International Journal of General Medicine最新文献

Patients with rheumatoid arthritis (RA) exhibit a significantly higher incidence of secondary osteoporosis compared to the general population, leading to substantially increased fracture risk, compromised quality of life, and poorer prognosis. Traditional views attribute this primarily to inflammatory activity, immobilization, and glucocorticoid use. However, the emergence of osteoimmunology has revealed deeper mechanisms, demonstrating that RA-induced osteoporosis represents a classic paradigm of osteoimmune dysregulation. This review systematically synthesizes recent advances (past 5-10 years) in understanding the pathophysiology of RA-induced osteoporosis from an osteoimmunological perspective. Research indicates that within the synovial and bone marrow microenvironments of RA, activated immune cells and stromal cells secrete abundant pro-inflammatory cytokines and express signaling molecules. This process severely disrupts core regulatory pathways of bone remodeling, leading to a profound imbalance characterized by excessive bone resorption and inadequate bone formation. Key mediators of this imbalance include dysregulation of the RANKL/RANK/OPG system and upregulation of potent inhibitors of the bone-forming Wnt pathway. Complex interactions between immune cells and bone cells are critical in establishing a localized bone-destructive microenvironment. Emerging research areas, including gut microbiota dysregulation, epigenetic mechanisms, and neuro-immune interactions, provide novel insights into these mechanisms. This review emphasizes that dysregulation of the osteoimmune system constitutes the core pathophysiological basis of RA-induced osteoporosis. A deeper understanding of these mechanisms is crucial for developing targeted bone-protective therapies and guiding future clinical strategies.

Objective: To investigate the therapeutic effects of Gupishengji-Huazhuojiedu Decoction (GHD) in inducing remission in Crohn's disease (CD) and to explore its potential underlying mechanisms.

Methods: A two-stage exploratory study was conducted. Stage one included a retrospective analysis (17 GHD, 27 infliximab [IFX]) and a prospective single-arm trial (n=8), assessing clinical remission (CDAI <150), endoscopic response (≥50% SES-CD reduction), and inflammatory biomarkers (CRP, fecal calprotectin). Stage two applied network pharmacology, machine learning (random forest, LASSO, XGBoost), and immunohistochemistry to explore GHD mechanisms.

Results: In the retrospective analysis, the GHD group exhibited a higher clinical remission rate than the IFX group (88.2% vs 51.9%, p=0.01), with trends toward higher clinical response (88.2% vs 63.0%, p=0.07) and endoscopic remission rates (58.8% vs 37.0%, p=0.16). In the prospective study, 87.5% (7/8) of patients achieved both clinical remission and endoscopic response after 12 weeks of treatment. CDAI, SES-CD, CRP, and fecal calprotectin levels were all significantly reduced compared with baseline (p<0.05). Bioinformatics analysis identified 13 key functional components (KFCGs) from GHD, and intersection of their 369 targets with CD differentially expressed genes yielded 36 candidate genes. Machine learning further prioritized six feature genes (IDO1, PRKG2, TGM2, ALDH1A2, ACPP, CASP1). Immune infiltration analysis revealed differences in immune cell populations between CD patients and healthy controls. Immunofluorescence experiments confirmed that GHD treatment significantly reduced the expression of CASP1, IDO1, CD11c, CD83, KLRG1, and CD45RO in intestinal mucosal tissue (p<0.05).

Conclusion: This study suggests that GHD may induce remission in CD through a multi-component, multi-target mechanism, particularly by modulating pathways related to CASP1 and IDO1, thereby improving clinical symptoms and endoscopic findings. The underlying mechanism may involve regulation of the intestinal immune-inflammatory microenvironment. GHD holds promise as a potential traditional Chinese medicine strategy for treating CD, but further validation in larger randomized controlled trials is warranted.

Acute promyelocytic leukemia(APL), a distinct subtype of acute myeloid leukemia(AML), has garnered significant attention in recent years regarding its pathogenesis and the molecular basis of its treatment response. With the rapid advancement of proteomics and metabolomics technologies, researchers can now delve deeper into revealing the molecular characteristics of acute promyelocytic leukemia and the regulatory role of its microenvironment. This review summarizes the latest research progress in proteomics and metabolomics within the acute promyelocytic leukemia field, focusing on analyzing the critical role of the the promyelocytic leukemia-retinoic acid receptor alpha (PML::RARα) fusion gene fusion protein in regulating cellular metabolism and protein expression. Furthermore, the article explores the importance of the immune system in acute promyelocytic leukemia treatment response and the impact of all-trans retinoic acid/arsenic trioxide therapy on the proteome and metabolome. By synthesizing existing research findings, this review aims to discuss how proteomic and metabolomic data elucidate the pathological mechanisms and therapeutic targets of acute promyelocytic leukemia, providing a theoretical basis for future precision medicine and translational research.

Objective: To explore the relationship between the triglyceride-glucose index (TyG), the monocyte to high-density lipoprotein cholesterol ratio (MHR) and the severity of coronary artery disease (CAD) under different glucose metabolism states.

