International Journal of General Medicine最新文献

Background: Myocardial infarction with non-obstructive coronary arteries (MINOCA) is a heterogeneous clinical entity in which coronary microvascular dysfunction plays a central pathophysiological role. The coronary slow flow phenomenon (CSFP) represents an angiographic manifestation of microvascular dysfunction; however, reliable and practical biomarkers for its identification remain limited. The stress hyperglycemia ratio (SHR) reflects acute metabolic stress beyond chronic glycemic status. This study aimed to investigate the association between SHR and CSFP in patients with MINOCA.

Methods: In this single-center retrospective cohort study, 2073 patients undergoing coronary angiography for suspected myocardial infarction between 1 January 2020 and 1 December 2025 were screened. 354 patients with MINOCA were included. Patients with CSFP were matched 1:2 with controls according to age and sex using exact matching. SHR and other laboratory parameters were assessed. Logistic regression and receiver operating characteristic (ROC) analyses were performed to identify independent predictors of CSFP.

Results: Among the study population, 118 patients (33.3%) had CSFP. Patients with CSFP had significantly higher SHR levels, along with increased C-reactive protein, triglycerides, low-density lipoprotein cholesterol, and uric acid, whereas HbA1c and serum albumin levels were lower (all p < 0.05). In multivariable logistic regression analysis, SHR emerged as the strongest independent predictor of CSFP (OR: 1.48, 95% CI: 1.30-1.69; p < 0.001). In ROC analysis, SHR demonstrated the highest discriminative performance for CSFP (AUC: 0.74), with an optimal cut-off value of 0.998, yielding a sensitivity of 66.1% and a specificity of 64.3%.

Conclusion: SHR is independently associated with CSFP in patients with MINOCA, suggesting that acute metabolic stress plays a key role in coronary microvascular dysfunction. SHR may serve as a simple and readily available marker for identifying high-risk microvascular phenotypes in MINOCA patients.

Objective: To develop a clinical risk stratification model for thyroid eye disease (TED) recurrence post-glucocorticoid therapy by integrating dynamic thyroid-stimulating hormone receptor antibody (TRAb), extraocular muscle (EOM) thickness, and baseline clinical-biochemical indicators, with only internal validation.

Methods: A single-center retrospective cohort study of 426 TED patients (2016-2023) was conducted. Recurrence (12-month follow-up) was adjudicated by two ophthalmologists. LASSO regression screened predictors, and multiple machine learning models were built and validated via 10-fold cross-validation. Model performance was assessed by AUC and decision curve analysis (DCA).

Results: 98 patients (23.0%) had recurrence, with 89% occurring after 6 months post-treatment. Recurrent patients showed slower TRAb decline and persistent EOM thickening. 15 key predictors were identified, and the random forest (RF) model had the best performance (AUC=0.92, 95% CI: 0.88-0.95; accuracy=0.87) with consistent subgroup results (Events Per Variable=6.5, potential overfitting risk).

Conclusion: This internally validated risk stratification model identifies factors associated with TED recurrence post-glucocorticoid therapy, with dynamic TRAb and EOM thickness as key indicators. The findings are preliminary due to no external validation and temporal limitations, and prospective multi-center studies are required before clinical implementation to inform individualized follow-up.

Objective: Recurrent pregnancy loss (RPL), defined as two or more consecutive spontaneous miscarriages before 20 weeks of gestation, affects 2-5% of reproductive-age women globally, and current clinical predictors for it lack sufficient accuracy. This study aimed to construct a machine learning (ML) model for RPL prediction by integrating serum IL-33, C-reactive protein (CRP), and lymphocyte subset counts, and validate its performance in a retrospective cohort.

Methods: A total of 340 reproductive-age women from XiDian Group Hospital and Xi'an Traditional Chinese Medicine Hospital (January 2020-December 2024) were enrolled. Baseline clinical characteristics, IL-33, CRP levels, and lymphocyte subset counts were collected as predictors, with RPL as the primary outcome. The dataset was split into a training set (70%) and a validation set (30%). Logistic regression, random forest, and XGBoost were trained with hyperparameter optimization via grid search, and model performance was evaluated by AUC, accuracy, sensitivity, specificity, PPV, and NPV.

Results: Of the 340 participants, 85 (25.0%) had RPL and 255 (75.0%) did not. The RPL group had significantly lower IL-33 and CD4+/CD8+ ratio, higher CRP and NK cell proportions (all p < 0.001). XGBoost outperformed the other two models, with an AUC of 0.89 (95% CI: 0.82-0.96) in the training set and 0.85 (95% CI: 0.76-0.94) in the validation set; its validation set accuracy, sensitivity, specificity, PPV and NPV were 88.1%, 82.4%, 88.7%, 28.6% and 98.7%, respectively.

Conclusion: The ML model integrating IL-33, CRP, and lymphocyte subset counts shows good discriminatory ability for RPL, providing a preliminary reference for identifying high-risk women in clinical practice.

