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.

Background and objectives: The efficacy and safety of PD-L1 inhibitors in the treatment of cervical cancer is an ongoing research question. This review aims to establish a clear profile of atezolizumab, examining its impact on survival outcomes, response rates, and safety measured by serious adverse events (SAEs). Materials and methods: A literature search was conducted using PubMed, Scopus, and Web of Science, focusing on articles published up to February 2024. The review followed the PRISMA guidelines and synthesized outcomes from four randomized trial studies involving atezolizumab administered at 1200 mg IV every three weeks, alone or in combination with chemoradiotherapy. Results: A total of 284 patients received atezolizumab, the majority being advanced stage cervical cancer (IVA-IVB). Median follow-up times ranged from 9 weeks to 32.9 months. It was found that combining atezolizumab with standard therapies extended median progression-free survival (PFS) from 10.4 to 13.7 months and overall survival (OS) from 22.8 to 32.1 months, according to the phase III trial. Monotherapy and initial treatment settings with atezolizumab also showed promising efficacy, with disease-free survival rates at 24 months reaching 79% compared to 52% with standard therapy alone. However, the treatment was associated with high rates of SAEs, reaching up to 79% in more intensive treatment combinations. Conclusions: Atezolizumab demonstrates significant potential in improving PFS and OS in patients with cervical cancer, supporting its inclusion as a first-line treatment option. Despite the efficacy benefits, the high incidence of SAEs necessitates careful patient selection and management strategies to mitigate risks. This systematic review supports the continued evaluation of atezolizumab in broader clinical trials to refine its therapeutic profile and safety measures in the context of cervical cancer treatment.

Background and Objectives: Hip fractures are a leading cause of morbidity in the elderly, often resulting in declining physical function, psychological distress, and diminished quality of life (QoL). This study aimed to evaluate changes in QoL among hip fracture patients preoperatively and postoperatively, comparing diverse patient subgroups to identify factors influencing recovery. Methods: We conducted a prospective longitudinal observational study at Victor Babeș University of Medicine and Pharmacy Timișoara, recruiting 77 adult patients admitted for surgical management of hip fractures between March 2023 and March 2025. Standardized questionnaires, including the Short Form-36 (SF-36), World Health Organization Quality of Life (WHOQOL-BREF), Hospital Anxiety and Depression Scale (HADS), and Generalized Anxiety Disorder-7 (GAD-7), were administered preoperatively and at 3 months postoperatively. Demographic, clinical, and surgical variables were also recorded. Results: Participants’ mean age was 72.6 years (SD 8.1), with 57.1% female. Postoperative QoL scores (SF-36 Physical Function domain mean 52.7 ± 9.2) improved significantly compared to preoperative scores (44.8 ± 8.7, p = 0.012). WHOQOL-BREF physical and psychological domain scores similarly increased (p < 0.05). Anxiety and depression symptoms, as measured by HADS and GAD-7, decreased markedly postoperatively in most subgroups. Subgroup analyses revealed that patients undergoing total hip arthroplasty demonstrated more pronounced QoL improvements than those receiving partial hip replacement. Older patients (≥80 years) exhibited improvements but at a slower rate. Conclusions: Quality of life indicators show notable improvement following surgical treatment of hip fractures, underscoring the significance of timely orthopedic intervention and comprehensive perioperative care. Anxiety and depression levels also declined, highlighting the benefits of a structured follow-up. These findings may guide clinicians toward optimizing patient-centered recovery protocols and targeted interventions, particularly for older adults or those with high baseline anxiety and depression levels.

Background and Objectives: Negative-pressure wound therapy (NPWT) expedites tissue repair, yet functional recovery depends on adjunct rehabilitation. Evidence from high-resource settings is difficult to translate to Romanian county hospitals, where advanced devices are scarce. The objective of this study is to determine whether two tiers of low-technology, therapist-delivered exercise improve mobility, oedema resolution, pain and quality-of-life (QoL) beyond NPWT alone in adults with acute lower-limb wounds. Methods: A single-centre, prospective observational study (January 2021–June 2024) enrolled 92 patients and randomised them unevenly into: Group A, NPWT only (n = 39); Group B, NPWT + routine physiotherapy (n = 33); Group C, NPWT + enhanced manual programme (n = 20). All received −125 mmHg continuous suction; rehabilitation started 48 h post-operation. Primary outcomes were ankle dorsiflexion and knee flexion at 12 weeks. Secondary outcomes included calf circumference, ultrasound oedema depth, Manual Muscle Testing (MMT), pain (VAS), analgesic use and SF-36 domains through 24 weeks. Results: Baseline characteristics were similar (p > 0.40). At 12 weeks dorsiflexion reached 20.1 ± 1.8° in Group C, surpassing Group B (18.4 ± 2.1°; p = 0.004) and Group A (16.0 ± 2.3°; p < 0.001). Knee flexion followed the same gradient (140.8 ± 3.2°, 137.6 ± 3.4°, 133.4 ± 3.8° respectively). Oedema depth fell fastest in Group C (0.4 ± 0.2 mm by day 42) versus B (0.6 ± 0.2 mm) and A (0.8 ± 0.3 mm). Week-12 MMT grade ≥ 4.5 was attained by 95% of Group C, 85% of B and 72% of A (χ² = 10.9, p = 0.004). VAS pain fell more steeply with each rehabilitation layer, paralleled by a stepwise decline in daily tramadol. All SF-36 domains were highest in Group C at 24 weeks (Physical Function 88.7 ± 4.8 vs. 85.1 ± 5.4 vs. 78.2 ± 5.9; p < 0.001). Mobility correlated positively with QoL (r = 0.66) and inversely with pain and oedema. Conclusions: In a resource-constrained Romanian setting, adding structured manual physiotherapy to NPWT produced meaningful functional and patient-centred gains, while an “enhanced” programme incorporating daily PNF and elastic-band strengthening delivered the largest observed benefit. These findings justify prioritising therapist-led interventions even where sophisticated equipment is unavailable.

