Background: To investigate the connections between microvascular complications (DMCs) and serum complement hs-CRP, C3d, and MBL levels in individuals with type 2 diabetes mellitus (T2DM). Methods: From January 2023 to January 2025, 100 patients with simple T2DM admitted to our hospital were selected as the T2DM group, 100 patients with T2DM combined with DMC were selected as the DMC group, and 100 healthy individuals who underwent physical examinations during the same period were selected as the control group. The serum levels of complement hs-CRP, C3d, and MBL were compared among the three groups. The relationships between complement hs-CRP, C3d, and MBL and the blood glucose and lipid markers of DMC patients were examined using Pearson correlation analysis. Binary logistic regression analysis was used to investigate the risk factors for DMC in patients with type 2 diabetes. The diagnostic value of blood complement hs-CRP, C3d, and MBL for DMC in T2DM patients was evaluated using the receiver operating characteristic curve (ROC) and the area under the curve (AUC). Results: Comparison of serum complement hs-CRP, C3d, and MBL levels revealed the following trend: DMC group > T2DM group > control group, with statistically significant differences (P<0.05). Body mass index (BMI), length of illness, fasting blood glucose (FPG), glycosylated haemoglobin (HbA1c), lipid markers (triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), insulin resistance index (HOMA-IR), blood uric acid (UA), and creatinine (Scr) were significantly different between the DMC and T2DM groups. In T2DM patients who developed DMC, blood complement hs-CRP, C3d, and MBL levels were favourably correlated with FPG, HbA1c, TG, TC, and LDL-C levels and negatively correlated with HDL-C levels (P<0.05), according to the Pearson correlation analysis. Binary logistic regression analysis revealed that disease duration and FPG, HbA1c, hs-CRP, C3d, and MBL levels were factors associated with DMCs in patients with T2DM (P<0.05). ROC curve analysis showed that the optimal hs-CRP cut-off value for detecting DMCs in patients with T2DM was 293.68 mg/L, with an AUC of 0.834 (95% CI 0.754–0.914), a sensitivity of 0.844, and a specificity of 0.803. The optimal C3d cut-off value was 394.25 mg/L, with an AUC of 0.835 (95% CI 0.741–0.919), a sensitivity of 0.830, and a specificity of 0.805. The optimal MBL cut-off value was 330.32 mg/L, with an AUC of 0.827 (95% CI 0.739–0.915), a sensitivity of 0.823, and a specificity of 0.776. Conclusion: The pathogenic progression of DMC in T2DM is significantly influenced by serum complement activation. Elevated levels of serum complement components hs-CRP, C3d, and MBL can increase the risk of DMC in T2DM patients. In patients with type 2 diabetes, these three markers can be used as trustworthy predictors of the development of DMC.
Background: Early identification of pregnancies at risk for fetal growth restriction (FGR) is essential for appropriate prenatal monitoring and timely intervention. First-trimester screening markers, including nuchal translucency (NT), pregnancy-associated plasma protein A (PAPP-A), and free β-human chorionic gonadotropin (free β-hCG), are routinely used in clinical practice and may provide early insight into placental function. Methods: This cohort study analysed first-trimester biochemical and ultrasound markers in pregnancies that later developed FGR and compared them with those of uncomplicated control pregnancies. NT was measured between 11 and 13+6 gestational weeks, while PAPP-A and free β-hCG concentrations were expressed as multiples of the median (MoM). Correlation analyses and logistic regression models were applied to evaluate associations and predictive value. Results: NT values were significantly higher in pregnancies complicated by FGR. Mean PAPP-A and free β-hCG levels did not differ significantly between the FGR and control groups. Correlations among first-trimester markers were more consistent in the control group, whereas disrupted relationships were observed in FGR pregnancies. Although mean PAPP-A values were similar, very low PAPP-A levels (<5th percentile) were associated with an increased risk of FGR. The combined presence of elevated NT and low PAPP-A improved the identification of high-risk pregnancies. Conclusion: NT may serve as a potential early indicator of FGR risk, particularly when interpreted within specific clinical sub-stratifications rather than as a standalone screening tool. Extremely low PAPP-A values may further contribute to early risk stratification. The combined interpretation of biochemical and sonographic markers in the first trimester may support earlier identification of pregnancies requiring closer surveillance.
Background: Long-term management of pharmacotherapy in patients with type 2 diabetes mellitus (T2DM) and ischemic stroke is challenging due to comorbidities, neurological impairment and functional limitations. Although clinical factors are known to influence adherence, the contribution of circulating biomarkers of neurological injury and repair remains poorly characterised. To investigate the clinical and biomarker-related factors associated with suboptimal medication adherence, and to develop a biomarker-enhanced nomogram for predicting poor adherence in patients with T2DM complicated by ischemic stroke. Methods: A retrospective cohort study was conducted in which 100 patients were screened, 100 enrolled, and 0 were excluded based on predefined inclusion and exclusion criteria. All the patients were treated from March 2025 to July 2025. Demographics, comorbidities, medication classes, National Institutes of Health Stroke Scale, Barthel Index, rehabilitation guidance, and circulating biomarkers, including neuron-specific enolase (NSE), S100 calcium-binding protein B (S100B), brain-derived neurotrophic factor (BDNF), high-sensitivity C-reactive protein, and HbA1c, were collected. Medication adherence was evaluated at 6 months post-discharge using the Morisky Medication Adherence Scale. Patients were randomly assigned to a training cohort (n=70) and a validation cohort (n=30). Univariate and multivariable logistic regressions were performed to find factors associated with poor adherence, and a biomarker-enhanced nomogram was built. Model performance was evaluated by the concordance index, calibration curves, receiver operating characteristic curves and net reclassification improvement (NRI). For NRI analysis, patients were categorised into three clinically interpretable predicted-risk groups: low risk (<30%), intermediate risk (30%–60%), and high risk (>60%). Results: Forty-three patients showed poor adherence to medication. Independent predictors of poor adherence were age ≥60 years, primary education or less, ≤2 types of medication, NIHSS score ≥4, Barthel Index ≤60, no guidance for rehabilitation, high NSE (>15 ng/mL), high S100B (>110 pg/mL) and low BDNF (<22 ng/mL). Discrimination of the nomogram, including the biomarker, was good, with C-indexes of 0.851 in the training cohort and 0.838 in the validation cohort. The area under the curve values were 0.873 and 0.851, respectively. Calibration plots showed little difference between predicted and observed probabilities. The inclusion of NSE, S100B, and BDNF in the clinical-only model improved risk classification of patients (NRI 0.324, 95% CI: 0.112–0.536) using the predefined low, intermediate, and high-risk categories. Conclusion: onclusion: Clinical characteristics, neurological function, rehabilitation guidance and serum neurological injury/ repair biomarkers were related to the medication adherence of the patients with T2DM and ischemic stroke. A nomogram combining NSE, S100B, and BDNF biomarkers improved the prediction of poor adherence. They may facilitate the identification of high-risk patients who need early, individualised adherence-support interventions.