Validate the clinical utility of exosome cargo (miRNAs/proteins) and NLRP3/BDNF as key regulatory molecules for acupuncture-mediated spinal cord injury (SCI) recovery. From the establishment of the database to May 2025, a literature search was conducted on PubMed, and Embase, using keywords ["exosome cargo" or "exosome"], ["acupuncture" or "acupuncture and moxibustion" or "electroacupuncture" or "EA"], ["spinal cord injury" or "SCI"], ["immune regulation"], ["inflammatory reaction"], ["neuroregeneration" or "nerve"]. Including peer-reviewed studies on human/animal models, articles that do not meet the requirements are excluded. Preclinically, MSC-exosomal miR-145-5p suppressed TLR4/NF-κB signaling, reducing spinal IL-1β by 47% in SD rats. Schwann cell-exosomal MFG-E8 activated SOCS3/STAT3, increasing M2 macrophage CD206 by 63% and raising rat BBB scores by 3.8 points; Treg-exosomal miR-2861 upregulated tight junction proteins (occludin/ZO-1) to repair the blood-spinal cord barrier. Acupuncture (EA at GV14/GV4) upregulated spinal BDNF by 72% and NGF by 58% via Wnt/β-catenin, while EA at GV6/GV9 downregulated NLRP3 by 42-58% and TNF-α by 35-47%. Clinically, EA at EX-B2 increased ASIA scores by 3.2±1.1 points (Guo et al). Besides, 5x/week EA improved ASIA vs 3x/week (+6.4 points). EA+exercise reduced MAS by 1.6-2.9 points, with outcomes correlated to peripheral NLRP3 reduction, BDNF elevation, and MBI/WISCIII increases. Exosome cargo (miR-145-5p/MFG-E8) and NLRP3/BDNF are key regulatory molecules underlying acupuncture-mediated SCI recovery. However, limitations (small RCT samples, heterogeneous acupuncture protocols, unstandardized exosome isolation) hinder translation. Future work should focus on standardized biomarker detection, exosome engineering, and large-scale clinical trials.

Glioblastoma (GBM) is the most malignant primary central nervous system tumor in adults, with strong invasiveness, high recurrence, and poor prognosis. Natural killer (NK) cells, innate immune cells that eliminate glioma stem cells without MHC matching, show promise for GBM immunotherapy, but their efficacy is limited by GBM's immunosuppressive tumor microenvironment (TME), especially via protein post-translational modifications (PTMs). This review summarizes seven key PTMs' (phosphorylation, acetylation, glycosylation, methylation, ubiquitination, SUMOylation, lactylation) dual regulation on NK cell therapy: physiological PTMs enhance NK cytotoxicity, targeting, and persistence; aberrant PTMs block NK activation, induce exhaustion, and promote GBM immune escape. It also analyzes bottlenecks (insufficient NK activity/persistence, GBM's PTM-mediated escape) and breakthroughs (PTM-targeted small molecules like TAK-981, CRISPR-edited NK cells, combination therapies). Future directions include BBB precision delivery, PTM-guided personalized therapy, and PTM crosstalk research, aiming to advance NK therapy's clinical translation for GBM.

Background: The atherogenic index of plasma (AIP) reflects lipid imbalances associated with early atherosclerosis, which is relevant to slow coronary flow phenomenon (SCFP). So in the present study, we aimed to investigate the correlation between AIP and slow coronary flow phenomenon.

Methods: In total, 1525 patients received coronary angiography for chest pain and found no obvious obstructive stenosis were consecutively enrolled in this study. Out of whom, 91 patients were diagnosed with SCFP. We selected 182 age and sex-matched patients with normal coronary arteries and normal blood flow as the controls. The clinical parameters were compared, and the association between AIP and SCFP was explored.

Results: Patients with SCFP had a higher level of uric acid, triglyceride (TG), AIP, while a lower high-density lipoprotein cholesterol (HDL-C) level. Multivariate logistic regression analyses showed that the AIP and uric acid levels were independent predictors of SCFP. When the AIP was ≥0.205, the specificity and sensitivity were 0.648 and 0.678, respectively (area under the curve [AUC] = 0.740; 95% confidence interval [CI], 0.684-0.797, P < 0.001).

Conclusion: AIP is an independent predictor of SCFP in patients with chest pain and angiography proven normal coronary arteries. AIP could offer a non-invasive, accessible tool for early SCFP detection, therefore improving patient outcomes.

Background: Severe traumatic brain injury (sTBI) is related to disturbances in iron metabolism, and hepcidin is involved in the regulation of this process. However, it is unclear about serum hepcidin levels after sTBI. In this study, serum hepcidin levels were detected for association with severity and worse outcomes of sTBI.

Methods: In this two-center observational analytical study, age, gender, alcohol drinking, cigarette smoking, hypertension, diabetes mellites and hyperlipidemia were not significantly different between 154 patients with sTBI and 154 controls; and serum hepcidin levels were measured. The Glasgow Coma Scale (GCS) and Rotterdam computed tomography (CT) classification were used as severity metrics. Patients got 180-day follow-up by adopting the extended Glasgow Outcome Scale (GOSE), with score of 1-4 signifying poor prognosis. The primary outcome was poor prognosis, and secondary outcomes included death, overall survival, and acute lung injury (ALI). Results were determined using multivariate approaches.

