Search Results (1,988)

Background/Objectives: Gestational diabetes mellitus (GDM) is an established risk factor for postpartum depression (PPD), yet its psychobiological mechanisms remain poorly characterized. This study aimed to profile the psychological and biochemical-associated factors of PPD among women with GDM in Jordan. Methods: A prospective observational study recruited 204 pregnant women from three Jordanian hospitals. The Edinburgh Postnatal Depression Scale (EPDS) was administered antepartum and at 4–9 weeks postpartum, with EPDS ≥ 13 used to define probable PPD. Antepartum serum serotonin, cortisol, and CRP were measured by ELISA in a biomarker subsample of 115 participants (84 non-GDM and 31 GDM). Of 54 women diagnosed with GDM, 44 completed the postpartum EPDS and were included in the within-GDM psychological analysis; 25 of these also had stored antepartum serum and were included in the within-GDM biomarker analysis. Analyses were exploratory, consistent with a pilot design. Results: Probable PPD was identified in 26 of 44 GDM women (59.1%). GDM status did not predict PPD in the full cohort (p = 0.237). Within the GDM subgroup, women with probable PPD had significantly higher antepartum EPDS scores (p = 0.003), and elevated perceived stress (p = 0.049), than those without probable PPD. In the within-GDM biomarker subsample (n = 25), antepartum serum serotonin was significantly lower in women with probable PPD (p < 0.001); CRP and cortisol did not differ significantly. Serotonin and cortisol showed the strongest inverse correlations with postpartum EPDS (both p < 0.01). Among GDM women without antepartum depression, 19.0% developed new-onset PPD. Conclusions: In our study, GDM women who develop probable PPD exhibit a distinct profile of antenatal vulnerability and lower serum serotonin levels. Routine perinatal mental health screening and biomarker investigation are warranted in this high-risk group. Findings should be confirmed in larger, adequately powered cohorts. Full article

Nutritional peripheral neuropathy is a clinically important condition associated with inadequate intake, malabsorption, bariatric surgery, aging, metabolic disease, and chronic medication exposure. B vitamins serve as essential coenzymes in mitochondrial energy metabolism, one-carbon metabolism, neurotransmitter synthesis, redox regulation, and myelin maintenance. This narrative review synthesizes mechanistic and clinical evidence linking B vitamin-dependent coenzyme systems to nutritional neuropathy and selected neuropsychiatric manifestations. Particular emphasis is placed on the tricarboxylic acid cycle, electron transport chain, urea cycle, folate–methionine cycle, and MTHFR-dependent one-carbon metabolism. The proposed “dynamic coenzyme network” is intended as an integrative mechanistic framework rather than a stand-alone therapeutic recommendation. Although biochemical interdependence among B vitamins supports evaluation for combined or functional deficiencies in selected patients, mechanistic plausibility should not be equated with clinical efficacy. Clinical consideration of B vitamin repletion should be guided by documented deficiency, dietary and gastrointestinal risk factors, medication exposure, neurological phenotype, and functional biomarkers such as homocysteine and methylmalonic acid. Adjunctive nutrients, including alpha-lipoic acid and acetyl-L-carnitine, may have context-specific relevance, particularly in metabolic neuropathies, but evidence for fixed multi-nutrient combinations remains heterogeneous. Further well-designed clinical studies are needed to determine whether this mechanistic framework translates into meaningful neurological or neuropsychiatric benefit beyond established deficiency states. Full article