Background: Individual cytokines have been implicated in the pathogenesis of acute myocardial infarction (AMI). However, the predictive utility of a comprehensive serum cytokine panel for post-infarction outcomes remains underexplored. Methods: We conducted a prospective cohort study of 184 patients presenting with ST-segment elevation myocardial infarction (STEMI). Blood samples were collected within 24 hours of primary percutaneous coronary intervention (PCI). We analysed a panel of 11 cytokines (GDF-15, IL-1β, IL-6, IL-8, IL-10, IFN-γ, VEGF, G-CSF, GM-CSF, TGF-β, and hs-cTnT) using a multiplex bead-based immunoassay. The primary endpoint was the occurrence of Major Adverse Cardiac Events (MACE) at 12 months. MACE was defined as cardiovascular death, recurrent MI, or heart failure hospitalisation. Results: Elevated levels of IL-6, IL-8, GDF-15, and hs-cTnT were significantly associated with 12-month MACE. Multivariable logistic regression identified GDF-15 (OR 3.58, 95% CI 1.82-7.04, p<0.001) and hs-cTnT (OR 2.94, 95% CI 1.53-5.65, p=0.001) as independent predictors. In univariable analysis, IL-6, IL-8, GDF-15, and hs-cTnT were elevated. Still, only GDF-15 and hs-cTnT retained independent prognostic significance in the multivariable model. A composite biomarker score showed an AUC of 0.86 (95% CI 0.80-0.92) for predicting MACE. Conclusion: A serum biomarker profile including GDF-15 and hs-cTnT may improve early risk assessment after primary PCI in STEMI, supporting routine biomarker profiling to enhance risk stratification beyond traditional variables.
Background: To determine the predictive efficacy of measuring fibroblast growth factor 23 (HPDR2) in postmenopausal individuals with osteoporosis, tartrate-resistant acid phosphatase 5b (TRACP-5b), and serum macrophage inflammatory protein-1 b (CCL4) for fractures. Methods: The osteoporosis group consisted of 242 postmenopausal individuals with osteoporosis who were admitted to the hospital between January 2023 and January 2025. There were two groups: 108 patients with fractures and 134 without. The decreased bone mass group (164 patients) and the control group (130 patients) consisted of postmenopausal women diagnosed with decreased bone mass and normal bone mass, respectively, at the hospital during the same time period. The levels of serum CCL4, TRACP-5b and HPDR2 in each group were compared. The predictive value of serum CCL4, TRACP-5b, and HPDR2 detection for fractures in postmenopausal patients with osteoporosis was assessed using univariate and multivariate analyses of fracture risk factors. The relationships between the levels of serum CCL4, TRACP-5b, and HPDR2 and fracture severity were analysed. Results: The levels of serum CCL4, TRACP-5b and HPDR2 in the osteoporosis group were significantly greater than those in the decreased bone mass group and the control group (P< 0.01), and the reduced bone mass group's serum CCL4, TRACP-5b, and HPDR2 levels were considerably higher than the control group's (P< 0.01). The fracture group had significantly greater serum levels of HPDR2, TRACP-5b, and cCl4 than the non-fracture group (P< 0.01). Multivariate analysis revealed that serum C C L4 > 7 1 9.75 pg/mL, TRACP-5b> 6.90 U /L and H PD R2> 247.35 pg/mL were risk factors for fractures in postmenopausal patients with osteoporosis (P< 0.01). Serum levels of cCL4, TRACP-5b, and HPDR2 are highly effective at predicting fractures in patients with osteoporosis (P< 0.01). The combined detection sensitivity of the three indicators was 90.0%, the specificity was 89.7%, and the area under the curve (AUC) was 0.949. The AUC was significantly greater than that of CCL4 (Z = 3. 415, P< 0.01), TRAC P-5 b (Z = 3.814 , P< 0.01), and HPDR2 (Z = 3.986 , P< 0.01) were detected as individual indicators. However, the AUC of each indicator did not change statistically significantly (P> 0.05). Conclusions: Serum CcL4, TRACP-5b and HPDR2 are involved in the occurrence and development of postmenopausal osteoporosis. The detection of their levels has high value in predicting fractures in postmenopausal osteoporosis patients.
