Journal of Inflammation Research最新文献

{"title":"Baricitinib Successfully Treated a Teenager with Refractory Livedoid Vasculopathy: A Case Report and Literature Review.","authors":"Chenxi Liu, Ying-Ying Jin, Xiqiong Han, Hua Huang, Shengfang Bao, Xuemei Xu, Liping Wang, Yanliang Jin","doi":"10.2147/JIR.S495481","DOIUrl":"10.2147/JIR.S495481","url":null,"abstract":"<p><strong>Background: </strong>The pathogenesis is of livedoid vasculopathy (LV)-a rare, chronic, and recurrent cutaneous vascular obstructive disease-is not fully understood. Conventional anticoagulant therapy sometimes exhibits limited efficacy, and although JAK inhibitors have demonstrated some efficacy in the treatment of refractory LV, the evidence remains insufficient.</p><p><strong>Case presentation: </strong>This study reports a case of a 14-year-old girl who were failed to maintain remission following treatment with oral rivaroxaban combined with external use of heparin sodium cream. However, the symptoms improved significantly 2 weeks after treatment with baricitinib, and remission was maintained during its gradual reduction.</p><p><strong>Conclusion: </strong>Successful treatment of this refractory patient with baricitinib provides another evidence for the potential therapeutic effect of JAK1/JAK2 inhibitors in LV, and also offers a reference for the dosage tapering regime of baricitinib in LV.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"1471-1477"},"PeriodicalIF":4.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11803417/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143382494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cucurbitacin IIa Alleviates Colitis via Promoting the Release of Host-Derived Extracellular Vesicles Encapsulating microRNA-30b-5p.","authors":"Yinyin Zhao, Binyuan Jiang, Shengnan Zuo","doi":"10.2147/JIR.S500722","DOIUrl":"10.2147/JIR.S500722","url":null,"abstract":"<p><strong>Purpose: </strong>Cucurbitacins have demonstrated anti-inflammatory effects and show promise for inflammatory bowel diseases. However, the underlying mechanisms by which cucurbitacins affect colitis remain largely unknown.</p><p><strong>Methods: </strong>In this study, we investigated the impact of cucurbitacin IIa on dextran sulfate sodium (DSS)-induced colitis in rats and the alterations in intestinal extracellular vesicles (EVs). EVs were isolated and characterized, followed by analysis of the small RNAs and proteins encapsulated within them using small RNA sequencing and proteomics, respectively.</p><p><strong>Results: </strong>Our results revealed that cucurbitacin IIa alleviated colitis symptoms in DSS-treated rats, along with changes in the morphology and composition of intestinal EVs. Notably, EVs from cucurbitacin IIa-treated rats also mitigated colitis symptoms in DSS-treated rats. Further analysis showed that cucurbitacin IIa modified the protein profiles and microRNA composition of EVs extracted from the feces of colitis rats. Specifically, microRNA-30b-5p, significantly increased by cucurbitacin IIa, was found to alleviate colitis symptoms in DSS-treated rats. In conclusion, cucurbitacin IIa appears to alleviate colitis by promoting the release of microRNA-30b-5p from host-derived extracellular vesicles.</p><p><strong>Conclusion: </strong>These findings enhance our understanding of cucurbitacin IIa's effects on intestinal health and offer potential new therapeutic targets for inflammatory bowel disease treatment.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"1447-1458"},"PeriodicalIF":4.2,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11793106/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and Validation of Pivotal Genes in Osteoarthritis Combined with WGCNA Analysis.","authors":"Chengzhuo Yang, Xinhua Chen, Jin Liu, Wenhao Wang, Lihua Sun, Youhong Xie, Qing Chang","doi":"10.2147/JIR.S504717","DOIUrl":"10.2147/JIR.S504717","url":null,"abstract":"<p><strong>Introduction: </strong>The prevalence of osteoarthritis (OA), the most common chronic joint condition, is increasing due to the aging population and escalating obesity rates, leading to a significant impact on human health and well-being. Thus, analyzing the key targets of OA through bioinformatics can help discover new biomarkers to improve its diagnosis.</p><p><strong>Methods: </strong>The microarray and RNA-seq results were screened from the Gene Expression Omnibus (GEO) database. Functional enrichment analyses, protein-protein interaction (PPI) analysis, and weighted gene co-expression network analysis (WGCNA) of the DEGs were performed. RT-qPCR and WB were further performed to verify the hub gene expression in OA rat.