Laryngeal vs. Esophageal Acid-Mediated Injury in Bulimia Nervosa: A Systematic Review.

Bulimia nervosa (BN) is a psychiatric eating disorder that can potentially be life-threatening and is characterized by recurrent binging and/or purging. During purging episodes that involve self-induced vomiting, laryngopharyngeal reflux (LPR) can occur as gastric acid is forcefully pushed through the esophageal sphincter and anteriorly to the acid-sensitive laryngopharyngeal tissue. While the esophageal mucosal lining can tolerate repeated exposure to acid before sustaining significant erosion, the laryngeal mucosa exhibits greater sensitivity, reacting to even mild exposure with inflammation. LPR has been shown to be associated with hoarseness, capillary dilation, enlargement of soft tissue, arytenoid, and thyroid cartilages, and thick mucus over the larynx. Individual studies have also been conducted on how the larynx sustains injury at higher pH levels compared to the esophagus. However, no literature review has yet synthesized why exactly the larynx experiences disproportionate vulnerability due to anatomical, histological, and acid-tolerance mechanisms. As such, this review aims to consolidate evidence on how injury to the larynx is greater than that to the esophagus among BN patients engaging in self-induced vomiting. The 2020 Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines were used for this analysis. A systematic review was conducted using PubMed, Web of Science, and Embase between 1957 and 2026 using two separate Boolean search strings: one primary search for primary, clinical, and population-level evidence on BN and/or laryngopharyngeal/esophageal pathology, and a secondary search to collect mechanistic and background literature. Eligible studies examined acid-mediated injury, laryngeal pathology, esophageal pathology, or comparative mucosal damage in BN or LPR. Excluded studies included non-peer-reviewed sources and opinion pieces unrelated to BN, LPR, or acid-mediated mucosal injury. Through the primary Boolean search (Search 1), nine studies met eligibility criteria and were used as primary evidence. These nine studies were supplemented by 12 mechanistic sources that were found through the second Boolean search string (Search 2); 10 foundational sources were identified through reference list chaining and included in this review. A total of 31 sources were included in the synthesis of this review, with two additional references used purely for methodological purposes (the PRISMA 2020 statement and the Newcastle-Ottawa Scale), for a total of 33 cited references. Across primary studies, 51 unique subjects were represented, 30 of whom had a formal BN diagnosis. An additional 380 subjects were represented throughout the mechanistic/supporting review literature examining general LPR and/or GERD populations. Across studies, laryngeal mucosa sustained earlier and more severe pathological changes compared to esophageal mucosa among BN patients. These findings indicate the larynx is disproportionately injured in BN due to markedly lower acid-exposure tolerance thresholds, thinner epithelium, and reduced buffering capacity of the mucosa. Prospective studies comparing laryngeal and esophageal mucosal outcomes among BN patients are warranted. Laryngeal symptoms in clinical settings, such as hoarseness, may help improve early diagnostic precision and implement interventional strategies, supporting otolaryngologic involvement in multidisciplinary care for this understudied patient population.