Biomarker, the short form of “biological marker”, appeared in the scientific literature in the 1940s. Since then, many different definitions have been suggested, but a generally applicable explanation of the term biomarker in science is extremely challenging. The word biomarker is found in 1.3 million articles in the scientific database PubMed^® that currently comprises more than 39 million citations for biomedical literature. Biomarkers are closely associated with human health and disease. The present article attempts to approach and evaluate the multifaceted term “biomarker” from a clinical perspective by searching the PubMed database. The search term biomarker was combined with other search terms related to medicine, physiology, biochemistry, and chemistry. Currently generally accepted clinical biomarkers, such as the high-molecular-mass N-terminal prohormone of brain natriuretic peptide (NT-proBNP, 60%), prostate-specific antigen (PSA, 67%), and troponin (37%), serve as a kind of positive control. The combination of the search term biomarker with selected low-molecular substances of clinically non-validated and hence rather experimental character yielded surprisingly high fractions of 41% for 8-iso-prostaglandin F_2α, 39% for symmetric dimethylarginine (SDMA), and 28% for asymmetric dimethylarginine (ADMA). The results of our survey are presented and discussed in detail for a wide spectrum of diseases. We focused on mechanisms that are assumed to underlie the biological activity and specificity of biomarkers. We also considered potential roles of the analytical chemistry of biomarkers including the emerging metabolomics and proteomics. Reliable analytical methods have been used for the quantification of the isomeric low-molecular-mass ADMA and SDMA in human biological samples. ADMA, but not SDMA, is considered an endogenous inhibitor of the endothelium-derived nitric oxide (NO) synthesis, one of the most potent endogenous vasodilators. Paradoxically, the utility of ADMA and SDMA as biomarkers in the renal and cardiovascular systems seems to contradict their main biological activity. This prominent pair is representative of many biomarkers and reveals that the supposed biomarker utility is likely to be predicated on not yet considered biological activity. The majority of human diseases are heterogenic, affect many organs and seem to include different and overlapping biochemical pathways. In recent years, especially proteomic studies provided a series of new potential candidate biomarkers. However, such biomarkers must still be validated in the clinic before they can be introduced into clinical practice. This is perhaps the most critical phase in the discovery of disease biomarkers. Our analysis reveals that the area of biomarker research is highly challenging. With minor exceptions, there is no specific biomarker for a single disease. In addition to clinical examinations, a combination of several biomarkers seems to be needed for reliable diagnosis and therapy. Analytical chemistry, especially proteomics, delivers a huge amount of data, which may complicate and even hinder progress in this area. Specific quantitative analysis of candidate biomarkers observed by proteomics (and metabolomics) is highly recommended to proceed with the same biological samples from studies in which the biomarkers were discovered. Full article

Background: Chronic kidney disease (CKD) is associated with early disturbances in mineral metabolism that contribute to bone fragility. Secondary hyperparathyroidism is a key component of chronic kidney disease–mineral and bone disorder (CKD-MBD) and may affect bone even during the early stages of CKD. This study evaluated the association between serum parathyroid hormone (PTH) concentrations and bone mineral density (BMD) in patients with stage 3 CKD. Methods: A multicenter cross-sectional observational study was conducted in 203 patients with stage 3 CKD. Blood and 24 h urine samples were collected to measure creatinine, calcium, phosphate, magnesium, 25-hydroxyvitamin D, fibroblast growth factor 23 (FGF23), and PTH. Bone mineral density was assessed by dual-energy X-ray absorptiometry (DXA). Associations between serum PTH concentrations and BMD were analyzed. Results: Elevated serum PTH concentrations were associated with lower femoral BMD and less favorable femoral T-scores, whereas no significant associations were observed at the lumbar spine. Serum PTH concentrations were inversely correlated with femoral BMD and femoral T-scores. Patients with reduced femoral BMD also showed higher FGF23 concentrations and lower renal function, while serum calcium, phosphate, magnesium, and 25-hydroxyvitamin D concentrations did not differ significantly among the groups. Conclusions: Elevated serum PTH concentrations were associated with reduced femoral BMD in patients with stage 3 CKD, supporting preferential early involvement of cortical bone. Serum PTH may represent an accessible biomarker for the early identification of patients at increased risk of cortical bone loss before conventional biochemical abnormalities become clinically apparent. Full article

Background: Although conventional cardiovascular risk scores are widely used, they do not fully capture the molecular mechanisms underlying vascular injury in type 2 diabetes mellitus (T2DM). This study investigated the association between the miR-34a/SIRT1 regulatory axis and cardiometabolic risk in T2DM by integrating biomarkers of inflammation, oxidative stress, and endothelial dysfunction. Methods: A cross-sectional study included 128 adults (96 with T2DM and 32 non-diabetic controls). Cardiometabolic risk was stratified using the Framingham Risk Score. Circulating miR-34a expression was quantified by RT-qPCR, whereas SIRT1 and biomarkers of inflammation (IL-6, TNF-α, and hs-CRP), oxidative stress (MDA and TAC), and endothelial dysfunction (VCAM-1 and ICAM-1) were measured using ELISA or standardized biochemical assays. Multivariate regression and receiver operating characteristic (ROC) analyses were performed. Results: Compared with medium-risk patients, individuals classified as high risk exhibited longer diabetes duration, higher body mass index, blood pressure, fasting glucose, and HbA1c levels (all p < 0.05), together with increased circulating miR-34a, inflammatory, oxidative stress, and endothelial dysfunction biomarkers, whereas SIRT1 and total antioxidant capacity were significantly reduced (all p < 0.001). These molecular alterations remained independently associated with risk after adjustment for age, sex, body mass index, smoking status, physical activity, dyslipidemia, HbA1c, and medication use. The combined biomarker model integrating miR-34a, SIRT1, hs-CRP, MDA, and VCAM-1 demonstrated excellent discriminatory performance for identifying high-risk individuals (AUC = 0.92; sensitivity = 86.4%; specificity = 85.5%). Conclusions: Cardiometabolic risk in T2DM is associated with a coordinated molecular signature characterized by miR-34a upregulation, SIRT1 suppression, systemic inflammation, oxidative stress, and endothelial dysfunction. These findings suggest that integrated biomarker profiling may complement conventional risk assessment and support future precision cardiometabolic strategies. Full article