Background: To explore the correlation between serum T cell replacing factor (TRF) and liver glutathione peroxidase 2 (LGP2) levels in patients with coronary heart disease (CHD) and cardiac function. Methods: From October 2023 to October 2025, 252 patients with CHD who visited our hospital were selected for the disease group, among whom 72 had NYHA cardiac function grade II, 124 grade III, and 56 grade IV The control group consisted of an additional 240 healthy patients who had physical examinations at our institution over the same time period. Baseline data for CHD patients were gathered. Enzyme-linked immunosorbent assays were used to evaluate the blood levels of TRF, LGP2, brain natriuretic peptide (BNP), and creatine kinase isoenzyme (CK-MB) in each patient group. A colour scale was used to quantify the left ventricular ejection fraction (LVEF), left ventricular end-systolic diameter (LVESD), left ventricular end-diastolic diameter (LVEDD), cardiac output (CO), interventricular septal thickness (IVS), and left ventricular mass (LV mass) of the CHD patients. Doppler ultrasound diagnostic apparatus. The relationship between blood TRF and LGP2 levels and cardiac function markers in CHD patients was examined using Pearson correlation analysis. Results: The disease group's systolic blood pressure and LDL-C levels were significantly higher than those of the control group, whereas serum TRF LGP2, and HDL-C (high-density lipoprotein cholesterol) levels were significantly lower in the disease group (P<0.05). Serum BNP and CK-MB levels were significantly higher in the illness group than in the control group, and LVESD, LVEDD, LV mass, and IVS were also significantly higher. At the same time, the LVEF and CO were significantly lower than those of the control group (P<0.05). NYHA-related cardiac function grade IV CHD patients had significantly lower LVEF, CO, and serum TRF and LGP2 levels than grade III and II patients did. The LVEF CO, and serum TRF and LGP2 levels of grade III CHD patients were significantly lower than those of grade II patients were, and the differences were statistically significant (P<0.05); NYHA-related cardiac function grade IV patients had significantly greater LVESD, LVEDD, LV mass, and IVS than grade III and II patients were, and the serum BNP and CK-MB levels were significantly greater than those of grade III and II patients were (P<0.05). The LVESD, LVEDD, LV mass, and IVS of grade III CHD patients were significantly greater than those of grade II patients, and the serum BNP and CK-MB levels were significantly greater in grade III CHD patients than in grade II patients (P<0.05). Serum TRF and LGP2 levels in patients with CHD were negatively correlated with BNP CK-MB, LVESD, LVEDD, LV mass, and IVS (P<0.05) and positively correlated with LVEF and CO (P<0.05). Conclusion: The serum levels of TRF and LGP2 in patients with CHD were significantly decreased, and both were closely related to cardiac function indicators.
Background: To explore the levels of serum Familial Cold Autoinflammatory Syndrome 1 (FCAS1), Procalcitonin, and Small Inducible Cytokine A25 (SCYA25) in patients with sepsis caused by drug-resistant Klebsiella pneumoniae (KP) infection and their relationship with prognosis. Methods: The study group consisted of 410 patients who were hospitalised to our hospital between March 2019 and March 2024 and had sepsis brought on by KP A total of 196 drug-resistant patients with sepsis caused by KPs were classified into the drug-resistant group, and 214 nondrug-resistant patients with sepsis caused by KPs were classified into the nondrug-resistant group. According to the severity of sepsis, 410 patients with KP-induced sepsis were divided into a severe sepsis group (178 patients) and a sepsis group (232 patients). The control group consisted of an additional 410 healthy volunteers who were physically examined at our hospital during the same time period. It was established that drug-resistant KPs were resistant to clinical medications. The prognosis of patients with drug-resistant sepsis caused by a KP infection was split into a survival group and a death group 28 days after admission. Serum FCAS1 levels were detected via an enzyme-linked immunosorbent assay, and serum Procalcitonin and SCYA25 levels were determined via the chemiluminescence method. The diagnostic value of serum FCAS1, Procalcitonin, and SCYA25 for drug-resistant KP-induced sepsis, as well as their predictive value for the mortality of patients with drug-resistant KP-induced sepsis, were examined using receiver operating characteristic (ROC) curves. Multivariate logistic regression analysis was used to investigate the factors impacting death in patients with sepsis and drug-resistant KP infection. Results: A total of 250 drug-resistant KP strains were detected in 196 patients with sepsis caused by drug-resistant KPs. The resistance rates of these strains to cefazoline, ceftriaxone, ceftazidime, amtronam, imipenem and meropenem were greater than 90%. Serum FCAS1, Procalcitonin, and SCYA25 levels exhibited a statistically significant difference (P<0.05) between the severe sepsis group and the control and sepsis groups. Additionally, the sepsis group's levels were higher than those of the control group. Serum FCAS1, Procalcitonin, and SCYA25 levels were considerably higher in the drug-resistant group than in the nondrug-resistant group (P<0.05). The nonsurviving group had higher levels of serum FCAS1, Procalcitonin, SCYA25, Acute Physiology and Chronic Health Evaluation II (APACHE II), and infection-related Organ Failure Assessment (SOFA) ratings than the surviving group, while the nonsurviving group's serum ALB level was lower (P<0.05). Patients with drug-resistant KP infection and sepsis had higher serum levels of FCAS1, Procalcitonin, and SCYA25, which were risk factors for death, according to multivariate logistic regression analysis (P< 0.05), whereas elevated levels of serum ALB were protective factors for death in patients with drug-resistant KP infection and sepsis (P<0.05). The results of the ROC curve analysis revealed that the areas under the curve (AUCs) of serum FCAS1, Procalcitonin, and SCYA25 and the combined diagnosis of drug-resistant KP infection sepsis were greater than those of FCAS1, Procalcitonin and SCYA25 (P< 0.05), and the AUCs of the combined prediction of the three indicators for the death of patients with drug-resistant KP infection sepsis were greater than those of FCAS1, Procalcitonin and SCYA25. The AUC was calculated separately (P<0.05). Conclusions: The levels of serum FCAS1, Procalcitonin and SCYA25 in patients with drug-resistant KP-induced sepsis are relatively high. The combined detection of these three indicators has high diagnostic value for drug-resistant KP-induced sepsis and is related to the death of patients.