Results: Serum hepcidin levels were markedly higher in patients than in controls. Serum hepcidin levels were linearly correlated with GCS scores, Rotterdam CT scores, GOSE scores, death risk, and possibilities of shorter overall survival, poor prognosis, and ALI, and were independently associated with preceding severity indicators and outcome variables. The results of regression analyses were robust, based on the E-value and sensitivity analyses. Serum hepcidin levels displayed analogous discrimination efficiency for death, poor prognosis, and ALI, compared to both GCS scores and Rotterdam CT scores. Moreover, ALI had a partial mediating effect on relationship between serum hepcidin levels, poor prognosis, and death.

Conclusion: Substantially elevated serum hepcidin levels, in tight correlation with trauma severity, are closely associated with poor outcomes; and ALI partially deciphers links between serum hepcidin levels and clinical outcomes, indicating that serum hepcidin may be a prognostic surrogate of sTBI.

Background: IgG4-related autoimmune pancreatitis (IgG4-AIP) is a rare autoimmune pancreatic disorder, with elevated carbohydrate antigen 19-9 (CA19-9) observed in some patients.

Objective: This study aims to compare the clinical features of IgG4-AIP patients with elevated versus normal CA19-9 levels to clarify the clinical significance of CA19-9 in this condition.

Methods: This study conducted a retrospective analysis of the clinical data of 41 patients with IgG4-AIP who underwent CA19-9 testing at Yichang Central People's Hospital from January 2019 to April 2025. In this study, the normal reference range for CA19-9 levels was defined as 0 to 39 U/mL.

Results: Among the 41 patients with IgG4-AIP, 23 patients (56.10%) had normal CA19-9 levels, while 18 patients (43.90%) exhibited elevated CA19-9 levels. Patients with elevated CA19-9 levels were more likely to be misdiagnosed as having pancreatic tumors (55.56% vs. 13.04%) and had a higher incidence of bile duct involvement (88.89% vs. 26.09%), whereas the incidence of lymph node involvement (22.22% vs. 56.52%) was lower (P<0.05). Compared to the normal CA19-9 group, patients in the elevated CA19-9 group had significantly higher levels of total bilirubin (TBIL), direct bilirubin (DBIL), alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), alkaline phosphatase (ALP), and complement C3 (C3) (P<0.05). Additionally, CA19-9 levels demonstrated a moderate positive correlation with TBIL, DBIL, ALT, AST, GGT, and ALP (P<0.05). However, no significant correlation was found between CA19-9 levels and C3 or serum immunoglobulin G4 (IgG4) levels (P>0.05).

Conclusion: Patients with elevated CA19-9 levels in IgG4-AIP exhibit more complex clinical features. Clinicians should consider CA19-9 level differences when evaluating and managing IgG4-AIP patients to guide personalized diagnostic and therapeutic strategies.

Objective: To synthesize 2020-2025 evidence on whether acupuncture (including electroacupuncture) modulates metabolic remodeling and mitochondrial function in atrial fibrillation (AF), summarize putative mechanisms, and define research priorities.

Methods: PubMed, Web of Science, Embase, and CNKI were searched from January 2020 to October 2025 using controlled vocabulary and free-text terms, supplemented by backward citation tracking. Eligible publications in English or Chinese included original studies and reviews addressing AF metabolomics, mitochondrial biology, and acupuncture. Priority was given to direct AF evidence pairing an acupuncture intervention with metabolic or mitochondrial readouts. Mechanistically relevant indirect evidence was also incorporated from AF metabolic characterization studies and acupuncture-related metabolic research in other conditions. Findings were synthesized qualitatively without meta-analysis. The review was not preregistered and no formal risk-of-bias tool was applied; evidence types and uncertainty were described narratively.

Results: AF is consistently associated with metabolic reprogramming in serum and atrial tissue, involving energy pathways, lipid metabolism, and amino acid/one-carbon metabolism. Mitochondrial abnormalities-impaired biogenesis, altered dynamics, and oxidative stress-are frequently linked to electrophysiological remodeling and pro-fibrotic signaling. Preclinical and small-sample clinical studies suggest acupuncture can shift metabolic profiles and improve mitochondrial-related parameters, with emerging signals implicating vagal-immune-metabolic coupling in AF models. However, rigorous randomized trials in AF patients with longitudinal metabolomics and prespecified mitochondrial endpoints remain scarce.

Conclusion: Acupuncture may modulate AF-relevant metabolic and mitochondrial dysfunction through coordinated autonomic, inflammatory, and metabolic regulation. Future studies should adopt multi-timepoint multi-omics designs, STRICTA-compliant protocols, and integrated clinical-mechanistic pipelines to test causal links to electrophysiological outcomes.