慢性鼻窦炎伴鼻息肉术后复发：内型机制、预测模型及精准治疗新策略

文献信息

中文摘要

背景： 慢性鼻窦炎伴鼻息肉（CRSwNP）术后复发是一个重大的临床挑战。传统的基于表型的分类已被证明不足以预测复发和指导个体化治疗，而免疫内型研究的进展正在揭示驱动复发的分子机制。
总结： 本综述系统性地探讨了CRSwNP术后复发的内型特异性机制、预测模型和治疗策略。它强调了五个核心争议：2型炎症是否真的是最强的复发驱动因素，鉴于有证据表明混合型1/3炎症可能导致更早的复发；缺乏生物制剂选择的头对头比较证据；内型分型在常规实践中的可操作性存疑；非2型和混合型内型持续缺乏有效疗法；以及缺乏内型驱动手术策略的前瞻性证据。本综述进一步批判了当前预测模型面临的转化障碍，包括复发定义不一致、外部验证不足以及输入变量可及性差。还总结了针对特定内型的药物治疗、生物制剂和手术策略。
关键信息： （1）2型炎症仍是复发的核心，但混合型内型可能导致更早和更难治的复发。（2）当前预测模型缺乏外部验证和校准数据，限制了其临床实用性。（3）靶向2型通路的生物制剂已改变治疗格局，但针对非2型患者的证据尚缺。（4）内型指导的精准管理——整合预测、药物治疗、生物制剂和手术——需要在多中心试验中进行前瞻性验证。

英文摘要

BACKGROUND: Postoperative recurrence of chronic rhinosinusitis with nasal polyps (CRSwNP) represents a significant clinical challenge. Traditional phenotype-based classifications have proven inadequate for predicting recurrence and guiding individualized management, while advances in immune endotype research are revealing the molecular mechanisms driving recurrence.
SUMMARY: This review systematically examines the endotype-specific mechanisms, predictive models, and treatment strategies for postoperative recurrence of CRSwNP. It highlights five core controversies: whether type 2 inflammation is truly the strongest recurrence driver, given evidence that mixed type 1/3 inflammation may lead to earlier relapse; the absence of head-to-head comparative evidence for biologic selection; the questionable operability of endotyping in routine practice; the persistent lack of effective therapies for non-type 2 and mixed endotypes; and the lack of prospective evidence for endotype-driven surgical strategies. The review further critiques the translational barriers facing current predictive models, including inconsistent recurrence definitions, insufficient external validation, and poor accessibility of input variables. Pharmacological treatments, biologics, and surgical strategies tailored to specific endotypes are also summarized.
KEY MESSAGES: (1) Type 2 inflammation remains central to recurrence, but mixed endotypes may drive earlier and more refractory relapse. (2) Current predictive models lack external validation and calibration data, limiting their clinical utility. (3) Biologics targeting type 2 pathways have transformed treatment, yet evidence for non-type 2 patients is absent. (4) Endotype-guided precision management-integrating prediction, pharmacotherapy, biologics, and surgery-requires prospective validation in multicenter trials.