Methods: A retrospective analysis was conducted on 526 patients who underwent coronary angiography (CAG) for the first time in the Affiliated Hospital of Xuzhou Medical University from January 2024 to January 2025. Among them, there were 122 patients in the non-CAD group and 404 patients in the CAD group. According to the Gensini score, the CAD group was further divided into a mild group (n = 147) and a moderate-to-severe group (n = 257). Meanwhile, they were divided into normal glucose regulation (NGR), prediabetes (Pre-DM), and diabetes mellitus (DM) groups according to the glucose metabolism state. Multivariate Logistic regression, restricted cubic spline (RCS), and receiver operating characteristic (ROC) curve analyses were used.

Results: Both the TyG index and MHR were independent risk factors for the occurrence and severity of CAD (P<0.05). In the DM group, the TyG index was significantly associated with the severity of CAD (OR=4.30, 95% CI: 1.48-12.49, P<0.01); in the NGR group, MHR was significantly associated with the severity of CAD (OR=436.1, 95% CI: 15.4-12342, P<0.001). RCS analysis suggested a significant linear positive correlation between the TyG index and the severity of CAD (P-overall=0.006, P-non-linear=0.917), while there was a non-linear relationship between MHR and the severity of CAD (P-overall=0.007, P-non-linear=0.033). ROC analysis showed that the area under the curve (AUC) of the combined prediction was 0.655, higher than that of the TyG index (0.618) and MHR (0.631).

Conclusion: TyG index and MHR can serve as independent biomarkers of new-onset CAD severity. In DM patients, TyG offers greater predictive value, while MHR is more predictive in NGR individuals.

Background: Lactobacillus paracasei (LP) may affect the efficacy of clopidogrel (CLP).

Methods:  Forty Sprague-Dawley (SD) rats were randomly divided into control group, LP group, CLP group, LP (pretreatment) + CLP group, and CLP + LP(posttreatment) group (n=6-8). The administration doses of CLP and LP in rats were 6.75 mg/kg/d and 10⁹ CFU/d, respectively, for 14 consecutive days. Tail vein blood was collected to detect blood drug concentration, platelet function. Then, a thrombosis model was constructed using 20% FeCl₃, the complete vascular occlusion time, thrombus weight, and thrombus inhibition rate, inflammatory factors, gut microbiota, short-chain fatty acids (SCFAs), trimethylamine N-oxide (TMAO) and mucosal barrier were evaluated.

Results:  Compared with the CLP group, the blood concentrations of AM and CA in the combined group were significantly decreased, while platelet aggregation (MPA) and platelet reaction index (PRI) were significantly increased. After model construction, the thrombosis formation time was significantly prolonged, the thrombus weight was significantly reduced, and the thrombus inhibition rate was significantly; the secretions of TNF-α, IL-1β, P-selectin, GPIIb/IIIa, and D-dimer were significantly decreased in the combined group. The structure of gut microbiota also changed significantly after CLP treatment, and LP combined with CLP could improve the dysbiosis caused by CLP through increasing SCFAs and decreasing TMAO. In addition, the expressions of ZO-1, Occludin, and P-gp were increased in the combined groups. It should be noted that there is a directional discrepancy between the changes in platelet function indices (MPA and PRI) and in vivo thrombosis outcomes, which may be related to the multi-factorial regulation of in vivo thrombosis.

Conclusion: LP may regulate the structure of gut microbiota (increasing SCFA-producing bacteria and inhibiting TMAO-producing bacteria), thereby protecting the intestinal mucosal barrier, inhibiting inflammatory responses, and cooperatively acting with CLP to inhibit platelet activation and improve coagulation function, although the specific mechanism needs further verification.

The cervical spine, a critical junction between the head and torso, is a rare but significant site for both primary and metastatic tumors. While primary tumors of the cervical spine are uncommon, certain types, such as chordomas and giant cell tumors, are particularly notable for their potential to affect this region. Metastatic lesions, although more frequent, present unique diagnostic and therapeutic challenges due to the complex anatomy of the cervical spine. Imaging is indispensable for the evaluation of cervical spine tumors, serving as the foundation for diagnosis, treatment planning, and monitoring therapeutic outcomes. Radiography, CT and MRI are the primary modalities used to assess tumor morphology, extent and relationship to surrounding structures. However, imaging alone may not always yield a definitive diagnosis, as some tumors lack distinctive features. Nevertheless, a combination of clinical presentation, epidemiological factors, and imaging findings often enables radiologists and clinicians to narrow the differential diagnosis and guide further management. Precise imaging interpretation is essential to prevent devastating clinical consequences resulting from diagnostic error, such as irreversible neurological damage, avoidable death, and significant long-term disability. This review provides a comprehensive overview of tumors that can involve the cervical spine, emphasizing their clinical and imaging characteristics. By highlighting key diagnostic features and discussing the latest advancements in imaging technology, aims to enable physicians in radiology, pathology, and clinical departments to gain a more comprehensive understanding of the imaging, pathological, and clinical characteristics of cervical spine tumors, thereby reducing misdiagnosis rates and alleviating the burden on patients.

