Abstract
Although patients with anorexia nervosa (AN) present with various gastrointestinal disorders, little has been understood regarding the incidence and pathophysiology of gastrointestinal ulcers related to AN. A 20-year-old woman with a past history of AN was hospitalized for further examination of dysphagia and chest pain. Her nutritional status was very poor as evidenced by very low body mass index. Esophagogastroduodenoscopy detected longitudinal and geographical ulcers in the entire circumference of the cervical and upper esophagus. Enhanced expression of autophagy-related proteins, LC3B and p62, was seen in the esophageal epithelium surrounding the active ulcers. Expression of these autophagy markers disappeared from the esophageal epithelium soon after the nutritional rehabilitation. Given the fact that starvation and malnutrition are potent inducers for autophagy, these findings suggest that autophagy might be involved in the development of gastrointestinal ulcers in patients with AN.


Similar content being viewed by others
References
Treasure J, Claudino AM, Zucker N. Eating disorders. Lancet. 2010;375:583–93.
Sato Y, Fukudo S. Gastrointestinal symptoms and disorders in patients with eating disorders. Clin J Gastroenterol. 2015;8:255–63.
Westmoreland P, Krantz MJ, Mehler PS. Medical complications of anorexia nervosa and bulimia. Am J Med. 2016;129:30–7.
Rautou PE, Cazals-Hatem D, Moreau R, et al. Acute liver cell damage in patients with anorexia nervosa: a possible role of starvation-induced hepatocyte autophagy. Gastroenterology. 2008;135:840–8 (8 e1–3).
Harada S, Nakagawa T, Yokoe S, et al. Autophagy deficiency diminishes indomethacin-induced intestinal epithelial cell damage through activation of the ERK/Nrf2/HO-1 pathway. J Pharmacol Exp Ther. 2015;355:353–61.
Liu JL, Chen FF, Lung J, et al. Prognostic significance of p62/SQSTM1 subcellular localization and LC3B in oral squamous cell carcinoma. Br J Cancer. 2014;111:944–54.
Mizushima N, Komatsu M. Autophagy: renovation of cells and tissues. Cell. 2011;147:728–41.
Rosenfeldt MT, Nixon C, Liu E, et al. Analysis of macroautophagy by immunohistochemistry. Autophagy. 2012;8:963–9.
Watanabe T, Sadakane Y, Yagama N, et al. Nucleotide-binding oligomerization domain 1 acts in concert with the cholecystokinin receptor agonist, cerulein, to induce IL-33-dependent chronic pancreatitis. Mucosal Immunol. 2016;9:1234–49.
Watanabe T, Yamashita K, Arai Y, et al. Chronic fibro-inflammatory responses in autoimmune pancreatitis depend on IFN-alpha and IL-33 produced by plasmacytoid dendritic cells. J Immunol. 2017;198:3886–96.
Sahani MH, Itakura E, Mizushima N. Expression of the autophagy substrate SQSTM1/p62 is restored during prolonged starvation depending on transcriptional upregulation and autophagy-derived amino acids. Autophagy. 2014;10:431–41.
Hoversten P, Kamboj AK, Katzka DA. Infections of the esophagus: an update on risk factors, diagnosis, and management. Dis Esophagus. 2018. https://doi.org/10.1093/dote/doy094.
Kim SH, Jeong JB, Kim JW, et al. Clinical and endoscopic characteristics of drug-induced esophagitis. World J Gastroenterol. 2014;20:10994–9.
Author information
Authors and Affiliations
Corresponding author
Ethics declarations
Conflict of interest
Sho Masaki, Tomohiro Watanabe, Kosuke Minaga, Ken Kamata, Yoriaki Komeda, Masatomo Kimura, and Masatoshi Kudo declare that they have no conflict of interest.
Human rights
All procedures followed have been performed in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki and its later amendments.
Informed consent
Informed consent was obtained from all patients for being included in the study.
Additional information
Publisher's Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Rights and permissions
About this article
Cite this article
Masaki, S., Watanabe, T., Minaga, K. et al. Possible involvement of autophagy in esophageal ulcers in anorexia nervosa. Clin J Gastroenterol 13, 473–476 (2020). https://doi.org/10.1007/s12328-019-01089-0
Received:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1007/s12328-019-01089-0