Background: Severe pneumonia in elderly patients is characterized by dysregulated inflammatory responses and impaired immune recovery. However, the dynamic interplay between inflammatory-immune biomarkers and clinical recovery remains insufficiently elucidated from a biochemical perspective. Methods: This prospective study included 276 elderly patients with severe pneumonia. Serial measurements of inflammatory biomarkers [C-reactive protein (CRP), procalcitonin (PCT), interleukin-6 (IL-6), and neutrophil-to-lymphocyte ratio (NLR)] and immune indicators (CD4+ T cells and natural killer cells) were performed at baseline, day 3, and end-of-treatment. Clinical recovery was evaluated using time to clinical stability, oxygenation index (PaO2 /FiO2), and length of hospital stay. Associations between biomarker dynamics and recovery outcomes were analyzed. Results: All inflammatory biomarkers exhibited significant declines over time, accompanied by partial restoration of immune function. Greater reductions in CRP PCT, and IL-6 at early time points were associated with faster clinical stabilization and improved oxygenation (all P < 0.01). NLR showed a pronounced early decrease, reflecting attenuation of systemic inflammatory stress. Notably, recovery of CD4+ T cells was significantly associated with improved clinical outcomes (P = 0.001), suggesting coordinated immune reconstitution. Patients with more favorable biomarker trajectories demonstrated shorter hospitalization and earlier transition to clinical stability. These findings indicate that integrated inflammatory-immune biomarker dynamics closely reflect the biological recovery process in severe pneumonia. Conclusion: Dynamic monitoring of inflammatory and immune biomarkers provides valuable biochemical insights into recovery trajectories in elderly patients with severe pneumonia. Combined biomarker profiling may serve as a practical tool for evaluating disease progression and guiding individualized management strategies.
Background: To explore the roles of urinep2-microglobulin (β2-MG) and the ratio of microalbuminuria (MAU) to uric acid (UA) in the diagnosis of renal damage and risk stratification assessment of the prognosis of essential hypertension with H-type (EH) hypertension. Methods: From January to December 2025, 204 patients with H-type EH and renal damage who were admitted to our hospital were selected and included in the renal damage group, whereas 102 patients with H-type EH but without renal damage were included in the EH group. Baseline data for all patients were collected. Urine β2-MG, urinary MAU, and UA levels were measured in all patients, and the MAU/UA ratio was calculated. The β2-MG levels and MAU/UA ratios of the two groups were compared, and multivariate logistic regression was used to identify factors influencing renal damage in patients with H-type EH. Patients with EH-related renal damage were divided into a low- to moderate-risk group and a high-risk group based on the prognostic risk stratification at admission. A receiver operating characteristic (ROC) curve was constructed to assess the predictive value of urine β2-MG concentration and the urine MAU/UA ratio for prognostic risk stratification of H-type EH renal damage. Results: Compared with those in the EH group, the proportion of patients with renal damage combined with diabetes, the urine β2-MG level, and the urine MAU/UA ratio were significantly greater (P<0.05). The results of multivariate logistic regression analysis revealed that elevated urine β2-MG levels and the urine MAU/UA ratio were independent risk factors for renal damage in H-type EH patients (P<0.05). The prognostic risk stratification revealed that 122 patients were in the low- to moderate-risk group and 82 in the high-risk group; urine β2-MG levels and urine MAU/UA ratios in the high-risk group were significantly higher than those in the low- to moderate-risk group (P<0.05). The ROC curve analysis revealed that the individual and combined predictions of urine β2-MG concentration and the urine MAU/UA ratio for high-risk renal damage in H-type EH patients had AUC values of 0.781, 0.786, and 0.860, respectively. The combined prediction AUC was significantly greater than the individual prediction AUC of the urine β2-MG concentration and the urine MAU/UA ratio (Z=2.035, 1.953; both P<0.05). Conclusion: The urine β2-MG level and urine MAU/UA ratio in patients with H-type EH renal damage are high. Moreover, increases in urine β2-MG levels and the urine MAU/UA ratio are independent risk factors for renal damage in H-type EH patients. The combined detection of these two indicators has high predictive value for the risk stratification assessment of renal damage in H-type EH patients.
Background: Circulating biomarkers that reflect tumor-associated immune-inflammatory activation may help refine breast cancer assessment. Triggering receptor expressed on myeloid cells-1 (TREM-1) amplifies myeloid-driven inflammatory signaling, and its soluble form (sTREM-1) can be measured in serum. However, the diagnostic and prognostic relevance of pretreatment circulating sTREM-1 in breast cancer remains insufficiently defined. Methods: This single-center retrospective observational study included 132 treatment-naive patients with stage I-III breast cancer, 68 patients with benign breast disease, and 60 healthy controls. Serum sTREM-1, conventional tumor markers, C-reactive protein (CRP), and derived inflammatory indices, including NLR, PLR, LMR, and SII, were analyzed. Associations with clinicopathological features, diagnostic performance, and disease-free survival (DFS) were evaluated using correlation analysis, receiver operating characteristic (ROC) curves, Kaplan-Meier analysis, and Cox regression models. Results: Serum sTREM-1 was significantly elevated in breast cancer compared with benign disease and healthy controls (P < 0.001). Higher sTREM-1 levels were associated with larger tumor size, lymph node involvement, advanced stage, high histological grade, and elevated Ki-67 expression (all P < 0.05). sTREM-1 correlated positively with CRP, NLR, PLR, and SII and negatively with LMR (all P < 0.001). For differentiating breast cancer from benign breast disease, sTREM-1 showed good diagnostic performance (AUC = 0.842), which improved when combined with CA15-3 and NLR (AUC = 0.889). Elevated sTREM-1 independently predicted shorter DFS in multivariate analysis (HR = 1.96, 95% CI: 1.01-3.80, P = 0.046). Conclusion: Circulating sTREM-1 is elevated in breast cancer and reflects myeloid-driven immune-inflammatory activation. As a measurable serum biomarker, sTREM-1 may provide complementary information for auxiliary diagnosis and prognosis evaluation. Larger multicenter studies are needed to validate its clinical utility and define standardized assay thresholds.
