Perananthan, Varan

Summary Barrett’s esophagus (BE) is the only recognized precursor to esophageal adenocarcinoma, but progression risk is highly heterogeneous. While most patients with nondysplastic BE have an annual cancer risk less than 0.5%, a subset with dysplasia or adverse molecular profiles carries markedly higher risk. This variability necessitates precision risk stratification to optimize surveillance and intervention. We review the evolution of BE risk stratification from historical consensus frameworks to contemporary clinical, histologic, and molecular models. Key clinical predictors, validated scoring systems, and recent advances in biomarker-based and imaging-driven surveillance are summarized, with emphasis on their validation and clinical applicability. Established clinical risk factors—age, male sex, smoking, segment length, and dysplasia—remain central to risk prediction. Biomarker assays, including p53 immunohistochemistry, tissue systems pathology and methylation-based assays may provide risk stratification beyond histology. Advances in endoscopic imaging, wide-area transepithelial sampling, and non-endoscopic capsule-based collection platforms could transform surveillance into a risk-adapted paradigm. The management of BE is shifting from a one-size-fits-all surveillance model toward personalized, biomarker-guided care. Integration of clinical, histologic, and molecular data—underpinned by artificial intelligence and real-world validation—promises to refine surveillance, reduce overtreatment, and improve early cancer detection in Barrett’s esophagus.

ABSTRACTBackgroundAchalasia is associated with an increased risk of esophageal cancer; though reported incidence rates vary widely (0.4% to 9.2%) due to differences in demographics, follow‐up duration, and diagnostic methods. This study evaluates the risk of esophageal cancer and Barrett's esophagus (BE) in achalasia using a large national database and a propensity‐matched control cohort.MethodsAchalasia patients were identified utilizing the TriNetX database based on International Classification of Diseases (ICD) and Current Procedural Terminology (CPT) codes for diagnostic procedures and lower esophageal sphincter (LES) directed therapies, including Heller myotomy, peroral endoscopic myotomy, and pneumatic dilation. A matched control group of celiac disease patients was used. A 1‐year lead time was applied to exclude secondary malignant achalasia. Outcomes included the incidence of esophageal cancer and BE, with subgroup analysis in patients following therapy.ResultsAmong 7863 achalasia patients (mean age 58.0, 51.9% female), the esophageal cancer risk was significantly higher than control (risk ratio 2.87, 95% CI: 1.56–5.27, p < 0.001). The absolute risk was low, with 40 cases (0.51%) over a mean follow‐up of 3.18 years. BE risk was also higher in achalasia (risk ratio 1.54, 95% CI: 1.24–1.90, p < 0.001), with 220 cases (2.80%). Subgroup analysis revealed no significant difference in BE risk between POEM and Heller myotomy (risk ratio 1.0, 95% CI: 0.42–2.40, p > 0.99).DiscussionThe elevated cancer risk in achalasia over a short follow‐up period warrants reconsideration of current endoscopic surveillance guidelines, despite the low absolute risk of esophageal cancer and BE.

ABSTRACTIntroductionEsophageal dysmotility following metabolic bariatric surgery (MBS) may relate to decreased gastric compliance. We investigated high‐resolution esophageal manometry (HRM) and secondary peristalsis assessed by functional lumen imaging probe (FLIP) and their association with intragastric pressure after MBS.MethodsPatients undergoing HRM, FLIP, and barium esophagram (BE) after MBS were included. HRM metrics and proximal intragastric pressure at baseline (IGP baseline), during wet swallow‐induced esophagogastric junction relaxation (IGP EGJ opening), and following wet swallow‐induced esophagogastric junction opening with subsequent closure (IGP post EGJ closure) were measured. Contractile response was assessed during FLIP.ResultsForty patients (26 Roux en Y gastric bypass, 14 sleeve gastrectomy) with FLIP a median of 4 years after MBS, were identified. HRM was normal or consistent with ineffective esophageal motility (IEM) in 33 (82.5%) patients, while the contractile response on FLIP was abnormal (disordered/impaired, absent, or spastic reactive) in 28 (70%). Delayed emptying on BE was numerically more frequent with abnormal FLIP (6% vs. 0%, p = 0.08). IGP post‐EGJ closure (median 21.8 vs. 15 mmHg, p = 0.03) and ∆ IGP post‐EGJ closure—IGP baseline (median 4 vs. 0 mmHg, p = 0.02) were greater and predictive of abnormal contractility on FLIP (OR 1.11, 95% CI 1.00–1.2, p = 0.03 and OR 1.6, 95% CI 1.07–2.39, p = 0.003, respectively).DiscussionAbnormal contractility on FLIP, reflecting disordered secondary peristalsis, frequently occurs despite normal HRM findings after MBS. Secondary peristalsis may be associated with reduced gastric compliance, reflected by elevated proximal intragastric pressure. FLIP contractility could serve as an early marker for post‐MBS esophageal dysfunction.