The skin surface is a dynamic biochemical interface where proteins, polysaccharides, lipids, and microbial or environmental molecules are continuously exposed to ultraviolet(UV) radiation, oxidative stress, mechanical stimulation, pH variation, host-derived enzymes, and microbial enzymes. These factors can generate heterogeneous macromolecular fragments on the skin surface through cleavage, oxidation, structural modification, or enzymatic degradation. However, current evidence does not support interpreting these fragments uniformly as active regulatory molecules. Instead, they should be considered a mixed molecular population that may include passive degradation products, stress-associated markers, host- or microbiome-derived cleavage products and, in some contexts, molecules with potential biological activity. This review summarizes current knowledge on the formation mechanisms, analytical detection, and possible biological relevance of skin surface macromolecular fragments, with emphasis on hyaluronic acid, collagen, keratin, lipids, and microbiome-associated fragments. Evidence from in vitro, ex vivo, and in vivo studies is distinguished to clarify the strengths and limitations of current interpretations. Particular attention is given to contradictory findings, concentration-dependent effects, source attribution, contamination, matrix interference, lack of reference standards, and insufficient functional validation. Overall, skin surface macromolecular fragmentation is better viewed as an emerging analytical and biological framework rather than as a proven regulatory mechanism. Future studies should combine standardized sampling, validated mass spectrometry(MS) workflows, multi-omics integration, reconstructed skin models, microbiota-related models, and controlled human studies to determine whether specific fragments are degradation products, biomarkers, or context-dependent functional molecules. Full article

Background: Children with Autism Spectrum Disorder (ASD) frequently exhibit severe food selectivity and micronutrient deficiencies, impacting growth and nutritional status. Evidence on integrated nutritional interventions in resource-constrained settings remains limited. Objective: To assess the feasibility and preliminary pre–post changes associated with a 12-week multicomponent nutritional intervention among Vietnamese children with ASD. Methods: In this exploratory single-arm pilot study, 56 children with ASD (mean age 59.0 ± 22.3 months; 80.4% male) were recruited from five community centers in Nghe An Province, Vietnam. The intervention comprised caregiver nutrition education, individualized dietary counseling, and daily multi-micronutrient supplementation. Anthropometric indicators, biochemical markers, feeding behaviors, and dietary intake were assessed at baseline and after 12 weeks. Pre–post changes were evaluated using paired statistical tests, and multivariable linear regression examined factors associated with growth response. Results: The study achieved a 100% completion rate, with all 56 recruited participants finishing the 12-week intervention and all scheduled follow-up assessments. Among children < 60 months, mean Weight-for-Age Z-score (WAZ) increased from −0.66 to −0.28 and mean Height-for-Age Z-score (HAZ) from −1.18 to −0.97 (p < 0.001). For children older than 60 months, mean HAZ increased from −0.87 to −0.58 (p < 0.001) and Body Mass Index-for-Age Z-score (BAZ) from −0.20 to 0.06 (p = 0.006). Significant increases occurred in serum zinc (10.29 to 11.72 µmol/L; p = 0.001), ferritin (31.74 to 34.79 ng/mL; p = 0.001), and hemoglobin (122.73 to 124.77 g/L; p = 0.002), while albumin remained unchanged. Concurrent improvements were observed in feeding behaviors and nutrient-dense food intake. Regression analysis indicated that lower baseline anthropometric status was significantly associated with greater gains in WAZ and HAZ. Conclusions: This community-based multicomponent intervention was feasible and associated with short-term improvements in feeding behaviors, dietary intake, selected biomarkers, and growth measures in children with ASD, supporting further evaluation in randomized controlled trials. Full article

