. The key criterion was the reticulocyte production index (RPI = 1.38), indicating ineffective erythropoiesis characteristic of PA rather than true hemolysis. Cyanocobalamin monotherapy caused a reticulocyte crisis, decreased LDH and bilirubin, and increased hemoglobin, confirming the false-positive nature of the DAT. The authors conclude that a positive Coombs test in PA does not require the administration of glucocorticosteroids; correct interpretation allows avoiding unnecessary immunosuppression.
ABSTRACT. The present clinical case demonstrates a rare variant of acute coronary syndrome, in which the most likely mechanism of myocardial ischemia was extrinsic compression of a coronary artery by an intrapericardial mass with magnetic resonance imaging features of a teratodermoid tumor. A 47-year-old woman was admitted with clinical signs of acute coronary syndrome with ST-segment elevation. Echocardiography revealed regional left ventricular wall motion abnormalities and a mass in the pericardial cavity adjacent to the anterior and anterolateral walls of the left ventricle. Contrast-enhanced cardiac magnetic resonance imaging showed a well-defined heterogeneous mass measuring 33 × 43 × 41 mm with features consistent with a teratodermoid lesion. The differential diagnosis included cardiac and pericardial tumors, metastatic disease, and visceral syphilis. The patient refused biopsy for morphological verification of the mass, as well as surgical treatment. During four years of follow-up, clinical deterioration associated with progression of chronic heart failure was observed. Thus, this case demonstrates a rare “non-classical” cause of the clinical presentation of “classical” acute coronary syndrome and is intended to broaden physicians’ understanding of the etiology of myocardial ischemia.
ABSTRACT. Osteoarthritis (OA) was previously considered primarily a degenerative disease associated with joint “wear and tear.” Nevertheless, recent studies indicate that chronic, low-grade inflammation is a central factor in its development. The aim of this review is to characterize the morphology of inflammation in OA, focusing on macrophage polarization mechanisms and the role of obesity. A literature review of the last 5 years was conducted using PubMed, MEDLINE, and eLibrary databases. The analysis focused on pathogenetic mechanisms of joint damage, macrophage polarization, and obesity’s impact on disease progression. The results of the analysis allow us to conclude that the morphology of inflammation in OA reflects a complex network of cellular interactions, in which macrophage polarization plays a pivotal role, and obesity serves as one of the factors precipitating this process.
ABSTRACT. Systemic sclerosis (SSc) is a rare systemic autoimmune disease of connective tissue characterized by a markedly heterogeneous clinical course and multiorgan involvement. The etiology of the disease is considered the result of a complex interaction between exogenous trigger factors and a genetic predisposition. Viral and bacterial infections, occupational hazards (exposure to silica dust, chemicals), and exposure to cold are discussed in the current literature as potential triggers. Along with studying these external factors, in recent years, scientists have focused on identifying new genetic markers for the development of SSc. An analysis of current data on the genetic basis of predisposition to SSс and the mechanisms of its development was conducted based on a review of literature data for the period from 2010 to 2026. A search for relevant sources was conducted in the international databases PubMed, Scopus, Web of Science, as well as in the Russian scientific electronic library eLibrary.ru.
ABSTRACT. Early osteoarthritis (OA) developing in young individuals is increasingly recognized as one of the clinical manifestations of heritable disorders of connective tissue (HDCTs). In contrast to age-associated osteoarthritis, degenerative joint changes in HDCTs arise in the context of primary defects of the extracellular matrix, impaired mechanotransduction, and dysregulation of tissue-remodeling signaling pathways, particularly transforming growth factor-β (TGF-β). This review discusses the hypothesis of distinct endophenotypes of early OA in HDCTs, including a fibrotic endophenotype (predominantly associated with Marfan syndrome), and osteopenic and mixed endophenotypes, more commonly observed in hypermobility-related conditions such as the hypermobile type of Ehlers–Danlos syndrome. Particular emphasis is placed on the role of subchondral bone as an active pathogenic compartment and on TGF-β-mediated transdifferentiation of resident fibroblasts into α-smooth muscle actin (α-SMA)-positive myofibroblasts, which may promote the formation of a functionally compromised collagen matrix. Phenotypic stratification of early OA in HDCTs is considered a prerequisite for a personalized approach to diagnosis and management in this patient population.
Background. Glucosamine and chondroitin sulfate are widely used symptomatic slow-acting drugs for osteoarthritis; however, their efficacy remains controversial.
Objective: to evaluate the efficacy of combined glucosamine and chondroitin sulfate therapy in knee osteoarthritis through a systematic review and meta-analysis of randomized controlled trials.