Background/Objectives: Native valvular heart disease (VHD) lacks established lesion-modifying pharmacotherapy. Sodium–glucose cotransporter 2 inhibitors (SGLT2is) improve heart-failure and cardiorenal outcomes, but their relevance to VHD differs by phenotype and treatment setting. Methods: MEDLINE/PubMed, Scopus, Web of Science Core Collection and Cochrane CENTRAL were searched from inception to 27 July 2026, together with trial registries, conference proceedings and reference lists. Evidence was synthesized by clinical setting, study design and mechanistic proximity to valve tissue. Results: Functional/secondary mitral regurgitation (MR) currently provides the most convincing valve-related signal: EFFORT and DEFORM showed concordant reductions in MR severity with favorable remodeling surrogates, consistent with HF-directed unloading rather than a primary leaflet effect. DapaTAVI provides the strongest hard-outcome evidence after the mechanical correction of aortic stenosis, reducing the 1-year death/worsening-HF composite in selected high-risk patients. In 28,940 HF patients from the SHEBAHEART registry, SGLT2i use was associated with reduced death/HF hospitalization and a 28% lower adjusted risk of tricuspid-regurgitation progression, but these data remain observational. Native aortic-stenosis progression is supported only by target-trial emulation, and no dedicated clinical evidence exists for native aortic regurgitation. Conclusions: SGLT2is should be integrated into guideline-directed HF therapy when indicated. In secondary MR, reassessment after optimized therapy should precede mitral intervention when clinically appropriate. A post-TAVI benefit should be interpreted as cardiorenal/HF protection, not valve modification. The current evidence does not justify SGLT2is solely to modify an untreated native valve lesion.

Background: Atrial Fibrillation (AF) is associated with a prothrombotic state and increased risk of ischemic stroke. Type 2 diabetes mellitus (T2DM) is a major cardiometabolic comorbidity in AF and independently increases thromboembolic risk. D-dimer is a well-established biomarker of coagulation activation and fibrin turnover, but the specific contribution of T2DM to D-dimer levels in AF remains insufficiently characterized in real-world cohorts. Methods: We conducted a retrospective, observational, single-center study including 300 adult patients with non-valvular AF evaluated at a tertiary university hospital. Patients were stratified according to the presence of T2DM (150 with T2DM and 150 without diabetes). Plasma D-dimer levels were compared between groups and analyzed across clinically relevant thresholds and CHA₂DS₂-VASc categories. Multivariable linear and logistic regression models were used to assess the independent association between T2DM and D-dimer levels after adjustment for demographic factors, comorbidities, renal function, prior stroke, CHA₂DS₂-VASc score components, and oral anticoagulation. Results: Patients with T2DM exhibited significantly higher D-dimer levels than non-diabetic patients (median 0.94 vs. 0.63 µg/mL FEU, p < 0.001). T2DM was independently associated with higher log-transformed D-dimer levels (adjusted β = 0.19, p < 0.001) and with increased odds of elevated D-dimer above both 0.5 µg/mL and 1.0 µg/mL thresholds. Across all CHA₂DS₂-VASc categories, patients with T2DM consistently showed higher D-dimer concentrations. Findings remained robust in sensitivity analyses restricted to anticoagulated patients. Conclusions: In patients with atrial fibrillation, type 2 diabetes mellitus is associated with increased coagulation activity as reflected by higher D-dimer levels, independent of clinical thromboembolic risk. These results support the concept of a diabetes-associated hypercoagulable AF phenotype and highlight the potential role of coagulation biomarkers in refining risk stratification.