Background: Cardiovascular disorders, especially atherosclerosis, have been associated with allergic inflammation. In addition to traditional inflammatory responses, there is evidence that the development and instability of coronary artery plaque may be influenced by effector cells of allergic inflammation. This review examines the phases of allergic pathology, the immunological mechanisms of atherosclerosis, and the clinical link between allergic diseases (asthma, atopic dermatitis, allergic rhinitis, and food allergy) and cardiovascular disease (CVD), along with future therapeutic perspectives. Material and Method: A literature search was conducted in PubMed, Google scholar; ScienceDirect, Scopus, and studies published between 2014–2024 were taken into consideration. Keywords included allergic inflammation, eosinophils, mast cells, reactive oxygen species, atherosclerosis, Th2 cells, and cytokines. Epidemiological studies and review articles were included. Results: Emerging evidence suggests that allergic inflammation contributes to atherosclerosis through interconnected mechanisms such as eosinophil activation, reactive oxygen species production, mast cell degranulation, and endothelial dysfunction. Th2-driven immune responses, which are mediated by cytokines such as IL-4, IL-5, and IL-13, as well as eosinophil activity and mast cell degranulation, play a crucial role in vascular inflammation and plaque progression. Additionally, changes in lipid metabolism contribute to this process. Epidemiological studies support this connection, indicating that patients with chronic allergic conditions such as asthma, allergic rhinitis, food allergy, and atopic dermatitis experience increased cardiovascular morbidity. However, most current data are observational, and our understanding of the underlying mechanisms in humans remains limited, often relying on insights gained from preclinical models. Conclusions: A potential mechanism for cardiovascular risk is suggested by the interaction between atherosclerosis and allergic inflammation. Promising alternatives for treating allergic inflammation and cardiovascular issues include novel treatments like cytokine inhibitors, mast cell stabilizers, and biologics that target certain pathways. Further research is necessary to see whether concentrating on allergy pathways could lead to innovative treatments for cardiovascular disorders or vice versa.

Antibiotic-induced dysbiosis has been increasingly implicated in a range of pediatric outcomes, yet the concept remains variably defined and often inconsistently applied. The purpose of this review is to provide an overview and critical evaluation of the available data regarding the effects of early-life exposure to β-lactam antibiotics on the developing microbiome. We conducted a narrative review of experimental and epidemiological studies examining β-lactam exposure during pregnancy, the perinatal period, and early childhood was conducted. β-lactams induce reproducible alterations in microbial composition, diversity, and metabolic function, including decreases in Bifidobacterium and Lactobacillus and a relative increase in Enterobacteriaceae and other facultative anaerobes, especially in early life. Reduced microbial diversity and changed short-chain fatty acid-producing taxa often accompany these compositional changes. However, associations with immune, metabolic, and neurodevelopmental outcomes are heterogeneous and frequently confounded by indication host-related factors. Evidence for causality in humans remains limited despite strong mechanistic support from animal models. Current data support cautious interpretation, even though β-lactam-associated microbiome perturbations may contribute to disease susceptibility during vulnerable developmental windows. While mechanistic and longitudinal evidence continues to develop, antibiotic stewardship focused on appropriate indication and duration is still crucial.

Background: Giant cell myocarditis (GCM) is a rare condition with an incompletely understood immune pathogenesis, characterized by inflammatory damage to the myocardium and the presence of multinucleated giant cells on histopathological examination. The frequently fulminant and severe course requires rapid intervention for a correct diagnosis and the initiation of immunosuppressive therapy, which is often life-saving. Materials and methods: This article contains information from observational studies and case reports, systematically collected from prestigious publications such as JACC, NEJN, ESC, JCC, Heliyon, and Cureus found in the PubMed and ClinicalTrials.gov databases. Thus, 25 patients diagnosed with giant cell myocarditis between March 2019 and May 2025 were analyzed, with a focus not only on the initial clinical evolution, mortality incidence, and the need for heart transplantation but also on the incidence of major complications such as cardiogenic shock and malignant rhythm and conduction disorders refractory to drug treatment. These parameters were studied according to certain intrinsic factors that cannot be influenced, such as age at onset, gender, and associated pathology of the patient, as well as extrinsic factors that can be influenced, such as the time of diagnosis and the start of immunosuppressive therapy. The results obtained were compared with those in the literature from previous years, considering the limitations of the current study. Results: The selected patients were 13 women (52%) and 12 men (48%), mostly from the US and Japan, aged between 22 and 76 years, with an average age of 44.92 years. An associated autoimmune pathology was found in 40% of patients in this group, and previous cardiovascular pathology in 28%. Only 8% had a history of GCM. The clinical onset of new-onset heart failure, refractory to usual therapy, with progressive dyspnea as the cardinal symptom was found in 12 patients, representing 48% of cases; palpitations as an expression of rhythm or conduction disorders were found in five patients, representing 20%; precordial discomfort to precordial pain accompanied or not by ST-T segment changes was present in four patients, representing 16%; and general signs and symptoms or those of other organs were present in three (12%) cases. The diagnosis was made by histological examination of the biopsy fragment obtained by endomyocardial biopsy or from the myocardial fragment obtained during the implantation of mechanical cardiovascular support devices and, less frequently, on the explanted heart and at autopsy. In terms of progression, of the 25 patients, four (16%) died, four (16%) required heart transplantation, and 16 (64%) had a severe progression with cardiogenic shock, which required mechanical circulatory support in 11 (44%) cases. The outcome was mainly influenced by the early diagnosis and administration of immunosuppressive medication, but also by the age of the patients and associated chronic diseases. Conclusions: Giant cell myocarditis is a serious condition that, in the absence of rapid diagnosis and appropriate immunosuppressive therapy, has a fulminant, often fatal course. Clinical suspicion of giant cell myocarditis remains important in the initial diagnosis. Raising this suspicion, together with modern and improved paraclinical investigations compared to previous years, has led to faster diagnosis and administration of immunosuppressive therapy in this pathology. Histological examination remains the gold standard for final diagnosis, but it should be noted that it may be non-diagnostic. In the face of a strong suspicion of giant cell myocarditis, the best approach is to start immunosuppressive therapy and monitor the patient’s progress. Immunosuppressive treatment remains decisive in influencing the evolution of this condition, both through prompt administration and through the adaptation of therapeutic regimens to the evolution of patients. A more detailed understanding of the immune-mediated pathogenesis of GCM and the identification of clinical risk factors for unfavorable short- and long-term outcomes may enable earlier risk stratification and the development of more targeted, individualized therapeutic strategies.