Background and Objectives: Eccentric hypertrophy (EH) represents a common physiological cardiac adaptation in athletes, particularly in endurance disciplines. However, the biological correlates underlying EH and potential sex-specific differences remain poorly understood. This study aimed to investigate clinical, echocardiographic, and biochemical determinants of EH in a large cohort of elite athletes. Materials and Methods: We evaluated 2522 elite athletes undergoing pre-participation screening for Olympic competitions. Athletes were classified according to cardiac geometry into EH or normal geometry (NG) based on echocardiographic parameters. Clinical, anthropometric, echocardiographic, and biochemical variables were compared between groups. Univariate and multivariable logistic regression analyses were performed to identify independent predictors of EH. Results: EH was present in 601 athletes (23.8%) and was more prevalent in endurance sports (51.1% vs. 14.3%, p < 0.0001). Athletes with EH showed greater cardiac chamber dimensions and mass, with preserved systolic and diastolic function. Several biomarkers differed between groups, including higher AST, ALT, CPK, eosinophils, and HDL, and lower creatinine and TSH in EH (all p < 0.01). Following multivariable analysis, lower creatinine (OR 0.28, 95% CI 0.14–0.52, p < 0.0001), higher AST (OR 1.02, 95% CI 1.02–1.03, p < 0.0001), and higher eosinophil count (OR 1.12, 95% CI 1.06–1.20, p < 0.0001) independently predicted EH. The model showed moderate discrimination (AUC 0.72). Sex-stratified analyses showed different biomarker associations with EH in men (creatinine and AST) and women (eosinophils and HDL), with similar model performance (AUC 0.71 vs. 0.73). Conclusions: EH in elite athletes is associated with distinct biological signatures reflecting multiple physiological pathways. Notably, sex-specific patterns emerge, suggesting different mechanisms underlying cardiac adaptation in male and female athletes. Full article

Postoperative wound healing complications present a major challenge in plastic and reconstructive surgery, prolonging recovery and impairing outcomes. Early risk identification is difficult due to complex interactions among clinical, laboratory, and molecular factors. This study developed and evaluated machine-learning (ML) models to predict wound healing outcomes and identify key complication predictors. Utilizing a dataset of 95 women and 76 variables (including hematological, biochemical, coagulation, and gene expression profiles), we evaluated several ML approaches, including Decision Tree, Extra Trees, Gaussian/Bernoulli Naive Bayes, Logistic Regression, and Support Vector Machine. Model performance was assessed via k-fold cross-validation, ROC analysis, and SHAP feature importance. Molecular markers (COL1A1, MMP9, MAPK1, MAPK8, IL10, and CCL2) emerged as the strongest predictors, whereas conventional clinical variables showed limited value. The models achieved high discriminative performance, with validation ROC–AUC values ranging from 0.903 to 0.913. Extra Trees and Gaussian Naive Bayes demonstrated the highest sensitivity for detecting complications (Recall = 0.820 ± 0.238 and 0.807 ± 0.246, respectively). These findings highlight the value of integrating molecular-genetic biomarkers with ML for personalized risk stratification and preventive care in reconstructive surgery. Full article

Cardiometabolic residual risk in type 2 diabetes mellitus (T2D) persists despite major advances in glucose-lowering therapy, lipid management, blood pressure control, weight reduction, and organ-protective strategies. This residual burden should not be interpreted solely as the consequence of incomplete achievement of conventional therapeutic targets, but rather as the clinical expression of persistent molecular activity involving multiple interconnected organs and pathways. Insulin resistance, metaflammation, oxidative stress, mitochondrial dysfunction, lipotoxicity, endothelial impairment, hepatic metabolic dysregulation, renal inflammation, fibrotic remodeling, and metabolic memory interact within a dynamic network linking adipose tissue, liver, kidney, immune cells, and vasculature. In this review, we discuss the biochemical and molecular drivers of cardiometabolic residual risk in T2D, with particular emphasis on impaired insulin receptor substrate/PI3K/Akt signaling, stress-kinase activation, NLRP3 inflammasome priming and assembly, MASLD-related lipotoxicity and fibrogenesis, podocyte and tubular injury, endothelial nitric oxide synthase uncoupling, AGE-RAGE signaling, and thrombo-inflammatory vascular injury. These pathways explain why biological vulnerability may persist even when conventional clinical parameters appear adequately controlled. We also examine the role of translational biomarkers and simple clinical indices, including TyG-derived indices, adiposity markers, hepatic steatosis and fibrosis scores, albuminuria, eGFR, and lipid-related markers, as accessible windows into active biological pathways. Finally, we review how contemporary therapeutic strategies may modulate selected components of this residual-risk network. A pathway-centered interpretation of T2D may support more precise residual-risk phenotyping and help move cardiometabolic care beyond isolated target control toward mechanism-based prevention. This review further links these mechanisms to the contemporary cardiovascular–kidney–metabolic (CKM) framework, as defined by the 2026 AHA/ACC/ADA/ASN CKM Guideline, and disaggregates the underlying molecular network into organ-specific pathway cascades that make the causal relationships between metabolic, inflammatory, hepatic, renal, and vascular injury more explicit. Full article

