Background and aims <p>Esophageal stricture is a common complication after esophageal endoscopic submucosal dissection (ESD). Pathological scars may predict stricture development, but clinical studies exploring their relationship are limited. This study aimed to investigate the link between concurrent pathological scarring and post-ESD esophageal stricture and develop a predictive risk model.</p> Methods <p>This retrospective single-center study included patients who underwent ESD for superficial esophageal lesions (SELs) over the past decade. Data on demographics, endoscopy, pathology, and concurrent scarring were collected. Multivariate logistic regression identified risk factors, followed by validation using subgroup analysis and propensity score matching. A nomogram was developed and internally validated.</p> Results <p>Of 255 patients, 28 (11.0%) developed esophageal stricture. Multivariate logistic regression identified concurrent pathological scarring as an independent risk factor for stricture development (OR 96.520 [10.641–875.536], <i>p</i> &lt; 0.001). Additional risk factors included lesions in the upper esophagus, lesions longer than 4 cm, circumferential involvement over 50%, infiltration depth beyond the epithelium, and muscular layer injury during the procedure. A predictive model incorporating these factors was developed, demonstrating high discriminative ability (AUC 0.943 [0.902–0.984]) with an optimal cutoff of 135.6, sensitivity of 82.4%, and specificity of 94.3%. The calibration curve showed good accuracy.</p> Conclusions <p>Concurrent pathological scarring is an independent risk factor for post-ESD esophageal stricture.</p>

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Concurrent pathological scar: independent risk factor for esophageal stricture after endoscopic submucosal dissection

  • Yue-Yi Zhang,
  • Zhi-Yu Yan,
  • Qing-Wei Jiang,
  • Yun-Lu Feng,
  • Ying-Yun Yang,
  • Sheng-Yu Zhang,
  • Dong-Sheng Wu,
  • Tao Guo,
  • Xi Wu,
  • Qiang Wang,
  • Ai-Ming Yang

摘要

Background and aims

Esophageal stricture is a common complication after esophageal endoscopic submucosal dissection (ESD). Pathological scars may predict stricture development, but clinical studies exploring their relationship are limited. This study aimed to investigate the link between concurrent pathological scarring and post-ESD esophageal stricture and develop a predictive risk model.

Methods

This retrospective single-center study included patients who underwent ESD for superficial esophageal lesions (SELs) over the past decade. Data on demographics, endoscopy, pathology, and concurrent scarring were collected. Multivariate logistic regression identified risk factors, followed by validation using subgroup analysis and propensity score matching. A nomogram was developed and internally validated.

Results

Of 255 patients, 28 (11.0%) developed esophageal stricture. Multivariate logistic regression identified concurrent pathological scarring as an independent risk factor for stricture development (OR 96.520 [10.641–875.536], p < 0.001). Additional risk factors included lesions in the upper esophagus, lesions longer than 4 cm, circumferential involvement over 50%, infiltration depth beyond the epithelium, and muscular layer injury during the procedure. A predictive model incorporating these factors was developed, demonstrating high discriminative ability (AUC 0.943 [0.902–0.984]) with an optimal cutoff of 135.6, sensitivity of 82.4%, and specificity of 94.3%. The calibration curve showed good accuracy.

Conclusions

Concurrent pathological scarring is an independent risk factor for post-ESD esophageal stricture.