</p><p><strong>Results: </strong>In this study, 35 key genes were identified through differential expression analysis and weighted gene co-expression network analysis (WGCNA) using the GSE169077 and GSE114007 datasets. Enrichment analysis revealed that these key genes were predominantly enriched in the HIF-1 signaling pathway, ECM-receptor interaction, and FoxO signaling pathway. Through the integration of protein-protein interaction (PPI) analysis, validation in animal models and ROC curve analysis, four pivotal genes (GADD45B, CLDN5, HILPDA and CDKN1B) were finally identified.</p><p><strong>Conclusion: </strong>In conclusion, these identified key genes could serve as novel targets for predicting and treating OA, offering fresh insights into its etiology and pathogenesis.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"1459-1470"},"PeriodicalIF":4.2,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11792882/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Significance of the Lesion-Pleura Relationship in Differentiating Peripheral Inflammatory Lesions and Lung Cancers.","authors":"Yang Tao, Wen-Tao Zhang, Can Ding, Bin-Jie Fu, Fa-Jin Lv, Zhi-Gang Chu","doi":"10.2147/JIR.S493062","DOIUrl":"10.2147/JIR.S493062","url":null,"abstract":"<p><strong>Purpose: </strong>To determine the significance of lesion-pleura relationship in differentiating peripheral inflammatory lesions (PILs) and peripheral lung cancers (PLCs).</p><p><strong>Patients and methods: </strong>From January 2017 to April 2022, a total of 743 patients with 501 PLCs and 292 PILs (≥1.5 cm) were retrospectively enrolled. The patients' clinical characteristics and CT features of lesions in these two groups were analyzed and compared, and the impact of the lesion-pleura relationship (broad or narrow basement and distance between lesion and pleura) on differentiation was specifically assessed.</p><p><strong>Results: </strong>Lesions attached to pleura were more frequent in PILs (188, 64.4%) than in PLCs (244, 48.7%) (<i>P</i> < 0.001), and those with broad basement-to-pleura were also more common in PILs (133, 70.7%) than in PLCs (47, 19.3%) (<i>P</i> < 0.001). Among the 296 lesions with a lesion-pleura distance ≤16 mm, the optimal cutoff value of distance was ≤8.9 mm (area under curve [AUC], 0.733; sensitivity: 0.770; specificity: 0.623; <i>P</i> < 0.001) for predicting PLCs. Regarding the 728 lesions attached to pleura or with a lesion-pleura distance ≤16 mm, the AUC of the model based on the clinical and CT features for predicting PLCs significantly increased from 0.812 to 0.879 after including lesion-pleura relationship (narrow basement or lesion-pleura distance ≤ 8.9 mm) (<i>P</i> < 0.001). Additionally, the lesion-pleura relationship was one of independent indicators for differentiation (odds ratio, 9.433; <i>P</i> < 0.001).</p><p><strong>Conclusion: </strong>When differentiating peripheral lesions (≥1.5 cm), it is crucial to consider the basement-to-pleura and lesion-pleura distance besides patients' clinical characteristics, laboratory parameters and morphological features.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"1425-1434"},"PeriodicalIF":4.2,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11794381/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143255775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynamic Complement Protein Changes in Aqueous Humor and Plasma of Patients With Retinal Vein Occlusion During Ranibizumab Treatment.","authors":"Tingting Guo, Yanying Zhao, Shengnan Liang, Jie Wang, Hengwei Liu, Yufan Zhou, Heping Xu, Zhongping Chen","doi":"10.2147/JIR.S502481","DOIUrl":"10.2147/JIR.S502481","url":null,"abstract":"<p><strong>Purpose: </strong>To assess dynamic changes of complement protein in aqueous humor (AH) and plasma of retinal vein occlusion (RVO) patients during ranibizumab treatment, and to explore the differential expression of complement proteins in branch retinal vein occlusion (BRVO) and central retinal vein occlusion (CRVO).</p><p><strong>Patients and methods: </strong>This prospective, consecutive case series study collected AH and plasma samples from 27 RVO patients at baseline, 1 and 2 months after ranibizumab treatment, including 19 BRVO and 8 CRVO patients. The concentrations of 13 complement proteins and vascular endothelial growth factor A (VEGF-A) were measured using Luminex^® × MAP^® technology.