Natural killer (NK) cells are key mediators of antitumor immunity; however, NK cell dysfunction in epithelial ovarian cancer should be considered not as a uniform defect, but rather as compartment-specific states that differ across the blood, ascites, primary tumor, and metastatic sites according to their local cellular interactions, soluble factors, and metabolic constraints. Peripheral blood provides an accessible systemic reference and may support immune monitoring. However, it does not fully reflect NK cell states in local or distant disease compartments. In ascites, cytokine-responsive and partially recoverable NK cell populations coexist with soluble, biochemical, and metabolic suppressive signals. In primary tumors, NK cells often acquire tissue-adapted suppressive phenotypes, characterized by altered activating receptors, increased inhibitory checkpoints, and reduced cytotoxic effector function. In metastatic lesions, NK cells appear to share suppressive phenotypes with primary tumors, although these phenotypes may be reinforced within metastatic niches through coordinated inhibitory receptor–ligand interactions. The above compartment-specific states imply that NK cell-targeted therapy for ovarian cancer should not rely on a unilateral strategy. Instead, therapeutic design may need to be multifaceted but coordinated, combining cytokine-based activation, adoptive NK cell transfer, checkpoint blockade, local delivery, and antigen-directed chimeric antigen receptor NK cell approaches according to the dominant biology of each compartment. Paired multi-compartment profiling and longitudinal functional assessment will be essential for biomarker development and compartment-guided treatment design. Full article

Traumatic brain injury (TBI) disrupts brain metabolism, which evolves over time and varies with the severity of the injury. Monitoring these metabolomic changes may reveal biomarkers indicating early damage, mechanisms of injury, and potentially help predict outcomes. This study used untargeted plasma metabolomics to investigate systemic time-dependent metabolic changes in mice exposed to controlled cortical impact (CCI) with or without replacement of a modified skull cap designed to reduce compensatory space for cerebral edema modelling a severe closed skull TBI, compared to sham controls. Male mice were subjected to CCI, CCI + CAP, or sham procedures comprised a scalp incision or a craniotomy. Plasma samples were collected at 4, 8, and 16 h, and 3 and 7 days after injury. Hydrophilic interaction liquid chromatography–mass spectrometry (HILIC-MS) was used to profile metabolites in all groups and time points, while ion-pair liquid chromatography–mass spectrometry (RPIPLC-MS) was used in CCI and sham mice at the early time points. The largest metabolic changes occurred at 8 h post-injury, distinguishing mice with CCI from sham controls. The early changes concerned metabolism of amino acids, energy, and nucleotide pathways, with metabolites such as succinate, phenylalanine, and cytidine showing significant changes. By 7 days, the metabolic patterns of the injured mice, especially CCI mice, had partially converged toward the sham state, although oxidative and mitochondrial disturbances persisted. The CCI + CAP mice had more pronounced and persistent metabolic disturbances compared to the CCI mice, which may reflect the effect of increased intracranial pressure post-injury. Plasma metabolomics can efficiently capture the evolving biochemical effects of TBI. The findings identified circulating metabolites that were associated with progression and severity of brain injury and provide a basis for future translational studies in human TBI. Full article

