At present, obesity, as a part of metabolic syndrome, represents the leading factor for disability, and is correlated with higher inflammation status, morbidity, and mortality. The purpose of our study is to add new insights to the present body of knowledge regarding the correlations between chronic systemic inflammation and severe obesity, which cannot be treated without considering other metabolic syndrome conditions. Biomarkers of high-level chronic inflammation are recognized as important predictors of pro-inflammatory disease. Besides the well-known pro-inflammatory cytokines, such as WBCs (white blood cells), IL-1 (interleukin-1), IL-6 (interleukin-6), TNF-alpha (tumor necrosis factor-alpha), and hsCRP (high-sensitivity C-reactive protein), as well as anti-inflammatory markers, such as adiponectin and systemic inflammation, can be determined by a variety of blood tests as a largely available and inexpensive inflammatory biomarker tool. A few parameters, such as the neutrophil-to-lymphocyte ratio; the level of cholesterol 25-hydroxylase, which is part of the macrophage-enriched metabolic network in adipose tissue; or levels of glutamine, an immune–metabolic regulator in white adipose tissue, are markers that link obesity to inflammation. Through this narrative review, we try to emphasize the influence of the weight-loss process in reducing obesity-related pro-inflammatory status and associated comorbidities. All data from the presented studies report positive results following weight-loss procedures while improving overall health, an effect that lasts over time, as far as the existing research data show.

Background and Objectives: Overweight and obesity are well-known conditions that negatively impact the health and lifestyle of an individual. Bariatric surgery is one of the most efficient weight loss techniques. Besides the main effect on the bodyweight, improvement in the levels of inflammatory biomarkers, such as interleukin 6 (IL-6), tumor necrosis factor alpha (TNFalfa), and others, has been observed. The purpose of this study was to establish the correlations between obesity-linked chronic systemic inflammation (estimated with inflammatory cytokine levels) and the weight loss process after metabolic surgery. Materials and Methods: An observational cohort study included two categories: the patients with obesity–bariatric group and the patients without obesity–control group. The study was performed between 1 February 2021 and 1 March 2023. Baseline characteristics, anthropometrics, biochemical assessment and inflammatory biomarkers were measured both before surgery and one year after the procedure, in the case of the bariatric group. The control group was assessed in the same period as the pre-surgery bariatric group. The bariatric group underwent two types of bariatric procedures: the majority underwent laparoscopic sleeve gastrectomy whereas a select few underwent one anastomosis laparoscopic gastric bypass. Results: We performed a prospective study comprising 55 Caucasian patients—from which 33 patients had morbid obesity, a mean age of 41.76 ± 10.78 and a mean BMI of 43.34± 7.51 kg/m². The preoperative levels of IL-6 were positively correlated with waist circumference (r = 0.354, p = 0.043), weight (r = 0.549, p = 0.001) and BMI (r = 0.520, p = 0.002). After applying the Kruskal–Wallis test and Dunn’s test, significant differences for IL-6 (p = 0.010) and adiponectin (p = 0.024) were obtained for values recorded pre- and post-surgery. No correlation was found between adiponectin, IL-6, TNF- α levels and anthropometric indices after surgery. Our study showed that bariatric surgery significantly changes the values of inflammatory cytokines one year after surgery. Nevertheless, we did not find significant correlations between the baseline values of these inflammatory markers and the weight loss process after surgery at a short-term (one-year) follow-up. Conclusions: Our study demonstrated that bariatric surgery significantly changes the level of inflammatory cytokines one year after operation. We demonstrate that preoperative levels of IL-6 are positively correlated with age, WC, and BMI.

Background/Objectives: Acute appendicitis (AA) is among the most common surgical emergencies. Differentiating between complicated (CAA) and uncomplicated (UAA) forms is essential for selecting the appropriate management—operative or non-operative—and for optimizing patient prioritization and outcomes. This study aimed to evaluate the diagnostic performance of emerging inflammatory indices in distinguishing these forms of AA. Methods: A total of 514 adult patients with surgically confirmed AA were retrospectively analyzed. Six immune-inflammatory indices—neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), monocyte-to-lymphocyte ratio (MLR), systemic immune-inflammation index (SII), systemic inflammation response index (SIRI), and pan-immune-inflammation value (PIV)—were calculated and compared with intraoperative and histopathological findings. Postoperative outcomes, including length of hospital stay (LOS) and hospitalization costs, were also evaluated. Results: All six indices were significantly higher in intraoperatively identified complicated cases (p < 0.0001). In histopathological analysis, five indices (NLR, MLR, SII, SIRI, and PIV) remained significantly elevated in patients with wall necrosis or perforation (p = 0.000–0.019), while PLR did not reach statistical significance. The indices showed fair diagnostic accuracy (AUC = 0.664–0.719, p < 0.0001). NLR and MLR were independent risk factors for CAA (p = 0.006 and p = 0.016), and MLR was also independently associated with complicated histopathological findings (p = 0.036). PIV independently predicted both increased LOS and higher hospitalization costs (p = 0.001 for each). Conclusions: These easily calculable inflammatory markers can serve as useful adjuncts for preoperative stratification of AA, supporting timely decision-making and contributing to more cost-effective emergency surgical care.