Background: To investigate the relationships among serum TNF-stimulated gene І4 (TSG-14), adipocyte lipid binding protein (ALBP), and Egl nine homolog 1 (EGLN1) levels and the severity of diabetic macular oedema (DME). A total of 314 patients with DME who were admitted to our hospital from March 2022 to March 2025 were selected (DME group). The patients were divided into mild, moderate, and severe groups based on their severity. Additionally, 314 patients with simple T2DM who were admitted to our hospital during the same period were selected (T2DM group). The levels of serum TSG-14, ALBP and EGLN1 were measured by ELISA. Logistic regression was used to identify determinants of severe DME, and receiver operating characteristic (ROC) curves were constructed to evaluate the blood levels of TSG-14, ALBP and EGLN1 in patients with severe DME.Results: There were significant differences in diabetes duration, fasting blood glucose, glycosylated haemoglobin, and homocysteine levels between the T2DM and DME groups (all P<0.05). Compared with those in the T2DM group, the levels of serum TSG-14, ALBP and EGLN1 in the DME group were considerably larger (all P < 0.05). Serum TSG-14, ALBP and EGLN1 levels in the moderate and severe groups were significantly higher (all P<0.05) than those in the mild group; serum TSG-14, ALBP and EGLN1 levels in the severe group were significantly higher (all P<0.05) than those in the moderate group. According to logistic analysis, EGLN1, ALBP and TSG-14 were risk factors for severe DME (all P<0.05). When evaluating patients with severe DME, ROC curve analysis showed that the AUCs for serum TSG-14, ALBP and EGLN1 alone and in combination were 0.781, 0.805, 0.817, and 0.950, respectively. The combined evaluation AUC was higher than in the individual evaluations (Z=2.699, 2.714, and 2.717, all P<0.05).Conclusion: The levels of TSG-14, ALBP and EGLN1 in the serum of DME patients were dramatically raised. These three signs are related to the severity of the condition. The combination detection approach has certain clinical utility for evaluating patients with severe DME.
Background: To explore the relationships between serum Interleukin-1 family member 4 (IL-1F4), Intercellular adhesion molecule-1 on endothelial cells (INCAM-1), and Vascular Permeability Factor (VPF) levels and disease progression and prognosis in patients with diabetic retinopathy (DR). Methods: Five hundred thirty-eight individuals with type 2 diabetes mellitus (T2DM) who were admitted to our hospital between February 2022 and February 2025 were chosen retrospectively. Based on their DR outcomes, these patients were divided into two groups: 178 with T2DM and 360 with DR. The evolution of these DR patients' illnesses led to further division into two groups: a non-PDR (NPDR) group (134 instances) and a proliferative DR (PDR) group (226 cases). Additionally, 134 healthy volunteers who underwent examinations during the same time frame comprised the control group. The differences in clinical data and serum levels of IL-1F4, INCAM-1, and VPF among the different groups were compared; the correlations among serum levels of IL-1F4, INCAM-1, and VPF were analysed, and to determine the variables affecting the course of DR. Based on the occurrence of visual impairment, DR patients were divided into two groups after a year of follow-up: those with a favourable prognosis (256 patients) and those with a poor prognosis (104 patients). Differences in clinical data and serum levels of IL-1F4, INCAM-1, and VPF among DR patients with different prognoses were compared. The factors influencing the poor prognosis of diabetic retinopathy (DR) were identified using multivariate logistic regression. The predictive value of serum IL-1F4, INCAM-1, and VPF for poor DR prognosis was assessed using receiver operating characteristic (ROC) curves. Results: The fasting blood glucose (FPG), glycosylated haemoglobin (HbA1c), IL-1F4, INCAM-1, and VPF levels in the control group, T2DM group, NPDR group, and PDR group increased successively (P<0.05), and the duration of diabetes in the T2DM group, NPDR group, and PDR group increased successively (P<0.05). The serum levels of IL-1F4, INCAM-1, and VPF in individuals with DR showed positive relationships (r=0.500, 0.489, and 0.564, respectively; P<0.05) according to Pearson analysis. High levels of FPG, HbA1c, IL-1F4, INCAM-1, and VPF, together with a longer duration of diabetes, were found to influence the progression of DR (P<0.05) in a multivariate logistic regression analysis. Groups with poor prognoses were older than those with good prognoses. Body mass index, FPG, HbA1c, IL-1F4, INCAM-1, and VPF were higher in the group with a poor prognosis than in the group with a good prognosis. Additionally, the duration of diabetes was longer in the poor prognosis group (P<0.05). Multivariate logistic regression analysis revealed that a longer duration of diabetes, as well as high levels of FPG, HbA1c, IL-1F4, INCAM-1, and VPF, were all variables affecting how DR progressed (P<0.05). The areas under the curve (AUCs) for forecasting a bad prognosis in individuals with diabetic retinopathy (DR) were found using ROC curve analysis. According to serum levels of IL-1F4, INCAM-1, and VPF were 0.771, 0.823, and 0.766, respectively. When these three indicators were combined, the area under the curve (AUC) for predicting a poor prognosis in DR patients was 0.873, which was higher than the AUC for any one sign alone (P<0.05). Conclusion: Serum IL-1F4, INCAM-1 and VPF may jointly participate in the process of DR. The elevated levels of these cytokines are closely related to the progression of DR and poor prognosis. Serum IL-1F4, INCAM-1, and VPF can serve as effective indicators of DR progression and visual disability.
