鸟分枝杆菌亚种。副结核病(MAP)已被确定为导致多发性硬化症(MS)的环境因素之一。多年来,MS的全球患病率一直在上升;然而,揭示MAP在MS中的作用的努力有限。因此,本研究旨在评估MAP与MS风险相关的奇数比率(OR)。使用术语“多发性硬化症”或“MS”和“副结核”从6个数据库中获得与MAP相关的MS数据,而不考虑PRISMA标准的时间或语言限制。来自12项研究的2,538名参与者的数据显示了4项研究的抗MAP抗体和MAPDNA,并在随机效应(RE)和固定效应(FE)荟萃分析模型中进行了拟合。此外,研究间异质性是使用I2值测量的,显著限值设定为I²>75%.使用留一法分析确定分析的严谨性和发表偏倚,Egger\'stests,和p曲线分析。在FE和RE模型中,抗MAP抗体数据与MS风险显著相关,MAP为10.71OR(95%-CI[7.78;14.74],p值<0.0001)和12.76OR(95%-CI[8.13;20.02],p值<0.0001)分别,I2值为34.9%(95%-CI[0.0%;67.2%];p值=0.11)。同样,FE中的MAPDNA数据集显着显示由于MAP导致的MS风险为5.53OR(95%-CI[3.54;8.66],p值<0.0001),而,RE显示5.27OR(95%-CI[3.22;8.60],p=0.0017),I2值=0.0%(95%-CI[0.0%;84.7%];p值=0.71)。Eggers\'测试,另一方面,在抗MAP抗体数据中发现发表偏倚(截距=1.61,95%CI:0.45-2.77,t=2.72,p=0.021),但不在MAPDNA数据集中(截距=-5.57,95%CI:-20.44-9.29,t=-0.74,p=0.54)。所有敏感性分析都证明了荟萃分析的稳健性。此外,没有观察到p-hacking的证据(右偏度检验(PFull<0.001,PHalf<0.001;统计功效≥94%(95%-CI:72.5%-99%))。总之,合成揭示了MAP和MS之间的强关联,表明MAP是可能触发MS的重要环境因子。因此,在MS病例中早期筛查MAP可能有助于其管理/治疗的治疗方法.因此,未来的研究应该针对MAP在MS表型严重程度中的作用,以及解决全球数据缺口和低疾病监测问题。
Mycobacterium avium subsp. paratuberculosis (MAP) has been identified as one of the environmental agents that causes multiple sclerosis (MS). The global prevalence of MS has been upsurging over the years; however, efforts to divulge the role of MAP in MS have been limited. As a result, the present study aimed at assessing the odd ratios (ORs) associated MAP with the risk of MS. MAP-related MS data were obtained from 6 databases using the terms \'multiple sclerosis\' or \'MS\' and \'paratuberculosis\' without regard for time or language restrictions following PRISMA standards. A total of 2,538 participants\' data from 12 studies presenting anti-MAP antibodies and MAP DNA from 4 studies were fitted in random-effects (RE) and fixed-effects (FE) meta-analytic models. Furthermore, the between-study heterogeneity was measured using I2-values with a significant limit set at an I² > 75%. Analytical rigor and publication bias was determined using leave-one-out-analytics, Egger\'s tests, and p-curve analysis. In the FE and RE models, anti-MAP antibodies data significantly associated MS risk with MAP as 10.71 OR (95%-CI [7.78; 14.74], p-value < 0.0001) and 12.76 OR (95%-CI [8.13; 20.02], p-value < 0.0001) respectively, with an I2 value of 34.9% (95%-CI [0.0%; 67.2%]; p-value = 0.11). Similarly, the MAP DNA dataset in FE significantly present MS risk due to MAP as 5.53 OR (95%-CI [3.54; 8.66], p-value< 0.0001) while, RE showed 5.27 OR (95%-CI [3.22; 8.60], p = 0.0017), with an I2-value = 0.0% (95%-CI [0.0%; 84.7%]; p-value = 0.71). Eggers\' test, on the other hand, found publication bias in anti-MAP antibodies data (intercept = 1.61, 95% CI: 0.45 - 2.77, t = 2.72, p = 0.021), but not in MAP DNA dataset (intercept = -5.57, 95% CI: -20.44 - 9.29, t = -0.74, p = 0.54). The robustness of the meta-analyses was demonstrated by all sensitivity analyses. In addition, there is no evidence of p-hacking observed (right-skewness test (PFull < 0.001, PHalf <0.001; statistical power ≥ 94% (95%-CI: 72.5%-99%)). In conclusion, the synthesis revealed a strong association between MAP and MS, indicating that MAP is a significant environmental agent that may trigger MS. Thus, early screening of MAP in MS cases may assist in the therapeutic approach to its management/treatment. Therefore, future studies should be tailored towards the role of MAP in the severity of MS phenotypes, as well as address global data gaps and low disease surveillance.