Although platelets have been traditionally thought of to be essential hemostasis mediators, new research shows how important they are for controlling cellular oxidative stress, inflammatory processes, and immunological responses—particularly during major surgery on the abdomen. Perioperative problems are largely caused by the continually changing interaction of inflammatory cytokines, the formation of reactive oxygen species (ROS), and platelet activation. The purpose of this review is to summarize the most recent data regarding the complex function of platelets in abdominal surgery, with an emphasis on how they interact with inflammation and oxidative stress, and to investigate the impact on postoperative therapy and subsequent studies. Recent study data on platelet biology, redox signals, surgical stress, and antiplatelet tactics was reviewed in a systematic manner. Novel tailored therapies, perioperative antiplatelet medication, oxidative biomarkers of interest, and platelet-derived microscopic particles are important themes. In surgical procedures, oxidative stress dramatically increases the reactive capacity of platelets, spurring thromboinflammatory processes that affect cardiac attacks, infection risk, and recovery. A number of biomarkers, including soluble CD40L, thromboxane B2, and sNOX2-derived peptide, showed potential in forecasting results and tailored treatment. Antiplatelet medications are still essential for controlling risk factors for cardiovascular disease, yet using them during surgery necessitates carefully weighing the risks of thrombosis and bleeding. Biomarker-guided therapies, antioxidant adjuncts, and specific platelet inhibitors are examples of evolving tactics. In abdominal procedures, platelets strategically operate at the nexus of oxidative stress, inflammatory processes, and clotting. Improved patient classification, fewer problems, and the creation of individualized surgical care strategies could result from an increased incorporation of platelet-focused tests and therapies into perioperative processes. To improve clinical recommendations, subsequent studies may want to focus on randomized studies, biomarker verification, and using translational approaches.

Anemia represents one of the most frequent systemic complications of inflammatory bowel disease (IBD), with a consistently higher prevalence reported in patients with Crohn’s disease (CD) compared with ulcerative colitis (UC). While chronic inflammation, impaired iron absorption, and intestinal blood loss are recognized contributors, microbiome-mediated mechanisms influencing host iron availability remain insufficiently explored. Emerging evidence indicates that CD-associated dysbiosis is characterized by an increased abundance of siderophore-producing bacteria, particularly members of the Enterobacteriaceae family. Because siderophores are high-affinity iron-chelating molecules capable of competing with host iron acquisition systems and partially escaping lipocalin-2-mediated sequestration, their expansion may contribute to reduced luminal iron bioavailability. In this systematic review, we analyzed comparative microbiome studies published between 2016 and 2026 that directly evaluated microbial differences between CD and UC. CD microbiota consistently demonstrated enrichment in siderophore-associated taxa relative to UC. Based on these findings, we propose that microbiome-driven iron competition may represent an additional mechanistic contributor to the increased prevalence and persistence of anemia observed in CD. Although direct in vivo quantification of siderophore activity in IBD remains limited, the convergence of ecological, functional, and strain-level microbiome evidence supports a biologically plausible interaction between microbial iron-scavenging strategies and host iron metabolism.

Myocardial ischemia–reperfusion injury (MIRI) represents a major contributor to morbidity and mortality in patients undergoing reperfusion therapy after acute myocardial infarction. Although timely restoration of coronary blood flow is essential for myocardial salvage, reperfusion paradoxically initiates a complex cascade of molecular and cellular events that may aggravate myocardial injury. Oxidative stress is considered one of the central mechanisms underlying MIRI, primarily through excessive production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), leading to mitochondrial dysfunction, calcium overload, endothelial injury, inflammatory activation, and cardiomyocyte death. This review summarizes the current understanding of the pathophysiological mechanisms involved in oxidative stress-mediated reperfusion injury, with emphasis on mitochondrial permeability transition pore opening, inflammasome activation, cytokine release, neutrophil extracellular trap formation, macrophage polarization, and interconnected cell death pathways including PANoptosis. Emerging evidence regarding immunometabolic regulation and epigenetic modulation in MIRI is also discussed. In addition, current pharmacological and non-pharmacological cardioprotective strategies targeting oxidative stress, mitochondrial dysfunction, and inflammatory signaling are reviewed, highlighting both promising experimental findings and the persistent challenges in clinical translation. A deeper understanding of the molecular interplay between oxidative stress and inflammatory pathways may facilitate the development of integrated therapeutic approaches aimed at improving myocardial recovery and long-term cardiovascular outcomes following reperfusion therapy.