Human epidermal growth factor receptor 2 (HER2) dysregulation contributes to tumorigenesis in gastric and gastroesophageal junction adenocarcinomas (GC/GEJ). HER2 overexpression has been associated in multiple cohorts with aggressive behavior and poor outcomes. While HER2 amplification has long guided therapy in HER2-positive disease, antibody–drug conjugates (ADCs) have shifted attention toward the HER2-low category, typically defined as immunohistochemistry (IHC) 1+ or IHC 2+ with negative in situ hybridization (ISH). This narrative review integrates evidence from the peer-reviewed literature, current testing recommendations, and registered clinical trials. It clarifies practical issues in HER2-low assessment and maps the evolving therapeutic landscape of HER2-targeted ADCs including rational combination strategies that may extend benefit beyond conventionally HER2-positive tumors. A cross-tumor perspective contrasts GC/GEJ testing and biology with the breast cancer paradigm and summarizes the importance of HER2-low expression in non-gastric malignancies. Finally, we discuss the therapeutic strategies in HER2-low GC/GEJ and highlight key safety and monitoring considerations for HER2-directed ADCs.

Background and Objectives: Atherosclerosis is a chronic inflammatory disease significantly contributing to cardiovascular morbidity and mortality. This study primarily aims to evaluate the role of baseline blood glucose levels and inflammatory markers in the histopathological features of atherosclerotic plaques in the carotid and femoro-popliteal arteries. Materials and Methods: In this retrospective, observational, and monocentric study, 165 patients diagnosed with infrainguinal peripheral arterial disease or carotid artery disease hospitalized in the Vascular Surgery Clinic, between January 2019 and December 2023, were included. From the electronic database of the hospital, we documented demographic data, cardiovascular comorbidities, including hypertension, atrial fibrillation, ischemic heart disease, and chronic heart failure, as well as chronic kidney disease, diabetes, and prevalent risk factors such as active smoking, dyslipidemia, and obesity. Additionally, we recorded the arterial site from which the atherosclerotic plaque was obtained, along with laboratory data obtained at the time of admission prior to the surgery. The patients were divided into “Carotid Artery” and “Femoro-Popliteal Axis” based on anatomical location. Results: A greater prevalence of male patients (p = 0.008) and dyslipidemia (p = 0.002) was found in the group with atherosclerotic plaques from the femoro-popliteal axis. Laboratory data also showed increased lymphocyte (p = 0.020) and PLT (p = 0.028) levels in this group. There was no significant difference in the types of atherosclerotic plaques between the two patient groups. However, those in the Carotid Artery group showed a higher rate of antiaggregant treatment and a reduced incidence of dual therapy (p < 0.001). The Spearman correlation analysis revealed a positive correlation between baseline glucose levels and NLR (r = 0.402, p < 0.001), MLR (r = 0.217, p = 0.005), PLR (r = 0.306, p < 0.001), and LGI (r = 0.693, p < 0.001). Furthermore, the predictive roles of glucose, NLR, MLR, and LGI were assessed through multivariate analysis. Consequently, elevated baseline values of the parameters above were associated with unstable atherosclerotic plaques, independent of demo-graphic data, standard cardiovascular risk factors, site of artery harvest, and chronic vascular treatments at the time of admission (for all p < 0.05). Conclusions: This study highlights the significant relationships between glucose levels and various inflammatory markers in patients with different histopathological diagnoses of atherosclerotic plaques. Additionally, elevated glycemic and systemic inflammation biomarkers were associated with unstable atherosclerotic plaque, independent of demographic data, comorbidities, cardiovascular risk factors, anatomical artery harvest, and vascular chronic medication at the time of admission.

Obesity and periodontitis are chronic diseases that share inflammatory and metabolic pathways. The RBFOX1 gene was selected as an exploratory candidate gene because it encodes an RNA-binding splicing regulator, has been implicated in obesity-related phenotypes, and has been reported in candidate-gene analyses of periodontitis/metabolic traits. This study investigated the association between obesity, periodontal disease severity, and RBFOX1 rs6500744 polymorphism. This case–control study enrolled 106 adults: 53 with obesity (BMI ≥ 30 kg/m²) and 53 normoweight controls. Clinical and radiographic periodontal assessments determined disease severity, complexity, staging, and grading. Genotyping of the RBFOX1 rs6500744 polymorphism (CC, CT, TT) was performed using the TaqMan^® SNP Genotyping Assay and the 7500 Fast Dx Real-Time PCR system. Multivariable models adjusted for age, sex, smoking status, and clinically confirmed type 2 diabetes. Participants with obesity showed higher levels of periodontal disease than normoweight controls, indicated by greater pocket depths, attachment loss, and bone loss. Advanced stage (Stage III/IV; p = 5.35 × 10⁻⁶) and Grade C periodontitis (p = 2.08 × 10⁻⁷) were significantly more frequent in the obese group. The rs6500744 T allele was more common among individuals with obesity (46.2% vs. 30.2%; OR 1.99, p = 0.023). Periodontal damage appeared to increase progressively from CC to CT to TT genotype, but genotype-stratified estimates, particularly for TT homozygotes, were interpreted cautiously because of the small subgroup size and multiple testing. Both obesity and the number of T alleles were associated with increased periodontal severity in adjusted statistical models. VIFs were low, residual diagnostics did not indicate major assumption violations, smoking-stratified sensitivity analyses were directionally consistent, and the obesity × T-allele interaction was not statistically significant. Obesity is associated with more severe and extensive periodontal disease in this exploratory case–control cohort; however, residual confounding from significant smoking imbalances between groups cannot be excluded. The RBFOX1 rs6500744 T allele may mark increased susceptibility to periodontal tissue destruction, but the findings do not establish causality or clinical prognostic utility and require longitudinal validation in larger, ancestry-controlled populations.