Materials and methods. A systematic search of Medline, EMBASE, Cochrane Library, and PubMed databases was conducted covering 2000–2024. Eligible studies were randomized controlled trials of duration ≥8 weeks comparing glucosamine and/or chondroitin sulfate with placebo in symptomatic knee osteoarthritis. Quality was assessed with Cochrane RoB 2.0 and Newcastle–Ottawa tools. Random-effects meta-analysis (DerSimonian–Laird method) was used to calculate pooled standardized mean differences (SMD) with 95% confidence intervals.
Results. Seventeen studies (n = 6,198) were included. The mean age of participants was 60.5 ± 10.1 years; 68.6% were women. The mean treatment duration was 34.7 ± 33.3 weeks. Combined therapy was associated with statistically significant improvements versus placebo in visual analogue scale pain (SMD -0.180; 95% CI: from -0.271 to -0.089; p < 0.001; I² = 81.7%) and WOMAC function (SMD -0.170; 95% CI: from -0.254 to -0.086; p < 0.001; I² = 78.1%). The safety profile was similar to placebo. Egger’s test did not detect publication bias (p >0.10).
Conclusion. Combined glucosamine and chondroitin sulfate therapy provides statistically significant but clinically small improvements in pain and function for knee osteoarthritis. The effect size is small (SMD <0.2) but may be clinically relevant for selected patients given the favorable safety profile.
Background. QRS complex fragmentation (fQRS) is regarded as an electrocardiographic marker of inhomogeneous intraventricular conduction that may reflect ischemic injury, scar formation, and myocardial electrical instability. In patients with ST-elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI), the presence of fQRS may be associated with an increased risk of early and long-term adverse cardiovascular outcomes.
Objective: To evaluate the prognostic value of fQRS in patients with STEMI who underwent PCI with respect to in-hospital mortality and major adverse cardiovascular events during long-term follow-up.
Materials and methods. A systematic search was conducted in the PubMed and Cochrane Library databases covering the period from January 1, 2010, to May 1, 2026. Prospective and retrospective observational studies of STEMI patients who underwent primary PCI were included if they reported data on in-hospital mortality and/or long-term adverse cardiovascular outcomes stratified by fQRS status. The quality of included studies was assessed using the Newcastle–Ottawa Scale. Quantitative synthesis was performed using a random-effects model to calculate the pooled odds ratio (OR) for in-hospital mortality and risk ratio (RR) for long-term outcomes. Heterogeneity was assessed using the I² statistic; the robustness of the findings was assessed by sequential leave-one-out sensitivity analysis.
Results. Nine studies comprising a total of 3,834 patients were included in the analysis. The presence of QRS complex fragmentation on ECG was associated with an increased risk of in-hospital mortality (OR 3.15; 95% CI: 1.70–5.84; p = 0.0003; I² = 65%) and adverse long-term cardiovascular outcomes (RR 3.43; 95% CI: 1.78–6.61; p = 0.0002; I² = 61%) in STEMI patients after primary PCI. Following exclusion of two outlier studies, heterogeneity for the in-hospital mortality outcome decreased (I² = 27%) while the statistical significance of the effect was maintained.
Conclusion. The results of this meta-analysis indicate an association between QRS complex fragmentation and an increased risk of in-hospital mortality and adverse long-term cardiovascular outcomes in STEMI patients who underwent primary PCI. However, the heterogeneity of results and the predominantly observational nature of the included studies necessitate cautious interpretation of the findings. Further prospective studies are warranted to clarify the prognostic value of fQRS.
ABSTRACT. Early, adequate cardiovascular risk stratification as part of primary prevention is most justified in young and middle-aged individuals due to its maximum clinical benefits. An analysis of the main actual risk assessment tools designed to identify and correct cardiovascular risk factors in the 20–59 age group is performed. The majority of existing risk assessment systems are most effective within the population groups for which they were developed; their informativeness decreases when used in other populations, even after calibration based on current morbidity and mortality rates. Furthermore, significant differences can be observed in the structure and predictive value of cardiovascular risk factors in age cohorts under and over 40 years. Despite the potential of artificial intelligence and machine learning to improve the accuracy of risk stratification for any age group, the widespread implementation of these methods is limited by the lack of sufficient evidence of their clinical superiority over traditional approaches to personalized prognosis in primary prevention. A solution to this problem may lie in validating existing risk stratification models for target patient groups, as well as increasing their informativeness by expanding the set or varying the range of cardiovascular risk markers. It is also important to consider the availability of assessment methods in clinical practice, particularly in primary healthcare.
