Oxidative stress and chronic inflammation are tightly interconnected biological processes that play central roles in colorectal cancer (CRC) initiation, progression, and resistance to therapy. Understanding their reciprocal interactions may identify novel biomarkers and therapeutic targets with translational relevance. Methods: This systematic review with qualitative synthesis was conducted in accordance with the PRISMA 2020 guidelines. A comprehensive literature search of PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar was performed from January 2005 to June 2025. Eligible studies investigated mechanistic links between oxidative stress and inflammation in colorectal cancer, assessed oxidative or inflammatory biomarkers, or explored redox- and inflammation-targeted therapeutic strategies. Study selection and data extraction were performed systematically. Due to heterogeneity in study designs and outcomes, a qualitative synthesis was undertaken without meta-analysis. Results: Twenty-six studies met the inclusion criteria. Evidence consistently demonstrated that redox-sensitive pathways—including NF-κB, NRF2, and IL-6/JAK/STAT3—drive colorectal carcinogenesis by promoting genomic instability, immune evasion, angiogenesis, and therapy resistance. Biomarkers such as 8-hydroxy-2′-deoxyguanosine, malondialdehyde, F₂-isoprostanes, C-reactive protein, interleukin-6, and tumor necrosis factor-α were frequently associated with tumor stage, prognosis, and treatment response. Therapeutic strategies targeting oxidative stress and inflammation showed promising preclinical and early translational results, particularly in combination with chemotherapy or immunotherapy. Conclusion: Oxidative stress and inflammation constitute a synergistic axis that critically influences colorectal cancer biology. Although several biomarkers and redox-targeted interventions demonstrate translational potential, robust clinical validation is still required before routine implementation. Integrative strategies guided by biomarker profiling may represent a future direction for personalized CRC management. Most therapeutic approaches discussed are supported by preclinical and early translational evidence, and their clinical applicability remains to be validated.

Background: Vulvar squamous cell carcinoma (VSCC) is an uncommon yet increasingly relevant malignancy characterized by two distinct etiopathogenetic pathways: HPV-associated and HPV-independent. Data from Eastern Europe remain scarce, where demographic and diagnostic variability may influence disease presentation and outcomes. Purpose: This study aimed to assess the epidemiologic characteristics, HPV status, surgical management, and postoperative morbidity of VSCC in a Romanian single-center cohort, providing real-world evidence from an underrepresented region. Methods: A retrospective analysis was conducted on all 35 consecutive patients with histologically confirmed vulvar squamous cell carcinoma (VSCC) diagnosed and treated between January 2017 and December 2024 at the Department of Obstetrics and Gynecology, County Emergency Clinical Hospital of Craiova, Romania. Demographic, histopathologic, and surgical data were reviewed. HPV genotyping was performed on formalin-fixed paraffin-embedded (FFPE) tissue using PCR-based methods. Results: HPV DNA was detected in 31.4% of cases, predominantly genotypes 16, 18, and 33. HPV-positive patients were significantly younger than HPV-negative ones (median 58 vs. 72.5 years, p < 0.001), supporting the dual-pathway model of carcinogenesis. Early postoperative complications occurred in 65.7% of patients and late morbidity in 71.4%, secondary lymphedema. Surgical radicality was not significantly associated with early complications or length of hospitalization. Conclusions: This study highlights the epidemiologic and surgical patterns of VSCC in an Eastern European population, showing that conservative surgical strategies can maintain oncologic safety while reducing morbidity. These findings emphasize the need for standardized HPV testing, optimized perioperative care, and improved surveillance programs to enhance outcomes and survivorship.

Background: Radiotherapy is a cornerstone of treatment for cervical and endometrial cancers but is associated with vascular and perivascular changes that can increase surgical complexity and perioperative morbidity. While these effects are well documented in head, neck, and mediastinal irradiation, the pelvic vasculature remains underexplored. Methods: We retrospectively analyzed 119 patients who underwent pelvic oncologic surgery after RT (57.1% cervical cancer, 42.9% endometrial cancer). Intraoperative vascular findings were recorded and correlated with tumor type, perioperative complications, and vascular injury. Logistic regression was used to identify predictors of perioperative morbidity. Results: Perivascular fibrosis (21.8%) and inflammatory thrombosis (10.1%) were the most frequent intraoperative vascular changes, with no significant differences between tumor types. Most patients required no vascular procedure; when needed, simple venorrhaphy was sufficient, and no complex vascular reconstructions were performed. Perioperative complications occurred more frequently in cervical cancer patients (RR = 2.66; p = 0.02), with hemorrhage and urinary tract injury being the most common. Cervical tumor site and perivascular fibrosis were borderline predictors of complications. Conclusions: Neoadjuvant RT induces measurable intraoperative vascular changes without significantly increasing major vascular injury, particularly in experienced surgical settings. Cervical cancer patients represent a higher-risk subgroup, underscoring the need for meticulous surgical planning and multidisciplinary perioperative management. Perivascular fibrosis may serve as a marker for operative risk stratification, and long-term vascular surveillance is warranted due to the potential for delayed macrovascular events.