Background: To explore the diagnostic efficacy of serum soluble tumorigenic factor-2 (sST-2), growth differentiation factor-15 (GDF-15), and the neutrophil/lymphocyte ratio (NLR) for the poor prognosis of pulmonary hypertension (PH) associated with chronic obstructive pulmonary disease (COPD). Methods: The COPD mixed with PH group consisted of 121 patients who received a diagnosis of COPD combined with PH at our hospital between January 2023 and December 2024. Patients with COPD and PH were further separated into two groups: those with a fair prognosis (93 patients) and those with a bad prognosis (28 patients). Forty-five healthy people who had physical examinations were chosen as the healthy control group, and another 75 patients with uncomplicated COPD within the same time period were chosen as the COPD group. Multivariate analysis of the effects of serum sST-2 and GDF-15 levels and the NLR on the prognosis of COPD combined with PH in each group, the relationships between serum sST-2 and GDF-15 levels and the NLR and the severity of COPD combined with PH, and the diagnostic value of COPD combined with PH for poor prognosis. Results: The COPD combined with the PH group's serum sST-2, GDF-15, and NLR levels were noticeably higher. Compared with the healthy control group, the COPD group showed significantly greater differences (P< 0.05) that increased with increasing PH severity. The group with a good prognosis had a considerably higher level of left ventricular ejection fraction (LVEF) than the group with a poor prognosis, whereas the levels of serum sST-2, GDF-15 and NLR in the poor prognosis group were significantly greater than those in the good prognosis group, and the differences were statistically significant (P< 0.05). There were no statistically significant differences in age, sex, disease duration, hypertension status, diabetes status, triglyceride, cholesterol, high-density lipoprotein or low-density lipoprotein levels (P> 0.05). Conclusions: The levels of serum sST-2, GDF-15 and the NLR are indicators reflecting the severity of COPD combined with PH. The combined detection of these three indicators helps improve diagnostic efficacy in patients with COPD and PH at high risk of a poor prognosis.
Background: To assess the value of the serum levels of sestrin 2 (SESN2), heme oxidase 1 (HO-1), and soluble haemoglobin scavenger receptor (sCD163) for the prediction of intrauterine fetal hypoxia in pregnant women with gestational hypertension disorder (HDCP). Methods: A total of 230 pregnant women with HDCP who were diagnosed and treated at this hospital from January 2023 to December 2024 were selected as the HDCP group, and 75 pregnant women with normal pregnancies who underwent prenatal examination at this hospital were included in the control group. Changes in the levels of serum SESN2, HO-1, and sCD163 were observed in the two groups. The levels of each index in pregnant women with HDCP of different severities were compared, and patients were divided into two groups based on whether intrauterine fetal hypoxia occurred: those with intrauterine hypoxia and those without. The factors influencing intrauterine fetal hypoxia in pregnant women with HDCP and the predictive efficacy of serum SESN2, HO-1, and sCD163 levels for intrauterine fetal hypoxia in pregnant women with HDCP were analysed. Results: The HDCP group had significantly higher levels of serum SESN2 and sCD163 than the normal pregnancy group (P< 0.01), while the normal pregnancy group had significantly lower levels of serum HO-1 (P< 0.01). Serum SESN2 and sCD163 levels were substantially greater in the severe preeclampsia group than in the moderate preeclampsia and gestational hypertension groups (P< 0.01), while the mild preeclampsia and gestational hypertension groups had significantly lower serum HO-1 levels (P< 0.01). Serum HO-1 levels in the mild preeclampsia group were significantly lower than those in the gestational hypertension group (P< 0.01), while serum SESN2 and sCD163 levels were significantly higher than those in the latter group (P< 0.01). While the intrauterine hypoxia group's prothrombin time and HO-1 levels were significantly lower than those of the nonintrauterine hypoxia group (P < 0 .0 1 ), the intrauterine hypoxia group's levels of serum D-dimer, fibrinogen (FIB), SESN2, and sCD163 were significantly higher. Multivariate logistic regression analysis revealed that elevated D-dimer, FIB, SESN2, and sCD163 levels were risk factors for intrauterine hypoxia in pregnant women with HDCP (P< 0.05), whereas elevated prothrombin time and HO-1 levels were protective factors (P< 0.05). The AUCs of individual and combined detection of serum SESN2, HO-1, and sCD163 for predicting intrauterine fetal hypoxia in pregnant women with HDCP were 0.823 (95% CI: 0.768-0.870), 0.868 (95% CI: 0.817-0.909), and 0.848 (95% CI: 0.795-0.8), respectively 92), 0.960 (95% CI: 0.926-0.981), and the AUC of the combined detection was significantly greater than that of SESN2 (Z = 4.665, P<0.001), HO-1 (Z = 4.876, P< 0.001), and sCD163 (Z= 4.228, P< 0.001) single detection. Conclusions: SESN2, HO-1, and sCD163 are involved in the occurrence and progression of HDCP and are closely associated with its severity. The combined detection of these three indicators helps determine a fetus's intrauterine hypoxic status.
Background: To explore the diagnostic value of serum Aldehyde dehydrogenase 5 (Ahd-5), IL-1 receptor-like 1 (IL1RL1), and CD138 in patients with chronic heart failure (CHF). Methods: The study group consisted of 256 CHF patients treated at our hospital between February 2023 and March 2025, whereas the control group consisted of 138 healthy volunteers who attended our hospital during that period for physical examinations. The cardiovascular function markers (LVEF, LVESV, and LVEEDV) and the serum markers (Ahd-5, IL1RL1, CD138, and N-terminal pro-Btype natriuretic peptide, or NT-proBNP) were identified and compared. According to LVEF results, CHF patients were divided into reduced ejection fraction heart failure (HFrEF), mildly reduced ejection fraction heart failure (HFmrEF), and preserved ejection fraction heart failure (HFpEF) groups. Serum Ahd-5, IL1RL1, and CD138 levels of CHF patients were correlated with cardiac function markers using Pearson correlation analysis. The associations among the various severities of CHF patients and their serum Ahd-5, IL1RL1, and CD138 levels were examined using Spearman correlation analysis. Factors influencing the occurrence of CHF were examined. The diagnostic value of serum Ahd-5, IL1RL1, and CD138 levels for CHF patients was examined using a receiver operating characteristic (ROC) curve. Results: Compared to the control group, the study group’s serum levels of Ahd-5 and LVEF were significantly lower (P<0.05). However, their blood levels of IL1RL1, CD138, NT-proBNP, creatinine, LVESV, and LVEDV were significantly greater. According to LVEF data, there were 72 patients in the HFrEF group, 88 in the HFmrEF group, and 98 in the HFpEF group. Serum Ahd-5 levels were substantially lower in the HFrEF and HFmrEF groups than in the HFpEF group (P<0.05), although serum IL1RL1 and CD138 levels were significantly greater. While the HFmrEF group had considerably greater serum IL1RL1 and CD138 levels (P<0.05), the HFrEF group had significantly lower serum Ahd-5 levels. According to the results of the Pearson correlation analysis, the serum Ahd5 level of CHF patients was positively correlated with LVEF (P<0.05) and negatively correlated with NT-proBNP, creatinine levels, LVESV, and LVEDV (P<0.05); the serum levels of IL1RL1 and CD138 were positively correlated with NT-proBNP, creatinine levels, LVESV, and LVEDV (P<0.05) and negatively correlated with LVEF (P<0.05). The serum Ahd-5 level showed a negative correlation with IL1RL1 and CD138 levels (P<0.05), and the serum IL1RL1 level had a positive correlation with the serum CD138 level (P<0.05). The areas under the curve (AUCs) of serum Ahd-5, IL1RL1, and CD138 for diagnosing CHF alone were 0.851, 0.830, and 0.860, according to ROC curve analysis. The combined diagnosis of CHF had an AUC of 0.946, which was substantially higher than the AUCs of serum Ahd-5 (Z=2.755, P=0.009), IL1RL1 (Z=3.071, P=0.002), and CD138 (Z=2.321, P=0.023). Conclusion: While serum IL1RL1 and CD138 levels considerably increased in CHF patients, serum Ahd-5 levels significantly decreased. When these three indications are detected together, they have a high diagnostic value for CHF and could be used as a novel auxiliary approach.