</p><p><strong>Results: </strong>During ranibizumab treatment, a reduction in the levels of C1q (p < 0.001), C2 (p = 0.030), C4 (p = 0.001), C4b (p = 0.026), C3b/iC3b (p < 0.001), C5 (p = 0.007), C5a (p = 0.005), CFD (p = 0.022), CFH (p < 0.001), and CFI (p < 0.001) in AH was observed. No significant changes were observed in the plasma levels of all measured factors. At baseline, CRVO had higher levels of C4 (p = 0.003), C4b (p < 0.001), C3b/iC3b (p < 0.001), C5 (p = 0.020), C5a (p = 0.007), CFD (p = 0.002), CFH (p < 0.001), and CFI (p < 0.001) in AH compared to BRVO.</p><p><strong>Conclusion: </strong>Ranibizumab treatment reduced the intraocular but not circulating activation of classical and alternative complement pathways in RVO patients. Differences in intraocular complement proteins were observed between BRVO and CRVO patients, which may reflect different pathogenesis.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"1435-1445"},"PeriodicalIF":4.2,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11790804/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rhein Mitigates Lung Injury in Severe Acute Pancreatitis Through the Inhibition of MARK4-Mediated Microtubule Destabilization.","authors":"Zhenxuan Sun, Jie Liu, Peng Ge, Yinan Cao, Jin Liu, Haiyun Wen, Xinyu Luo, Boliang Pei, Zuocang Jin, Huijuan Li, Lu Xun, Yalan Luo, Qi Yang, Hailong Chen","doi":"10.2147/JIR.S505049","DOIUrl":"10.2147/JIR.S505049","url":null,"abstract":"<p><strong>Purpose: </strong>Explore the therapeutic effect and molecular mechanism of rhein on severe acute pancreatitis associated acute lung injury (SAP-ALI).</p><p><strong>Methods: </strong>The SAP-ALI rat model was constructed by retrograde injection of 5% sodium taurocholate into the pancreaticobiliary duct, and pulmonary microvascular endothelial cell (PMVEC) injury model was induced by LPS. The potential therapeutic effects and appropriate dosages of rhein on SAP-ALI and PMVEC were investigated in both in vivo and in vitro experiments. Furthermore, the regulatory role of MARK4 in the related pathological process were confirmed by some experimental methods. RNA sequencing analysis was performed to explore the potential downstream genes of MARK4. Moreover, the regulatory effect of rhein on MARK4 was validated through molecular docking and rescue experiments.</p><p><strong>Results: </strong>Rhein intervention had potential therapeutic effects on acute lung injury triggered by SAP and pulmonary endothelial cell injury induced by LPS. MARK4 may contribute to pulmonary endothelial cell injury through the modulation of microtubule structure. Compared with LPS stimulation, a total of 2081 differentially expressed genes were identified after MARK4 knockdown. The results of molecular docking and rescue experiments indicated that rhein may exert its protective effects by targeting MARK4.</p><p><strong>Conclusion: </strong>Rhein may regulate the microtubule structure by targeting MARK4, thereby alleviating SAP-ALI and LPS-induced pulmonary endothelial cell injury.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"1395-1412"},"PeriodicalIF":4.2,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11791671/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Novel Nomogram for Predicting the Risk of Pneumonia After Intracerebral Hemorrhage.","authors":"Yuanyuan Sun, Lei Zhang, Baisong Huang, Quanwei He, Bo Hu","doi":"10.2147/JIR.S490064","DOIUrl":"10.2147/JIR.S490064","url":null,"abstract":"<p><strong>Background: </strong>Pneumonia is among the most dangerous complications of infection after intracerebral hemorrhage. We aimed to create a novel nomogram for pneumonia after intracerebral hemorrhage.</p><p><strong>Methods and results: </strong>The data from the Chinese Cerebral Hemorrhage: Mechanism and Intervention (CHEERY) study was analyzed. Thirty percent of qualified patients were placed in the validation group (n=763) while seventy percent of them were randomly placed in the training group (n=1784). In the multivariate analysis, ten variables were included in the model: age (β= 0.023, P<0.001), hospital days (β=0.392, P<0.001), baseline mRS score (β=0.484, P<0.001), baseline GCS score (β=-0.285, P<0.001), hs-CRP (β=0.328, P<0.001), hematoma volume (β=0.376, P<0.001), brainstem hemorrhage (β=0.956, P=0.002), intraventricular hemorrhage (β=0.629, P=0.001), and β-blocker (β=0.899, P<0.001) In the training subset, the areas under curve were 0.805 (95% CI, 0.773-0.833). The model was subsequently examined in the validation group, with the area under curve 0.767 (95% CI, 0.716-0.807). There was strong agreement between the anticipated and actual survival rates in the nomogram calibration curves for both the training and validation groups. The clinical value of the model is assessed by means of Decision Curve Analysis. In addition, we validated other models with this cohort, which showed that our model had better discrimination. Moreover, the area under the curve of the catboost model established using the above nine variables in the training set and the validation set is 0.87(95% CI, 0.80-0.90) and 0.77(95% CI, 0.72-0.80).