We thank Professor Vasant and Dr. Sasegbon for their thoughtful editorial and for placing our study within the broader context of post-infective disorders of gut-brain interaction (DGBI) 1. Prior cohort studies and meta-analyses have established that infectious enteritis is associated with subsequent irritable bowel syndrome (IBS), and more recent evidence has shown that functional dyspepsia (FD) may also emerge after acute gastroenteritis 2-6. Adding to this body of literature, we believe our study helps address an important evidence gap: the lack of large-scale, population-based, long-term data quantifying the risk trajectory of both IBS and FD following infectious enteritis. By assembling matched cohorts of 202,244 patients from a real-world U.S. collaborative network, we were able to assess incident IBS and FD at 1, 5 and 10 years, while also characterising downstream healthcare utilisation, including medication use, abdominal imaging, endoscopy and hospitalisation 7. In this respect, our findings extend prior literature beyond diagnosis alone and provide a broader view of the sustained clinical burden of post-infective DGBI. We also appreciate the editorialists' emphasis on the pathogen-specific gradient observed in our study 1. The higher subsequent IBS risk associated with Salmonella/Shigella (RR 6.48) and Giardia lamblia (RR 5.05), compared with viral enteritis (RR 3.52), likely reflects heterogeneity in host-pathogen interactions, mucosal injury and downstream immune activation 5, 7. The invasive bacterial pathogens are known to cause deeper lymphoid and epithelial disruption in the distal ileum and colon, while Giardia's non-invasive but persistent brush border injury, with secondary dysbiosis and barrier dysfunction, may perpetuate gut–brain dysregulation even after eradication. In addition, our multivariable analysis showed independent associations of obesity and psychological comorbidity with post-infective IBS, which are consistent with an evolving biopsychosocial model of DGBI 7-9. In parallel, emerging data suggest that symptom burden and healthcare utilisation are closely linked in IBS, reinforcing the potential value of earlier risk stratification and targeted follow-up 10. The editorial appropriately identifies three residual knowledge gaps: the absence of consistent Rome IV-based diagnostic criteria in longitudinal studies, the lack of validated patient-reported outcome measures across time points, and the absence of studies examining temporal overlap between IBS and FD in post-infective DGBI 1. We fully endorse these priorities. Our reliance on ICD codes rather than Rome IV criteria remains an acknowledged limitation; however, our sensitivity analyses and evaluation of IBS-directed medication and procedural utilisation support the robustness of our diagnostic signal 7. Prospective studies using validated instruments, particularly those capturing symptom severity, psychological burden, and quality of life at serial time points, are now urgently needed to translate these epidemiological findings into personalised, preventive care models. We hope these data support a more risk-stratified post-infectious approach, particularly for high-risk patients recovering from higher-risk pathogens and for those with obesity or psychological vulnerability. Future prospective studies are warranted to identify individuals most likely to benefit from early multidisciplinary follow-up and targeted intervention. Mohamed H. Eldesouki: conceptualization, writing – review and editing, writing – original draft. Swapna Gayam: supervision, writing – review and editing. The authors' declarations of personal and financial interests are unchanged from those in the original article. The authors have nothing to report. This article is linked to Eldesouki et al. papers. To view these articles, visit https://doi.org/10.1111/apt.70602 and https://doi.org/10.1111/apt.70627. The authors have nothing to report.
Eldesouki et al. (Wed,) studied this question.