[This corrects the article DOI: 10.2147/IJGM.S545850.].

Objective: This study aimed to analyze the correlation between serum levels of Procalcitonin (PCT) and C-reactive protein (CRP) and the occurrence and severity of Bronchopulmonary Dysplasia (BPD) in Extremely Low Birth Weight (ELBW) and Very Low Birth Weight (VLBW) neonates, and to identify associated risk factors.

Methods: A retrospective analysis was conducted on 213 ELBW/VLBW neonates admitted between January 2021 and January 2024. According to BPD diagnosis, they were categorized into a control group (n=62, without BPD) and an observation group (n=151, with BPD). The observation group was further stratified by severity into mild (n=71), moderate (n=46), and severe (n=34) BPD. Serum PCT and CRP levels were compared across groups. The correlation between these biomarkers and BPD severity was analyzed, and risk factors for BPD were investigated.

Results: PCT and CRP levels were significantly higher in the observation group than in the control group (P<0.05). A significant increasing trend in both PCT and CRP levels was observed with worsening BPD severity (P<0.05). Spearman analysis confirmed positive correlations between BPD severity and PCT (r=0.354) and CRP (r=0.472) levels (P<0.05). Multivariate logistic regression identified intrauterine infection, gestational age <28 weeks, assisted ventilation >2 weeks, infectious pneumonia, and FiO₂ >40% as independent risk factors for BPD (P<0.05).

Conclusion: In this retrospective study, elevated serum PCT and CRP levels were positively associated with the severity of BPD in ELBW/VLBW neonates. The identified risk factors, including intrauterine infection, gestational age <28 weeks, prolonged assisted ventilation, infectious pneumonia, and high FiO₂, are independently associated with BPD. These findings suggest that monitoring these biomarkers and risk factors may warrant intensified clinical attention.

Purpose: Heart rate recovery, measured during exercise testing, is an important marker of cardiovascular function. The Heart Rate Recovery Index, a recently proposed parameter derived from heart rate recovery, has shown predictive outcomes in patients undergoing cardiac resynchronization therapy. However, its role in heart failure identification remains unexplored. This study aimed to assess differences in the heart rate recovery index between patients with heart failure and individuals without heart failure undergoing exercise testing.

Patients and methods: 194 patients (mean age 58.3 ± 11.7 years; 57.7% men) with heart failure or other cardiovascular conditions requiring exercise testing were prospectively enrolled and underwent cycle ergometer testing. The index was calculated as the ratio between heart rate acceleration and deceleration time during exercise testing. Differentiation ability was assessed using receiver operating characteristic curve analysis. Subgroup and two-step cluster analyses examined heart rate recovery index differences across heart failure phenotypes and severity.

Results: Heart Rate Recovery Index was significantly lower in heart failure patients compared to those without (1.87 ± 0.68 vs 2.65 ± 1.08, p < 0.01). An optimal HRRI cut-off of 2.225 identified heart failure, while a lower cut-off of 1.555 differentiated patients with mildly reduced and reduced ejection fraction from those with preserved ejection fraction (AUC = 0.647). The index correlated significantly with systolic and diastolic parameters on echocardiography. In multivariable analysis, it remained an important predictor of heart failure (p < 0.01). Cluster analysis identified four phenotypic groups, with the index helping to differentiate early or less severe from advanced heart failure, according to the ejection fraction.

Conclusion: HRRI is a simple parameter that distinguishes the heart failure status and provides discrimination across its phenotypes. Its strong correlation with echocardiographic and functional markers supports its potential role in the assessment and characterization of heart failure.

Objective: Mast cells drive allergic diseases (asthma, rhinitis, dermatitis) via degranulation and pro-inflammatory mediator release. This review explores acupuncture's role in modulating mast cells to alleviate allergic symptoms.

Methods: We screened PubMed and Embase databases from January 2010 to January 2025 to search for published studies. The search keywords used are as follows: ["acupuncture" or "electroacupuncture"], ["allergic disease" or "asthma" or "allergic rhinitis" or "dermatitis" or "urticaria"], ["mast cell"]. 365 peer-reviewed studies on human/animal models were included, and articles that did not meet the requirements were excluded.

Results: Acupuncture inhibited mast cell degranulation, reducing histamine and IgE levels. It downregulated pro-inflammatory cytokines (TNF-α, IL-4, IL-5, IL-13) and upregulated anti-inflammatory IL-10, via suppressing NF-κB, MAPK (p38, ERK), and TLR4/MyD88 pathways. Clinically, it improved asthma (FEV1/PEF elevation), allergic rhinitis, and atopic dermatitis. Preclinically, it reduced eosinophil infiltration and inhibited NLRP3/caspase-1-mediated pyroptosis, further mitigating inflammation.

Conclusion: Acupuncture alleviates allergic disorders by targeting mast cells and inflammatory cascades, supporting its potential as a safe, effective therapeutic option.