Background: The incidence of benign thyroid nodules (TN) is high. Minimally invasive ablation is a commonly used treatment in clinical practice. However, the distinctions in efficacy and safety between different ablation techniques still need to be clarified. This study aimed to compare the effects of ultrasound-guided radiofrequency ablation (RFA) and microwave ablation (MWA) on serum inflammatory factors, vascular endothelial growth factor (VEGF) expression, nodule volume reduction, thyroid function, and coagulation function in patients with benign thyroid nodules. Methods: One hundred and three patients with benign TN were retrospectively included and allocated to an RFA group (n = 58) or an MWA group (n=45). Baseline data and serum levels of inflammatory factors, nodule volume, thyroid function indicators (FT3, FT4, TSH), coagulation function parameters (PT, APTT), and vascular endothelial growth factor (VEGF) expression in nodule tissues preand post-surgery were extracted. Results: No distinctions in baseline data were noted (P> 0.05). On day 1 after surgery, the levels of inflammatory factors were lower in the RFA group versus the MWA group; The volume reduction rate of the RFA group was higher at each time point after surgery; At 6 months after surgery, the RFA group had a lower rate of VEGF-positive cells and a higher proportion of negative + weakly positive cells (P< 0.05). The RFA group had a superior response rate (94.83% vs 77.78% in the MWA group) and a lower incidence of adverse reactions (ARs) (13.79% ), with faster recovery (P< 0.05). On postoperative day 1, thyroid function indicators and coagulation parameters in both groups fluctuated slightly. Still, they remained within the normal range, with no significant difference between groups (P> 0.05). Conclusion: For the treatment of benign thyroid nodules, ultrasound-guided RFA was superior in alleviating inflammatory stress, promoting nodule reduction, and inhibiting VEGF expression. Its safety profile was reliable in protecting thyroid function and maintaining stable coagulation function, demonstrating greater comprehensive efficacy and safety. Thus, it can be considered a preferred minimally invasive treatment option.
Background: This study aimed to explore the relationships between serum α1-acid glycoprotein (AAG), lactate dehydrogenase (LDH), and blood lactate (BLa) levels and the severity and prognosis of severe pneumonia (SP) complicated with shock in elderly patients to provide useful references for clinical diagnosis and treatment. Methods: From May 2024 to July 2025, 364 elderly patients with SP combined with shock who were admitted to our hospital composed the SP combined with shock group. Depending on their severity, patients were divided into low-, medium-, and high-risk groups. A good-prognosis group and a bad-prognosis group were subsequently assigned to patients based on follow-up data. An additional 364 elderly patients with SP who did not experience shock and were admitted to our hospital during that time frame were included in the SP group. Following measurements of each research participant's serum levels of AAG, LDH, and BLa, the AAG/LDH ratio was calculated. APACHE II (Acute Physiology and Chronic Health Evaluation II) and CPIS (clinical pulmonary infection) scores, and AAG, LDH, and BLa levels in elderly patients with SP combined with shock were correlated using Spearman correlation. Results: While the SP group's serum LDH level was lower than the SP group's, the SP combined with shock group's serum AAG and BLa levels and AAG/LDH ratios were higher. Each of these variations was statistically significant (P<0.05). The low-risk group had 120 patients, the medium-risk group had 158, and the high-risk group had 86. While the low-risk subgroup's serum LDH level was higher than that of the medium-risk and high-risk subgroups (P<0.05), the low-risk subgroup's serum AAG levels, BLa levels, AAG/LDH ratios, APACHE II scores, and CPIS scores were lower. The medium-risk subgroup's blood AAG, BLa, AAG/LDH ratio, APACHE II score, and CPIS score were all lower than the high-risk subgroup's. Still, the high-risk subgroup's serum LDH level was greater (P<0.05). Spearman correlation analysis revealed a negative correlation (P<0.05) between the serum LDH level and the APACHE II score and CPIS score, and a positive correlation (P<0.05) between the serum AAG level, BLa level, AAG/LDH ratio, and APACHE II score in elderly patients with SP and shock. There were 94 patients with poor prognoses and 270 with good prognoses. While the good-prognosis group had higher serum LDH levels than the bad-prognosis group, it had lower serum AAG and BLa levels, a lower AAG/LDH ratio, a lower APACHE II score, and a lower CPIS score (P<0.05). Multivariate logistic regression analysis showed that elevated blood AAG/LDH and BLa levels were independent risk factors for progression to high-risk and poor prognosis in elderly SP patients with shock (P<0.05). In predicting poor prognosis in older patients with SP and shock, the areas under the receiver operating characteristic (ROC) curves for blood AAG/LDH and BLa were 0.841 and 0.823, respectively, according to the ROC analysis. When predicting poor outcome in elderly patients with SP and shock, the combined AUC of AAG/LDH and BLa was 0.934, higher than the AUC of each sign alone (P<0.05). Conclusion: In elderly patients with SP complicated by shock, serum AAG/LDH and BLa levels are abnormal and closely related to disease severity and patient prognosis. The combination of serum AAG/LDH and BLa for predicting the prognosis of elderly patients with SP complicated by shock has relatively high value.