Background: Advanced stages of peripheral arterial disease, particularly chronic limb-threatening ischemia, are characterized by unfavorable limb outcomes and a substantial risk of major amputation. Clinical evaluation traditionally focuses on arterial obstruction; however, venous dysfunction may coexist and contribute to local limb pathophysiology in advanced PAD, remaining insufficiently recognized in routine practice. Methods: We performed a retrospective cohort analysis of consecutive patients with advanced peripheral arterial disease managed at the First Surgical Clinic of the Emergency County Clinical Hospital of Craiova over a five-year period (January 2020 to December 2024). Venous disease was defined using a clinically oriented composite definition incorporating imaging-confirmed venous pathology, prior deep venous thrombosis, and persistent lower-limb edema attributable to venous dysfunction. Arterial disease severity was assessed using multimodal imaging. Analyses were performed at both patient and limb levels to evaluate associations between venous disease, arterial severity markers, and clinical outcomes. Results: Among 241 patients (482 limbs), concomitant venous disease was identified in 68.9% at the patient level and was predominantly unilateral. At the limb level, venous disease was significantly associated with markers of severe arterial involvement, including inflow disease, higher segment occlusion scores, impaired tibial runoff, and absence of a patent pedal arch. Despite greater arterial severity, patients with venous disease exhibited a lower unadjusted rate of major amputation compared with those without venous involvement. Conclusions: Concomitant venous disease is highly prevalent in patients with advanced PAD and is closely linked to arterial disease severity. These findings suggest that venous dysfunction represents an integral component of advanced limb-threatening ischemia rather than an isolated comorbidity. Incorporating clinically oriented venous assessment may improve understanding of limb pathophysiology and support a more integrated arterio-venous approach to advanced PAD management.

Background: Vascular access dysfunction remains a major challenge in maintenance hemodialysis (HD). Although chronic kidney disease–mineral and bone disorder may contribute to vascular pathology, the relationship between mineral metabolism markers and cumulative vascular access deterioration remains poorly defined. Methods: This retrospective single-center study included 74 patients receiving maintenance HD. Cumulative vascular access burden was defined by reinterventions, definitive access losses, and additional vascular accesses. Associations with parathyroid hormone (PTH), calcium, phosphorus, calcium–phosphorus product, and alkaline phosphatase (ALP) were evaluated using group comparisons, correlation analysis, and logistic regression. Results: Patients with cumulative vascular access burden had higher ALP levels than those without burden (92.0 vs. 78.0 U/L, p = 0.010), whereas PTH, calcium, phosphorus, and calcium–phosphorus product did not differ significantly. ALP correlated with cumulative burden (Spearman’s ρ = 0.303, p = 0.009), and this association remained statistically significant after adjustment for age, BMI, PTH, and phosphorus (OR per 10 U/L increase = 1.226, 95% CI 1.059–1.418; p = 0.006). Conclusions: Higher ALP levels were associated with greater cumulative historical vascular access burden after adjustment for selected clinical and biochemical variables. These exploratory findings do not establish the prognostic value of ALP for future vascular access outcomes and require prospective validation.

Background/Objectives: Type 2 diabetes mellitus (T2DM) and atherogenic dyslipidemia have been implicated in colorectal cancer (CRC) development, but their prognostic relevance after cancer diagnosis remains unclear. This study aimed to evaluate the association between T2DM, lipid-derived atherogenic indices, and survival outcomes in patients with CRC. Methods: We conducted a retrospective cohort study including 240 CRC patients, of whom 60 had coexisting T2DM. Overall survival (OS) and disease-free survival (DFS) were analyzed using the Kaplan–Meier (KM) method and log-rank tests. In the absence of recurrence-specific data, DFS was defined as time to death or last follow-up. Lipid-related indices, including the atherogenic index of plasma (AIP), atherogenic coefficient (AC), remnant cholesterol (RC), non-high-density lipoprotein cholesterol (non-HDL-C), triglyceride–glucose (TyG) index, and triglyceride-to-HDL cholesterol ratio (TG/HDL-C), were evaluated by tertiles in KM analyses. Multivariable Cox proportional hazards models were constructed to assess the independent prognostic value of AIP, AC, and RC (entered separately as a continuous variable standardized to 1 standard deviation), adjusted for age, sex, adjuvant chemotherapy, radiotherapy, and T2DM status. Sensitivity analyses were performed in stage III–IV patients. Results: During follow-up, 28 deaths occurred. OS did not differ significantly between CRC patients and those with CRC coexisting with T2DM (log-rank p-values = 0.220). DFS analyses showed no significant differences across tertiles of any lipid-related index (all log-rank p-values > 0.05), with overlapping survival curves and no consistent dose–response patterns. In adjusted Cox models, AIP (hazard ratio [HR] per 1 SD = 0.71, 95% CI 0.48–1.06), AC (HR = 0.72, 95% CI 0.44–1.20), and RC (HR = 0.66, 95% CI 0.39–1.12) were not independently associated with DFS. Results were consistent in advanced-stage disease (stage III–IV). Conclusions: In this cohort of patients with CRC, neither T2DM nor lipid-derived indices reflecting atherogenic dyslipidemia and insulin resistance were independently associated with OS or DFS. These findings help refine the clinical interpretation of lipid-derived biomarkers in CRC, suggesting limited prognostic utility beyond established oncologic factors.