</p><p><strong>Conclusion: </strong>We have established a simple and easy predictive tool. By evaluating the incidence of pneumonia after intracerebral hemorrhage, we can identify high-risk groups early. At the same time, our study also suggests that doctors should be cautious in the use of β-blocker in clinical decision-making.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"1333-1351"},"PeriodicalIF":4.2,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11789516/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143123081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CLEC11A-Driven Molecular Mechanisms in Intervertebral Disc Degeneration: A Comprehensive Multi-Omics Study.","authors":"Nizhou Jiang, Quanxiang Wang, Zhenxin Hu, Xiliang Tian","doi":"10.2147/JIR.S505296","DOIUrl":"10.2147/JIR.S505296","url":null,"abstract":"<p><strong>Background: </strong>Intervertebral disc degeneration (IVDD) is a common chronic degenerative disease with a complex etiology involving genetic and environmental factors. However, the genetic pathogenesis and key driving factors of IVDD remain largely unknown.</p><p><strong>Methods: </strong>In this study, we combined MR with transcriptomic sequencing to identify key pathogenic genes implicated in IVDD. Further exploration using single-cell transcriptomics elucidated the specific cell types and pathways through which these genes modulate IVDD. Mediational MR analysis provided insights into the intermediary roles of 91 inflammatory factors and serum metabolites in the genetic causation pathway of IVDD. Finally, we validated these findings through in vitro experiments, confirming the regulatory roles of these critical genes in the progression of IVDD.</p><p><strong>Results: </strong>Transcriptomic and MR analyses identified six candidate pathogenic genes (AEN, CLEC11A, HMGN1, LRRC25, TAF7, and TREM1) significantly associated with IVDD. Subsequent single-cell analysis suggested that CLEC11A, TREM1, and HMGN1 may play pivotal roles in IVDD progression by modulating chondrocyte function and inflammatory responses. Mediation MR analysis further indicated that CLEC11A might significantly elevate IVDD risk by upregulating the inflammatory mediator ARTN and the uncharacterized serum metabolites X-12731 and X-18901 (ARTN: OR=1.078, 95% CI: 1.004-1.158, P=0.038; X-12731: OR=0.906, 95% CI: 0.852-0.960, P=0.043; X-18901: OR=1.090, 95% CI: 1.007-1.179, P=0.034). In vitro experiments demonstrated that overexpression of CLEC11A in nucleus pulposus cells significantly enhanced mRNA and protein expression of IVDD-related inflammatory markers; conversely, silencing CLEC11A markedly reduced these expressions. Similarly, overexpression of ARTN significantly increased, while knockdown decreased, the expression of these inflammatory markers in nucleus pulposus cells.</p><p><strong>Conclusion: </strong>Our integrative multi-omics analysis indicates that CLEC11A exacerbates IVDD by upregulating ARTN and inducing metabolic dysregulation, thereby amplifying the inflammatory pathways that drive disease progression.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"1353-1375"},"PeriodicalIF":4.2,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11787784/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143079825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative Bioinformatics Analysis to Identify Key Ferroptosis-Related Genes and Immune Infiltration in Aortic Aneurysm and Dissection: Implication of PTGS2.","authors":"Weiwei An, Jun Luo, Cheng Zhang, Qingzhong Xiao","doi":"10.2147/JIR.S488651","DOIUrl":"10.2147/JIR.S488651","url":null,"abstract":"<p><strong>Background: </strong>Aortic aneurysm and dissection (AAD) represent a highly lethal cardiovascular condition. Ferroptosis has recently been implicated in AAD development and progression. However, ferroptosis-related genes (FRGs) have not been systematically identified and verified in AAD.