Management of microaspiration and gastrointestinal dysfunction after lung transplantation: A narrative review

René Hage , Carolin Steinack , Macé M. Schuurmans
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Abstract

Background

Chronic Lung Allograft Dysfunction (CLAD) is the leading cause of late morbidity and mortality following lung transplantation. Increasing evidence implicates microaspiration, often secondary to gastroesophageal reflux disease (GERD) and gastrointestinal (GI) dysfunction, as a critical non-alloimmune driver of CLAD. However, its often silent presentation, diagnostic complexity, and heterogeneous management contribute to persistent knowledge and treatment gaps.

Methods

This narrative review synthesizes recent literature on the pathophysiology, diagnosis, and clinical impact of microaspiration and GI dysfunction in lung transplant recipients. We focus on emerging biomarkers (e.g., conjugated bile acids and pepsinogen A4), diagnostic modalities, and both medical and surgical treatment strategies aimed at mitigating aspiration-induced graft injury.

Key Content and Findings

Microaspiration leads to epithelial damage, surfactant disruption, immune activation, and microbial dysbiosis, collectively promoting allograft dysfunction. Conjugated bile acids in large airway bronchial wash fluid and pepsinogen A4 have shown superior specificity as aspiration biomarkers compared to pepsin alone. Gastrointestinal disorders, such as GERD, gastroparesis, and esophageal dysmotility, frequently co-exist post-transplant and contribute to aspiration risk. Pharmacologic interventions provide limited benefit, while anti-reflux surgery significantly improves graft outcomes, particularly when performed early. Conservative measures such as head-of-bed elevation also reduce reflux burden and may complement therapeutic strategies.

Conclusions

Microaspiration is a modifiable and underrecognized contributor to allograft injury. Integration of aspiration biomarkers, early reflux evaluation, and personalized stepwise management, including surgical intervention when indicated, may improve long-term transplant outcomes. This review provides clinicians with a structured framework for diagnosis and management of microaspiration-related injury in lung transplantation.
肺移植术后微吸和胃肠功能障碍的处理:一个叙述性的回顾
背景:慢性同种异体肺移植功能障碍(chronic Lung Allograft Dysfunction,简称CLAD)是肺移植术后晚期发病和死亡的主要原因。越来越多的证据表明,微吸,通常继发于胃食管反流病(GERD)和胃肠道(GI)功能障碍,是一个关键的非异体免疫驱动因素。然而,其通常沉默的表现,诊断的复杂性和异质性管理导致了持续的知识和治疗差距。方法本文综述了近年来关于肺移植受者微吸和胃肠道功能障碍的病理生理、诊断和临床影响的文献。我们专注于新兴的生物标志物(例如,共轭胆汁酸和胃蛋白酶原A4),诊断方式,以及旨在减轻吸入性移植物损伤的医疗和手术治疗策略。微吸导致上皮损伤、表面活性剂破坏、免疫激活和微生物生态失调,共同促进同种异体移植物功能障碍。与单独胃蛋白酶相比,大气道支气管洗涤液和胃蛋白酶原A4中的共轭胆汁酸显示出优越的特异性。胃肠道疾病,如胃反流、胃轻瘫和食管运动障碍,经常在移植后共存,并增加误吸风险。药物干预提供有限的益处,而抗反流手术可显著改善移植物预后,特别是在早期进行时。保守措施如床头抬高也可减少反流负担,并可作为治疗策略的补充。结论微吸是引起同种异体移植物损伤的一个可改变的、未被充分认识的因素。吸入生物标志物、早期反流评估和个性化分步管理的整合,包括指征时的手术干预,可能改善移植的长期结果。本综述为临床医生提供了一个诊断和处理肺移植中微吸入相关损伤的结构化框架。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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