Digestive Diseases and Sciences | 2021
Half-Full or Half-Empty: Does Gastroparesis Affect Lung Transplantation Outcomes?
Abstract
Although significant advances in solid organ transplantation have been made in the past decades, outcomes inferior to those with other organ transplantations remain for lung transplantation [1]. Chronic lung allograft dysfunction (CLAD) remains the largest barrier to improved morbidity and mortality in lung transplant recipients [2]. Limiting effective management of CLAD is the multiplicity of pathophysiologic mechanisms that contribute to progressive transplant decline [3]. Any investigation into the factors that can be associated with CLAD is welcome; once such mechanism is gastroparesis. In this issue of Digestive Diseases and Sciences, Blackett et al.[4] make an important contribution to the understanding of the factors associated with the development of gastroparesis after lung transplantation. Using a single-center, retrospective design, they identified 616 patients who underwent lung transplantation at a large, diverse transplant center. More than 17% (107) were diagnosed with gastroparesis within 3 years of transplant, with the most significant risk factor being Black race. Most interestingly, a new diagnosis of gastroparesis post-transplant was associated with an increased odds of CLAD, though there was no impact on overall mortality. Given inconsistent use of gastric emptying scintigraphy (GES, the most widely accepted means of diagnosing gastroparesis [5]) in this population, the current work raises the question as to whether GES should be considered as the newest addition to post-transplant protocols. Gastroparesis is fundamentally a sensorimotor disorder provoked by a variety of processes. While the most common etiology is “idiopathic,” post-surgical interventions may result in gastroparesis—presumably via disruption of vagal nerve fibers [6]. Gastroparesis has been described after fundoplication for gastro-esophageal reflux as well as after solid organ transplantation, including lung transplantation. Whereas gastroparesis is typically thought of as a delay in gastric emptying (as defined by retention of 10% or more of tracer-labeled gastric contents at 4 h), the severity of emptying delay does not necessarily correlate with symptoms, which makes singular use of the scintigraphy to define gastroparesis problematic [7]. Historically, management of gastroparesis has been difficult [6]. Pharmacologic targeting of motilin receptors (such as with erythromycin) or use of dopaminergic agents (such as metoclopramide or domperidone) can be limited by potentially irreversible side effects or medication-medication interactions that can be particularly problematic post-transplant. When pharmacologic management of gastroparesis failed, more invasive interventions were used cautiously, including surgical pyloroplasty or gastric electrical stimulation. Many patients were left unsatisfied and symptomatic. With newer effective and safer pharmacologic agents now available or in the pipeline and the evolution of per oral pyloroplasty, diagnosing gastroparesis is no longer merely an academic exercise. The current study suggests that transplant patients with gastroparesis may be missed despite potential benefits of treatment. Nevertheless, disorders of esophageal peristalsis and gastro-esophageal reflux disease (GERD) are likely still the major GI contributors to CLAD [8]. Blackett et al. have access to a robust single-center database of lung transplant patients that facilitates rigorous study of the factors associated with development of gastroparesis after lung transplantation. Their definition of incident GES as occurring within 3 years is a reasonable time frame, as undoubtedly confounders exist shortly after lung transplantation including the use of opiate analgesia, which may pharmacologically delay gastric emptying. Their study has some notable strengths including a large number of patients * Kyle Staller [email protected]