Recurrent spontaneous miscarriages represent a significant reproductive challenge, often associated with inherited thrombophilia. Among the genetic factors involved, methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms have been increasingly studied. The two main variants, MTHFR C677T and MTHFR A1298C, have been suggested to contribute to thrombotic events and adverse pregnancy outcomes. This study aims to evaluate the higher prevalence and potential role of MTHFR gene polymorphisms (C677T and A1298C) in the etiology of recurrent spontaneous miscarriages in pregnant women with inherited thrombophilia, in comparison with the classical thrombophilia-associated SNPs—F5 Leiden and the F2 G20210A gene mutation. In this single-center retrospective observational study, 64 women with recurrent pregnancy loss and confirmed inherited thrombophilia were evaluated. Genomic DNA extracted from peripheral blood samples was analyzed for thrombophilia-associated polymorphisms, including F5 Leiden (G1691A), F2 G20210A, MTHFR C677T, MTHFR A1298C, SERPINE1 4G/5G, and F13A1 V34L, using a real-time PCR-based Bosphore^® Thrombophilia Panel. The presence of MTHFR C677T and A1298C polymorphisms was investigated and compared to the incidence of F5 Leiden and F2 G20210A gene SNPs. Associations between genotypes and clinical characteristics, including the number of pregnancy losses, were assessed using chi-square tests, Kruskal–Wallis analysis, and logistic regression models. The most frequently detected polymorphisms were heterozygous variants of the MTHFR gene, with prevalences of 57.8% for C677T and 53.1% for A1298C. Homozygous MTHFR C677T was significantly associated with a higher number of pregnancy losses (Kruskal–Wallis test, p = 0.001). Similarly, the homozygous MTHFR A1298C genotype showed a significant association with increased miscarriage frequency (p = 0.012). Classical thrombophilic mutations were less frequent, with F2 G20210A identified in only two patients, although its presence was associated with a higher number of pregnancy losses (p = 0.030). These findings suggest that combined thrombophilic polymorphisms may contribute to recurrent pregnancy loss, although larger studies are required to confirm these observations.

Pediatric inflammatory bowel disease (PIBD), encompassing Crohn’s disease (CD) and ulcerative colitis (UC), is associated with inflammation that extends beyond the gastrointestinal tract. Among the most significant extraintestinal complications are anemia and thrombosis, both of which can impact disease severity, quality of life, and long-term outcomes. This review aims to explore the intertwined pathophysiology of anemia and thrombosis, clinical implications of these two complications, and management strategies for anemia and thrombosis in PIBD. Anemia is the most common systemic complication in PIBD, with multifactorial etiologies, including iron deficiency, chronic inflammation, and nutritional deficiencies. Despite its high prevalence, it remains underdiagnosed and undertreated. Thrombosis, although less frequent, poses significant risk, particularly during disease flares, hospitalizations, and in the presence of central venous catheters or corticosteroid therapy. The proinflammatory and hypercoagulable state in inflammatory bowel disease (IBD) increases thrombotic risk, necessitating early identification and, in high-risk cases, consideration of thromboprophylaxis. Anemia and thrombosis represent significant yet often overlooked complications in PIBD. Proactive screening, individualized risk stratification, and integrated management approaches are critical to improving outcomes. Further pediatric-specific research is needed to develop tailored prevention and treatment strategies.

Orthopedic trauma surgery is associated with an increased risk of postoperative hypercoagulability, predisposing patients to potentially life-threatening thromboembolic complications, including deep vein thrombosis (DVT) and pulmonary embolism (PE). Conventional coagulation tests, including prothrombin time (PT), activated partial thromboplastin time (aPTT), and international normalized ratio (INR), have limited sensitivity in detecting the complex hemostatic alterations that occur following orthopedic trauma procedures. In recent years, viscoelastic hemostatic assays—thromboelastography (TEG) and rotational thromboelastometry (ROTEM)—alongside specific coagulation biomarkers, such as D-dimer, fibrinogen, thrombin–antithrombin (TAT) complexes, and prothrombin fragments F1+2, have emerged as promising tools for a more comprehensive assessment of coagulation status in the perioperative setting. This narrative review, conducted using a structured literature search strategy with systematic elements, aims to synthesize the current evidence regarding the use of TEG/ROTEM and coagulation biomarkers in evaluating hypercoagulability following orthopedic trauma surgery, identify patterns of hemostatic dysregulation across different surgical procedures and patient populations, and highlight existing gaps in the literature. A structured search was conducted across major electronic databases, including PubMed, Scopus, Web of Science, Embase, and the Cochrane Library. The findings of this review provide clinicians with a clearer framework for perioperative coagulation monitoring and inform future research aimed at optimizing individualized thromboprophylaxis strategies in orthopedic trauma patients.