Çetin Eyüp, Başgül Sagiri Dilara, Kahraman Özlü Eylem Burcu, Akar Ezgi, Güler Eray Metin, Kocaoğlu Sarper, Beyaztaş Hakan, Demir Emine
Neurosurgery Clınıc, Health Sciences University Haydarpaşa Training and Research Hospital, Istanbul, Turkey.
Department of Medical Biochemistry, Hamidiye Faculty of Medicine, University of Health Sciences Turkey, Istanbul, Turkey.
Med Sci Monit. 2025 Mar 25;31:e947508. doi: 10.12659/MSM.947508.
BACKGROUND Ligamentum flavum (LF) hypertrophy is a key contributor to spinal pathologies such as lumbar and cervical disc herniations and spinal stenosis. Smoking, as a modifiable lifestyle factor, is implicated in systemic inflammation and oxidative stress, potentially exacerbating LF hypertrophy. This study aimed to compare the expression of alpha-1 antitrypsin (AAT), interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) in the lumbar ligamentum flavum from 27 smokers and 31 non-smokers. MATERIAL AND METHODS LF tissue samples were collected during spinal surgeries. Demographic, anthropometric, and clinical data were recorded. ELISA was used to quantify levels of AAT, IL-1ß, IL-6, and TNF-alpha. Statistical analyses included t-tests, Mann-Whitney U tests, and receiver operating characteristic (ROC) curve analyses. Statistical significance was set at p<0.05. RESULTS Smokers exhibited significantly higher levels of IL-1ß (p<0.001), IL-6 (p=0.004), and TNF-alpha (p<0.001), while AAT levels were significantly lower (p<0.001) compared to non-smokers. ROC analysis identified IL-1ß (AUC=0.828; p<0.001) and TNF-alpha (AUC=0.801; p<0.001) as highly effective markers for distinguishing smokers from non-smokers, while IL-6 (AUC=0.730; p=0.003) showed moderate diagnostic accuracy. AAT (AUC=0.867; p<0.001) demonstrated excellent sensitivity (96.3%) for detecting smoking-related effects. CONCLUSIONS Smoking contributes significantly to systemic inflammation and oxidative stress, leading to biochemical changes that may drive LF hypertrophy. These findings underscore the importance of smoking cessation as a modifiable risk factor in the management of spinal pathologies.
背景 黄韧带（LF）肥厚是腰椎和颈椎间盘突出症及椎管狭窄等脊柱疾病的关键促成因素。吸烟作为一种可改变的生活方式因素，与全身炎症和氧化应激有关，可能会加剧黄韧带肥厚。本研究旨在比较27名吸烟者和31名非吸烟者腰椎黄韧带中α-1抗胰蛋白酶（AAT）、白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）的表达。
材料与方法 在脊柱手术期间收集黄韧带组织样本。记录人口统计学、人体测量学和临床数据。采用酶联免疫吸附测定（ELISA）法对AAT、IL-1β、IL-6和TNF-α水平进行定量分析。统计分析包括t检验、曼-惠特尼U检验和受试者工作特征（ROC）曲线分析。设定统计学显著性水平为p<0.05。
结果 与非吸烟者相比，吸烟者的IL-1β（p<0.001）、IL-6（p=0.004）和TNF-α（p<0.001）水平显著更高，而AAT水平显著更低（p<0.001）。ROC分析确定IL-1β（曲线下面积[AUC]=0.828；p<0.001）和TNF-α（AUC=0.801；p<0.001）是区分吸烟者和非吸烟者的高效标志物，而IL-6（AUC=0.730；p=0.003）显示出中等诊断准确性。AAT（AUC=0.867；p<0.001）在检测吸烟相关影响方面表现出出色的敏感性（96.3%）。
结论 吸烟对全身炎症和氧化应激有显著影响，导致可能促使黄韧带肥厚的生化变化。这些发现强调了戒烟作为脊柱疾病管理中一个可改变的风险因素的重要性。