</p><p><strong>Methods and results: </strong>Seven human AAD datasets downloaded from Gene Expression Omnibus were analyzed, and 113 potential AAD-related FRGs were identified. Function enrichment analyses revealed that the FRGs were mainly associated with responses to chemical stress and cytokine signaling in the immune system. Protein-protein interaction network analyses identified 8 hub FRGs including <i>EZH2, EGFR, HIF1A, IL6, PTGS2, MAPK1, IL1B and SRC</i>. All these FRGs were significantly increased in patients with aortic aneurysm. Additionally, immune cell infiltration analyses revealed these FRGs were strongly correlated with the higher CD4⁺ Tem and macrophages fraction in AAD patients. Particularly, increased expression of PTGS2 in AAD patients was further validated using our newly collected clinical aortic specimens. Importantly, we found that PTGS2 knockdown could reduce the expression of MMP9 and MMP2 but increase GPX4 expression in macrophages. Conversely, while PTGS2 overexpression upregulated MMP9 and MMP2 expression but downregulated GPX4 expression, the regulatory effects of PTGS2 on these genes were largely blunted by ferroptosis inhibitors. Functionally, administration of celecoxib, a PTGS2-specific inhibitor, into mice significantly reduced β-aminopropionitrile-induced AAD development and progression.</p><p><strong>Conclusion: </strong>Through an integrative bioinformatics analysis, we have identified multiple key AAD-related FRGs including PTGS2. Functional studies also suggest a functional role of PTGS2 in ferroptosis and AAD development, offering novel insights into pathogenesis of human AAD.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"1377-1394"},"PeriodicalIF":4.2,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11787787/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143080052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development and Validation of the Systemic Inflammatory Response Index-Based Nomogram for Predicting Short-Term Adverse Events in Patients With Acute Uncomplicated Type B Aortic Intramural Hematoma.","authors":"Yasong Wang, Xuan Wu, Yue Wang, Zhiqiang Zhang, Xuanze Liu, Dongyuan Sun, Xue Liu, Tienan Zhou, Xiaozeng Wang","doi":"10.2147/JIR.S496007","DOIUrl":"10.2147/JIR.S496007","url":null,"abstract":"<p><strong>Purpose: </strong>This study aims to develop and validate a nomogram based on the Systemic Inflammatory Response Index (SIRI) to predict short-term aortic-related adverse events (ARAEs) in patients with acute uncomplicated Type B intramural hematoma (IMH).</p><p><strong>Patients and methods: </strong>We retrospectively analyzed 332 patients diagnosed with acute uncomplicated Type B IMH between April 2018 and April 2024. Patients were categorized into the stable group (N=225) and the exacerbation group (N=107) based on the occurrence of ARAEs within 30-day observation period. SIRI was calculated using neutrophil, monocyte, and lymphocyte counts. ARAEs were defined as death related to aortic disease, and the progression of IMH to aortic dissection or penetrating aortic ulcer. The nomogram was developed incorporating SIRI and other significant clinical variables. The model's performance was evaluated using the area under the curve (AUC), calibration curves, decision curve analysis (DCA), and net reclassification index (NRI).</p><p><strong>Results: </strong>Among the 332 patients, 217 were male (65.4%), with a mean age of 64.3±9.4 years. Multivariate logistic regression and LASSO regression analyses identified SIRI, anemia, diabetes, maximum diameter of aortic diameter (MDAD), and ulcer like projection (ULP) as independent predictors of ARAEs. Two nomogram models were developed: the Clinical model, including anemia, diabetes, MDAD, and ULP; and the Clinical-SIRI model, incorporating SIRI to the Clinical model. The Clinical-SIRI model demonstrated higher predictive accuracy, with an AUC of 0.788 (95% CI: 0.740-0.831), compared to the Clinical model's AUC of 0.742 (95% CI: 0.691-0.788, P = 0.012). SIRI improved predictive accuracy, as shown by a continuous NRI of 0.521 (95% CI: 0.301-0.743). Calibration curves and DCA further supported the clinical utility of the Clinical-SIRI model.</p><p><strong>Conclusion: </strong>The SIRI-based nomogram is a valuable prognostic tool for predicting short-term ARAEs in patients with acute uncomplicated Type B IMH.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"1303-1316"},"PeriodicalIF":4.2,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786605/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143079922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}