Background: Varicose veins (VVs) are an overlying manifestation of chronic venous disease, commonly occurring in the lower extremities. While typically linked to primary venous insufficiency, they can occasionally be secondary to systemic disease, e.g., malignancies, by various mechanisms such as tumor compression, hypercoagulability, and paraneoplastic syndromes. Bilateral varicose veins, as a presenting symptom of gastric cancer, are extremely rare and poorly documented. Materials and Methods: A comprehensive literature search was conducted to identify reports and studies linking varicose veins and malignancies, with particular focus on gastric cancer. The search was performed using the PubMed, Scopus, and Web of Science databases covering the last 13 years. Results: Literature Review: A review of the literature in the past decade identified publications, mostly case reports, describing associations between varicose-like venous changes and malignancies such as gastric, pancreatic, hepatic, and small-bowel tumors. The predominant mechanisms reported were inferior vena cava obstruction, tumor-related thrombosis, and paraneoplastic migratory superficial thrombophlebitis (Trousseau’s syndrome). Only a few cases involved gastric cancer as the primary site, with venous changes often being the first clinical sign. There is limited experience with gastric cancer that presents alongside bilateral collateral or varicose veins initially. Apart from the various reports having malignancies and varicose veins we also describe the case of a 50-year-old man who had extended history of bilateral lower-limb varicose veins. Severe, unexplained anaemia without obvious bleeding was discovered during examination. A biopsy verified a gastric adenocarcinoma, while upper gastrointestinal endoscopy revealed an ulcerated mass on the stomach’s greater curvature. Peritoneal dissemination was discovered with additional staging. A palliative subtotal gastrectomy was carried out because of the patient’s ongoing anaemia and suspected chronic bleeding caused by the tumour. The venous symptoms preceded any gastrointestinal issues. Conclusions: Although uncommon, malignancy should be considered in the differential diagnosis for atypical or rapidly progressing bilateral varicose veins, especially when accompanied by systemic symptoms or lab results such as unexplained anemia. Increased suspicion may lead to earlier cancer detection in some patients.

Background: Atrial fibrillation (AF) is a prevalent condition with a major influence on patients’ quality of life, especially when blood glucose and heart rate are disrupted and systemic inflammation is present. Objective: This study aimed to compare Kansas City Cardiomyopathy Questionnaire (KCCQ) scores of diabetic patients by AF type and their correlations with different clinical and biological parameters. Material and methods: The retrospective study included 220 patients, from which only 200 were selected because of missing data. Patients were divided into three groups: paroxysmal AF (n = 49), persistent AF (n = 54), and permanent AF (n = 97). Demographic, clinical, and analytical data, echocardiographic parameters, heart rate, blood glucose, renal function, and inflammatory markers were compared between the three groups and their relationship with KCCQ scores. Results: The KCCQ score was significantly higher in patients with paroxysmal AF (69.50 ± 5.93), compared to persistent AF (56.92 ± 3.04) and permanent AF (42.28 ± 5.89), p < 0.001. In subanalyses, based on left ventricular ejection fraction (LVEF), the same trend was maintained, with lower KCCQ scores associated with more severe forms of AF. Significant negative correlations of the KCCQ score with blood glucose level (r = −0.2535, p = 0.0003), heart rate (r = −0.3071, p < 0.0001), and neutrophil–lymphocyte ratio (NLR) (r = −0.2395, p = 0.0006), and a positive correlation with glomerular filtration rate (GFR) (r = 0.4349, p < 0.0001) were identified. Conclusions: The type of atrial fibrillation significantly influences the quality of life assessed by the KCCQ score. Clinical and analytical parameters such as blood glucose, heart rate, systemic inflammation, and renal function significantly correlate with patients’ perception of health, indicating the importance of integrated management of AF.