Oral ulcerations are complex pathological lesions with multifactorial etiology and diverse clinical manifestations. Current treatment options are mostly symptomatic with a different adverse effect. Therefore, this study aimed to develop a mucoadhesive oral gel containing Potentilla erecta L. ethanol extract (PEOG) and evaluate its healing effects in a rat model of oral ulceration. Dried rhizomes of Potentilla erecta were extracted with 70% ethanol using ultrasonic extraction, followed by low-pressure evaporation. The extract was incorporated into a gel base composed of poloxamer 407 and carbomer 934. Rheological characterization was performed to assess the viscoelastic and flow properties of the formulation. Therapeutic efficacy was evaluated through macroscopic assessment of ulcer healing, histopathological analysis, and determination of systemic oxidative stress biomarkers. Animals were assigned to three groups: untreated control, gel base (GB), and PEOG-treated. Rats were sacrificed on days 0, 3, 6, and 10 for blood and tissue sampling. PEOG treatment significantly accelerated ulcer healing, resulting in a marked reduction in ulcer size compared with controls. Histopathological findings indicated enhanced collagen deposition, while biochemical analyses suggested attenuation of oxidative stress. These results demonstrate that PEOG possesses considerable ulcer-healing potential and may represent a promising mucoadhesive formulation for the treatment of oral ulcerations. Full article

Skeletal safety of glucagon-like peptide-1 receptor agonists (GLP-1RAs) remains uncharted, with emerging evidence suggesting a divergence between mono- and dual-agonist therapies. GLP-1RA monotherapy appears bone-neutral, with modest or no adverse effects on bone mineral density (BMD), whilst dual agonists may confer a relatively higher risk of osteoporosis and fractures, plausibly mediated by greater weight loss magnitude and concomitant reductions in lean body mass (LBM) rather than direct osteotoxicity. Intensified surveillance is warranted in susceptible phenotypes, including older adults and postmenopausal women with low baseline BMD under conditions of rapid weight loss. Osteoporosis risk is further amplified by pre-existing osteopenia, nutritional deficiencies, and concomitant exposure to bone-active agents. Given the limitations of serial dual-energy X-ray absorptiometry (DXA), including cumulative radiation exposure and limited sensitivity to early remodeling changes, biochemical markers potentially depict bone turnover more dynamically. Measurement of dynamic bone resorption markers enables early identification of skeletal disturbances, supporting proactive adjustment of therapeutic strategy, dosing, and duration. Specifically, deoxypyridinoline (DPD), a bone-specific collagen crosslink, is a highly sensitive and rapidly responsive urine biomarker of osteoclastic activity. Incorporating DPD urine testing into monitoring frameworks potentially facilitates individualized therapeutic modulation, optimizing the metabolic efficacy of GLP-1RAs while safeguarding skeletal integrity. Full article

Objective: Obesity is a systemic disease characterized by low-grade chronic inflammation and increased metabolic risk. Although bariatric surgery is known to improve metabolic and inflammatory status, the longitudinal behavior of emerging inflammatory biomarkers such as procalcitonin (PCT) remains insufficiently characterized. This study aimed to evaluate postoperative changes in serum procalcitonin (PCT) levels in patients undergoing bariatric surgery and to investigate their associations with anthropometric measurements, liver enzymes, and novel inflammatory indices. Methods: In this retrospective longitudinal cohort study, 38 patients who underwent sleeve gastrectomy and had complete preoperative and postoperative follow-up data at months 1, 3, and 6 were included. Anthropometric and biochemical parameters were analyzed, and systemic inflammation was assessed using PCT, Systemic Immune-Inflammation Index (SII) and the Systemic Inflammation Response Index (SIRI). Repeated-measures analyses were performed according to data distribution, and correlations were evaluated using Spearman analysis. Results: PCT levels showed a significant reduction at postoperative month 1 compared with the preoperative period. However, despite continued reductions in body weight, BMI, and fat mass at postoperative months 3 and 6, PCT levels plateaued without further significant change. In the preoperative period, PCT demonstrated strong positive correlations with liver enzymes (p < 0.01). At postoperative month 1, PCT was significantly associated with glucose and HbA1c levels. Although SII and SIRI decreased after surgery, no significant correlation with PCT was observed. Conclusions: PCT decreased in the early postoperative period after sleeve gastrectomy and may reflect early metabolic and inflammatory changes associated with rapid weight loss. However, its sensitivity for monitoring long-term inflammatory changes appears limited. The observed preoperative associations with liver enzymes may suggest a potential relationship between PCT levels, liver enzyme alterations, and metabolic alterations in obesity. Full article