Type 2 diabetes mellitus (DM) is a chronic metabolic disorder posing multifaceted challenges to global public health. Among its numerous complications, infected diabetic foot ulcers (IDFUs) represent a particularly debilitating consequence. Beyond cardiovascular implications, there is an emerging understanding of the interconnectedness among IDFUs, neuropathy, atherosclerosis, and dyslipidemia. IDFUs, peripheral neuropathy, and atherosclerosis share common risk factors and mechanistic pathways. The primary objective of this study was to characterize the lipid profiles in DM patients with IDFUs, comparing them with DM patients without foot ulcers, and with a control group of healthy subjects. The secondary objectives included evaluating apolipoprotein E (ApoE) levels across these study groups and comparing lipid profiles within IDFU subgroups. A total of 160 patients were assessed for this study. After applying exclusion criteria, 140 participants were included, divided into three groups: Group IDFU (80 patients with IDFUs), Group DM (32 patients with DM but no foot ulcers), and Group Controls (28 healthy controls). Compared to Group DM, Group IDFU demonstrated lower levels of high-density lipoprotein cholesterol (HDL-C) (30.9 ± 12.6 mg/dL vs. 40.8 ± 16.6 mg/dL, p = 0.002), but improved levels of ApoE (160.9 ± 68.4 mg/dL vs. 197.2 ± 69.6 mg/dL, p = 0.01), triglycerides (TG) (126.9 ± 56.2 mg/dL vs. 165.8 ± 79.0 mg/dL, p = 0.004), low-density lipoprotein cholesterol (LDL-C) (84.2 ± 32.3 mg/dL vs. 92.3 ± 39.3 mg/dL, p = 0.1), and total cholesterol (133.6 ± 43 mg/dL vs. 164.6 ± 44.4 mg/dL, p = 0.002). The IDFU patients exhibit improved lipid profiles, excepting HDL-C, which is unusual because IDFU follows complications related to dyslipidemia for DM patients. Anemia, impaired renal function, and elevated TG levels were identified as biomarkers for mortality among patients with IDFUs. The data suggest that a lower level of HDL-C and an improved lipid profile may indicate a systemic end-stage disease manifestation in DM patients with IDFUs.

Strategies have been researched and implemented to reduce the number of people with diabetic foot ulcers (DFUs). One problem is the accurate assessment of DFU severity, which is the main factor in resource allocation and treatment choice. The primary objective of this study was to assess pentraxin-3 as a biomarker of an infected DFU (IDFU), the limb amputation level prognosis, and patient survival. The secondary objectives were to evaluate and compare other markers, including white blood cells (WBCs), C-reactive protein (CRP), the erythrocyte sedimentation rate (ESR), and procalcitonin (PCT), for identifying IDFUs. Over a period of two years, 145 patients were followed; 131 of these were analyzed for this study. Pentraxin-3 was found to be a good predictor of death (p = 0.047). A comparison between IDFUs and DFUs revealed the following differences: PCT had the highest AUROC of 0.91, sensitivity of 93.7, and specificity of 83.3%. CRP had a cutoff value of 226 mg/L, an AUROC of 0.89, a sensitivity of 95.5%, and a specificity of 83.3%. Fibrinogen had an AUROC of 0.87 at a cutoff value of 5.29 g/L, with a good sensitivity and specificity of 85% and 87%, respectively. ESR had a cutoff value of 46 mm/h, an AUROC of 85%, a sensitivity of 83.7%, and a specificity of 83.3%. Pentraxin-3 showed promising results in predicting IDFUs and DFUs, and it served as a marker for the risk of death in IDFU patients during the 6 month follow-up. Other markers, including CRP, PCT, ESR, and fibrinogen, were more effective in differentiating between IDFUs and DFUs.

Background and Objectives: Bronchial asthma (BA) and chronic obstructive pulmonary disease (COPD) are not only common obstructive respiratory conditions but also major causes of morbidity and mortality worldwide. There is, however, a surprising lack of blood-based biomarkers for separating between these pulmonary disorders. The aim of this study was to assess the practical relevance of using serum YKL-40, single or combined, for this purpose. Materials and Methods: Subjects included Romanian patients with BA (n = 24) or COPD (n = 27). YKL-40, fibrinogen, pre-treatment C-reactive protein (CRP), post-treatment CRP, erythrocyte sedimentation rate, interleukin 6 (IL-6), procalcitonin (PCT), absolute neutrophil count, neutrophil percentage, absolute lymphocyte count, lymphocyte percentage, absolute eosinophil count, and eosinophil percentage were measured and compared between these patients. Results: This is the first study investigating the clinical significance of serum YKL-40 in delineating between COPD and BA in Caucasian populations. Only fibrinogen and YKL-40 levels were different between COPD and BA, with the measured values being significantly elevated. These patients exhibited distinct inflammatory profiles. Using the upper quartiles of these variables for the pooled study population (YKL-40: 5100 pg/mL; fibrinogen: 552 mg/dL) as cut-off values, subjects were classified into high or low groups. High YKL-40 adults revealed significantly increased PCT levels. High fibrinogen subjects, by contrast, showed significantly elevated IL-6 concentrations and pre-treatment CRP levels. Low YKL-40 and fibrinogen patients showed the absence of COPD. Conclusions: Combined use of serum YKL-40 and fibrinogen may be useful for identifying the absence of COPD.

Background/Objectives: Gastric cancer remains a leading cause of cancer mortality worldwide. Reliable biomarkers are crucial for early detection, prognostication, and therapy monitoring. While classical tumor markers such as carcinoembryonic antigen (CEA), cancer antigen (CA)19-9, CA72-4, and alpha-fetoprotein (AFP) are used in clinical practice, their accuracy can be limited. Tumor necrosis factor alpha (TNF-α) is an inflammatory cytokine implicated in tumor progression, yet its relationship with established gastric cancer tumor markers has not been fully clarified. This study aimed to determine whether elevated TNF-α correlates with key tumor markers and disease stage in gastric cancer. Methods: In this prospective observational study, we enrolled 80 gastric cancer patients and 20 non-neoplastic controls. Baseline clinical data, laboratory parameters, and tumor markers (CEA, CA19-9, CA72-4, AFP) were recorded. TNF-α concentrations were measured using enzyme-linked immunosorbent assays. Correlation analyses and multivariate regression were performed to assess the relationship of TNF-α with tumor markers, inflammatory indices, and disease stage. Results: TNF-α was significantly elevated in gastric cancer patients (median 4.5 pg/mL) compared to controls (2.9 pg/mL). TNF-α showed a robust correlation with CA19-9 (rho = 0.502) and CA72-4 (rho = 0.385), and a moderate correlation with CEA (rho = 0.279). TNF-α concentrations were highest in Stage IV disease and in the intestinal-type histology. In regression analysis, only CA19-9 and CA72-4 remained independent predictors of TNF-α after controlling for clinical confounders. Conclusions: TNF-α is strongly associated with CA19-9 and CA72-4 and rises with advancing stage, highlighting its potential as an adjunct marker for assessing gastric cancer burden. These findings provide a rationale for further research on TNF-α as both a prognostic biomarker and a possible therapeutic target in gastric cancer.