National Institute for Health Research (NIHR) Nottingham Biomedical Research Centre at the Nottingham University Hospitals NHS Trust and University of Nottingham, Nottingham, UK.
Nottingham Digestive Diseases Centre, University of Nottingham, Nottingham, UK.
J Magn Reson Imaging. 2021 May;53(5):1422-1431. doi: 10.1002/jmri.27463. Epub 2020 Dec 16.
Increased small bowel permeability leads to bacterial translocation, associated with significant morbidity and mortality. Biomarkers are needed to evaluate these changes in vivo, stratify an individual's risk, and evaluate the efficacy of interventions. MRI is an established biomarker of small bowel inflammation.
To characterize changes in the small bowel with quantitative MRI measures associated with increased permeability induced by indomethacin.
Prospective single-center, double-blind, two-way crossover provocation study.
A provocation cohort (22 healthy volunteers) and intrasubject reproducibility cohort (8 healthy volunteers).
FIELD STRENGTH/SEQUENCE: 2D balanced turbo field echo sequences to measure small bowel wall thickness, T , and motility acquired at 3T.
Participants were randomized to receive indomethacin or placebo prior to assessment. After a minimum 2-week washout, measures were repeated with the alternative allocation. MR measures (wall thickness, T , motility) at each study visit were compared to the reference standard 2-hour lactulose/mannitol urinary excretion ratio (LMR) test performed by a lab technician. All analyses were performed blind.
Normality was tested (Shapiro-Wilk's test). Paired testing (Student's t-test or Wilcoxon) determined the significance of paired differences with indomethacin provocation. Pearson's correlation coefficient compared significant measures with indomethacin provocation to LMR. Intrasubject (intraclass correlation) and interrater variability (Bland-Altman) were assessed.
Indomethacin provocation induced a significant increase in LMR compared to placebo (P < 0.05) and a significant increase in small bowel T (0.12 seconds compared to placebo 0.07 seconds, P < 0.05). Small bowel wall thickness (P = 0.17) and motility (P = 0.149) showed no significant change. T and LMR were positively correlated (r = 0.68, P < 0.05). T measurements were robust to interobserver (intraclass correlation 0.89) and intrasubject variability (Bland-Altman bias of 0.005 seconds, 95% confidence interval [CI] -0.04 to +0.05 seconds, and 0.0006 seconds, 95% CI -0.05 to +0.06 seconds).
MR measures of small bowel wall T were significantly increased following indomethacin provocation and correlated with 2-hour LMR test results.
1 TECHNICAL EFFICACY STAGE: 2.
小肠通透性增加会导致细菌易位，从而导致发病率和死亡率显著增加。需要生物标志物来评估体内这些变化，对个体的风险进行分层，并评估干预措施的效果。MRI 是评估小肠炎症的一种既定的生物标志物。
用定量 MRI 测量来描述与吲哚美辛诱导的通透性增加相关的小肠变化。
前瞻性单中心、双盲、双向交叉激发研究。
激发队列（22 名健康志愿者）和受试者内可重复性队列（8 名健康志愿者）。
磁场强度/序列：在 3T 上获取用于测量小肠壁厚度、T1 和运动的二维平衡涡轮场回波序列。
参与者被随机分配接受吲哚美辛或安慰剂，然后进行评估。在至少 2 周的洗脱期后，用替代分配重复测量。每次研究访问时的 MR 测量（壁厚度、T1、运动）与实验室技术员进行的 2 小时乳果糖/甘露醇尿排泄比（LMR）测试的参考标准进行比较。所有分析均在盲法下进行。
用 Shapiro-Wilk 检验检验正态性。配对检验（Student's t 检验或 Wilcoxon）确定吲哚美辛激发引起的配对差异的显著性。Pearson 相关系数比较了吲哚美辛激发与 LMR 之间有显著意义的测量值。评估了受试者内（组内相关）和观察者间（Bland-Altman）变异性。
与安慰剂相比，吲哚美辛激发显著增加了 LMR（P<0.05），并显著增加了小肠 T1（0.12 秒，安慰剂 0.07 秒，P<0.05）。小肠壁厚度（P=0.17）和运动（P=0.149）无显著变化。T1 和 LMR 呈正相关（r=0.68，P<0.05）。T1 测量值具有较强的观察者间一致性（组内相关 0.89）和受试者内变异性（Bland-Altman 偏差 0.005 秒，95%置信区间 [CI] -0.04 至 +0.05 秒，0.0006 秒，95%CI -0.05 至 +0.06 秒）。
吲哚美辛激发后，小肠壁 T1 的 MRI 测量值显著增加，并与 2 小时 LMR 测试结果相关。
1 技术功效分期：2。
