Eryptosis is a type of regulated cell death of mature erythrocytes characterized by excessive Ca²⁺ accumulation followed by phosphatidylserine externalization. Eryptosis facilitates erythrophagocytosis resulting in eradication of damaged erythrocytes, which maintains the population of healthy erythrocytes in blood. Over recent years, a wide array of diseases has been reported to be linked to accelerated eryptosis, which leads to anemia. A growing number of studies furnish evidence that eryptosis is implicated in the pathogenesis of liver diseases. Herein, we summarize the current knowledge of eryptosis signaling, its physiological role, and the impact of eryptosis on anemia and hypercoagulation. In this article, upon systemically analyzing the PubMed-indexed publications, we also provide a comprehensive overview of the role of eryptosis in the spectrum of hepatic diseases, its contribution to the development of complications in liver pathology, metabolites (bilirubin, bile acids, etc.) that might trigger eryptosis in liver diseases, and eryptosis-inducing liver disease medications. Eryptosis in liver diseases contributes to anemia, hypercoagulation, and endothelial damage (via ferroptosis of endothelial cells). Treatment-associated anemia in liver diseases might be at least partly attributed to drug-induced eryptosis. Ultimately, we analyze the concept of inhibiting eryptosis pharmaceutically to prevent eryptosis-associated anemia and thrombosis in liver diseases.

Introduction: Compensated cirrhosis carries a significant risk of progression to decompensation, which substantially worsens prognosis. Accurate prediction of decompensation events is critical for guiding surveillance, optimizing intervention timing, and improving patient outcomes. Although many prognostic biomarkers have been studied, findings remain heterogeneous. This umbrella review synthesizes evidence from systematic reviews and meta‐analyses to identify and appraise biomarkers predicting decompensation in alcoholic and nonalcoholic compensated cirrhosis. Methods: PubMed, Scopus, and Web of Science were searched to August 15, 2025, for English‐language systematic reviews and meta‐analyses. From the included meta‐analyses, prognostic performance, heterogeneity, and publication bias were recorded. Results: Four systematic reviews were included, two with meta‐analyses. Strong predictors across reviews were serum albumin, INR, bilirubin, platelet count, and liver stiffness measurement. HVPG remained a robust invasive predictor, while emerging biomarkers—interleukin‐6, keratin‐18, and extracellular vesicles—were associated with an increased risk of decompensation, although the certainty of evidence was limited by heterogeneity and methodological constraints. Composite scores enhanced predictive accuracy. AMSTAR 2 ratings ranged from high to low, with common reporting limitations. Overlap analysis indicated moderate redundancy among primary studies. Conclusions: Both established and emerging biomarkers predict decompensation in compensated cirrhosis. Integrated multidomain models combining clinical, biochemical, and imaging‐derived measures may provide the greatest predictive value for guiding clinical decision‐making.

Long COVID-19 is characterized by the persistence of symptoms and immune alterations beyond the acute phase of SARS-CoV-2 infection. Understanding the demographic, clinical, and immunological differences between individuals with and without long COVID-19 is crucial for developing targeted interventions. This observational study included 206 participants, comprising 90 patients with long COVID-19 and 116 without. Data on demographic, lifestyle, and clinical characteristics were collected, alongside immune cell profiles and SARS-CoV-2 antibody levels. Statistical analyses compared these parameters between the two groups. Long COVID-19 patients were predominantly female (77.8%), older (47.78% aged 41–60, 20% >60 years), and had higher BMI, hypertension (31.1%), and autoimmune diseases (11.1%) compared to nonlong COVID-19 individuals (P < 0.001). Clinical symptoms unique to long COVID-19 included memory loss (40.0%), hair loss (37.8%), fatigue (35.6%), and myalgia/arthralgia (28.9%), all absent in the control group (P < 0.001). Immunologically, patients with long COVID-19 exhibited distinct immune profiles, including elevated cytotoxic T cells (CD3+CD8+), reduced B cells, and higher CD4/CD8 ratios. Moreover, long COVID-19 patients had higher SARS-CoV-2 antibody levels, with 15.5% showing levels between 1000–2500 BAU/ml, compared to 6.9% in controls. These immunological biomarkers, including altered T cell subsets and antibody levels, highlight the complex immune dysregulation associated with long COVID-19. These findings could inform future clinical management and therapeutic strategies targeting immune modulation.

The COVID-19 pandemic has prompted an urgent need to understand the differences between vaccine-induced and natural immunity, particularly in the context of post- COVID syndrome (long COVID). This review compares the immune responses elicited by natural infection and vaccination, focusing on their duration, strength, and effectiveness in mitigating long COVID symptoms. Vaccine-induced immunity, primarily targeting the spike protein of SARS-CoV-2, often produces a more consistent antibody and T-cell response, especially when bolstered by booster doses. In contrast, natural immunity, though broader in scope, is more variable and influenced by factors such as infection severity. Hybrid immunity, resulting from both infection and vaccination, may offer superior protection against long COVID. This comparative analysis highlights the importance of understanding these immune mechanisms to optimize protection strategies against SARS-CoV-2 and its variants.

Studying the consequences of coronavirus infections caused by the SARS-CoV- 2 virus has become crucial in light of its widespread occurrence in society, and the frequent observation of persistent symptoms and health impairments following recovery from the acute phase of the illness. The pandemic has brought about a new chronic, debilitating condition known as long COVID, which deserves serious attention from scientific and medical communities. Currently, we have conflicting knowledge about the factors that may increase the risk of developing such a debilitating condition. The aim of this review was to assess prognostic risk factors for the development of post-COVID-19 conditions. We conducted a systematic search in the databases PubMed, Web of Science, Scopus, CyberLeninka, and the eLibrary electronic library for reports on post-COVID-19 conditions up to April 2024. A total of 52 full-text studies meeting the inclusion criteria were analyzed from both Russian and international sources. The resulting review paper presents a comprehensive overview of recent studies aimed at examining factors preceding COVID-19 infection (gender, age, comorbidities, and others), factors related to COVID-19 infection (severity of acute phase, influence of biomarkers), and the impact of vaccinations on longterm consequences. Much remains unclear regarding long COVID and its risk factors due to conflicting data, possibly caused by the variety of symptoms and complex pathophysiology, including long-term organ damage and unresolved inflammatory processes. This review underscores the high prevalence of post-COVID conditions and the ambiguity in identifying risk factors, necessitating further research for effective management of these conditions.