Background: To explore the roles of Human Leukocyte Interferon (HLI) and Receptor for Advanced Glycation Endproducts (RAGE) in the occurrence and development of systemic lupus erythematosus (SLE), as well as their associations with the disease activity and clinical symptoms of SLE, and to evaluate the clinical application value of their detection. Methods: The levels of serum RAGE and HLI in SLE patients were detected via ELISA. The immunomagnetic bead method was used to measure the amounts of interleukin (IL)-1β, IL-2, IL-4, IL-5, and IL-6. Serum HLI and RAGE levels were measured in the active and inactive groups to assess the trial's effectiveness. Results: The SLE group had higher levels of HLI and RAGE than the RA group (P<0.05), while the RA group had lower levels of IL-2 and IL-6 (P<0.05). The active group had higher levels of RAGE, IL-6, and HLI than the inactive group (P<0.05). Positive correlations were found between RAGE and HLI (r=0.79, P=0.015) and between RAGE and HLI and the SLEDAI (r=0.65, P=0.016; r=0.44, P=0.034). RAGE is related to the cytokines IL1β, IL-4, and IL-5, whereas HLI is related to IL-1β and IL-4. Conclusion: HLI and RAGE support one another and play a role in the onset and progression of SLE. Both HLI and RAGE are associated with disease activity and clinical manifestations such as fever and kidney damage in patients with SLE. Their detection has significant clinical utility for distinguishing active from inactive SLE patients.
Background: Neonatal respiratory distress syndrome (NRDS) remains a major cause of early morbidity in preterm infants. Although exogenous pulmonary surfactant (PS) replacement therapy has improved short-term respiratory outcomes, the laboratory biochemical alterations accompanying PS treatment across different body fluid compartments have not been fully characterised. This study aimed to describe multi-domain biochemical changes associated with PS replacement therapy in preterm infants with NRDS. Methods: A total of 99 preterm infants with NRDS admitted to our hospital from January 1 to December 31, 2025, were included and divided into the PS treatment group (n=47) and the control group (n=52) according to treatment strategy. Fifty biochemical indicators involving nine core biochemical pathways were measured in serum, cerebrospinal fluid, and bronchoalveolar lavage fluid before treatment, 72 h after treatment, and 7 d after treatment. These pathways included bronchial development, intracranial injury, oxidative stress, inflammatory response, coagulation-fibrinolysis, vascular endothelial function, energy metabolism, hepatic function, and pulmonary surfactant function. Results: Before treatment, no significant differences were found in any biochemical indicators between the two groups (P>0.05). At 72 h and 7 d after treatment, the levels of markers related to bronchial epithelial injury, intracranial injury, oxidative injury, inflammatory response, coagulation-fibrinolytic disorder, and vascular endothelial injury were lower in the PS treatment group than in the control group (P<0.05). In contrast, indicators related to endogenous antioxidant capacity, pulmonary surfactant function, mitochondrial energy metabolism, and hepatic synthetic function were higher in the PS treatment group than in the control group (P<0.05). No significant changes were observed in the cerebrospinal fluid/serum S100 b ratio or serum pyruvate level at any time point in either group (P>0.05). These negative findings suggest that PS treatment was not associated with laboratory evidence of blood-brain barrier disruption and that pyruvate-related glycolytic homeostasis remained broadly stable in both groups. Conclusion: In this retrospective cohort, PS replacement therapy was associated with coordinated improvements in several biochemical domains in preterm infants with NRDS, including pulmonary surfactant function, oxidative-inflammatory status, coagulation-fibrinolytic balance, vascular endothelial markers, energy metabolism, and hepatic synthetic function. These findings provide exploratory laboratory evidence for multi-domain biochemical changes after PS treatment.
Background: Small Cell Lung Cancer (SCLC) is a deadly cancer with few reliable prognostic biomarkers. Although systemic inflammation contributes to SCLC progression, no studies have combined cellular senescence biomarkers with inflammatory markers. We proposed that measuring both serum inflammatory cytokines and cell-free telomere length together could improve prognostic accuracy. Methods: We enrolled 187 patients with extensive-stage SCLC before they started first-line chemo-immunotherapy. At baseline, we measured serum levels of IL-6, IL8, TNF-a, CRP, and cell-free telomere length (cfTL). We used Cox regression to create an Inflamm-Ageing Index (IAI). The main outcome was overall survival (OS). Results: High IL-6 (HR 2.14, 95% CI 1.45-3.16, p<0.001) and short cfTL (HR 2.87, 95% CI 1.92-4.29, p<0.001) were each linked to worse overall survival. The IAI grouped patients into low-, intermediate-, and high-risk groups, with median OS of 14.2, 9.1, and 5.3 months, respectively (p<0.001). The IAI stayed an independent predictor after adjusting for other factors (HR 3.42, 95% CI 2.18-5.37, p<0.001) and outperformed individual biomarkers (C-index 0.78). Conclusion: After a median follow-up of 16.8 months and 148 events (79.1%), the Inflamm-Aging Index, which combines inflammatory cytokines and cellular senescence biomarkers, showed promise for risk stratification in extensive-stage SCLC. However, since the biomarker thresholds were set using this cohort, external validation with pre-set cutoffs is needed before clinical use.
