Diagnosis: Heterotopic gastric mucosa (inlet patch) Heterotopic gastric mucosa is characterized by normal, functional gastric glands and tissue in an anatomically aberrant location. First described in 1805, the presence of such tissue in the upper esophagus is also known as a gastric mucosal rest or, more commonly, an inlet patch. The morphological features of the inlet patch may include any combination of gastric-type mucosa of cardiac-, antral-, or corpus-type glands with parietal and chief cells. Inlet patch lesions may be single or multiple and are most often found in the postcricoid portion of the esophagus at, or within 3 cm below, the upper esophageal sphincter.1-3 Grossly, the lesions are described as round or oval, discrete, salmon-pink or yellow, with a velvety texture against a silvery, normal esophageal background. Their surface may be flat or polypoid, with elevations or depressions. The lesions are often seen on withdrawal of the endoscope on the lateral or posterior surface of the proximal esophagus, usually near the cricopharyngeus.2,3 The origin of the inlet patch is thought to be an early developmental anomaly. In approximately the 14th week of gestational age, or when the fetus is 10 cm, the columnar epithelium lining the lumen of the esophagus is replaced by squamous mucosa, starting in the midesophagus and progressing cephalocaudally. According to the most popular theory, inlet patch lesions develop when the tissue replacement does not occur in discrete areas. The cervical esophagus is the most susceptible area because it is the last region to undergo change.4 Interestingly, heterotopic gastric mucosa has been reported in the oral cavity, most commonly in the floor of the mouth, the anterior aspect of the tongue, and the nasopharynx.5,6 Head and neck gastric heterotopic mucosa is believed to have originated from rests of primordial stomach endoderm that become separated and eventually are influenced to differentiate into gastric mucosa.6 Although the pathogenetic schema described herein is the one that is most widely published, there are alternate pathogenetic theories. Frequent coexistence and similarities of the histochemical mucin profile between the inlet patch and BE have led to the theory that there is a pathophysiologic link. Lauwers et al7 suggested that the inlet patch, like BE, may arise from multipotent stem cells of the submucosal esophageal glands, representing a “metaplastic inflammatory acquired process” based on mucin core protein expression and cytokeratin reactivity. Other evidence of a noncongenital origin includes a discrepancy between the mucin profiles of inlet patch lesions and Meckel diverticula, which are intestinal abnormalities of established congenital origin.7 The reported incidence of inlet patch varies widely in the literature, ranging from 0.1% to 10% in the adult population.1-3 The exact prevalence is difficult to determine because some patches are an incidental, often asymptomatic, endoscopic finding. Furthermore, observation of an inlet patch is heavily dependent on the expertise and awareness of the endoscopist because the frequent contractions of the upper esophageal sphincter make examination, photodocumentation, and biopsy of this region difficult. Therefore, it is likely that the cervical inlet patch is an underrecognized entity. Clinically, inlet patches are often asymptomatic. The range of symptoms and sequelae that are reported, however, vary widely in severity. The patches have been associated with laryngopharyngeal symptoms such as dysphagia and odonyphagia, globus pharyngeus, retrosternal pain, cricopharyngeal spasm, cough, pharyngitis, hoarseness, and dyspnea.2,7-9 The symptoms are thought to result from increased acid secretion. Support for this theory includes a positive correlation of the size of the inlet patch with the severity of symptoms as well as a significant reduction in the complaints of patients who received acid suppression treatment.3 Some authors have suggested that there is an association between colonization of the inlet patch with H pylori, which is a known producer of chronic inflammation, and subjective complaints, eg, globus sensation. Changes in gastric physiology after H pylori infection of gastric mucosa have been indicated in nonulcer dyspepsia, and an analogous model of H pylori infection of inlet patches leading to globus sensation has been described.10 Inlet patches may be a predisposing factor for the development of the specialized columnar metaplasia seen in BE, although the etiopathogenesis of this theory is not well described. Likely because of the reported coexistence between the 2 conditions, there have been several attempts to relate BE and inlet patches in the literature.1 Some authors suggest that having an inlet patch may predispose patients with BE to develop a high-grade dysplasia. It has also been suggested that inlet patches and BE are distinct entities but that congenital inlet patches may become superimposed with acquired metaplastic features in a similar progression to the specialized columnar metaplasia of BE.1 These differing explanations of the coexistence between BE and inlet patches indicates that the association between the 2 conditions has not yet been clearly defined. Also, because most lesions are asymptomatic and because of the controversy regarding the pathogenesis of the lesions, the treatment of inlet patches is not well established. However, once the condition is identified, most authors recommend endoscopic surveillance in symptomatic patients given the rare, but reported incidence of inlet patches undergoing specialized columnar metaplasia that is indistinguishable from that of BE, with a subsequent step-wise progression to adenocarcinoma. Symptomatic patients may benefit from pharmacological acid suppression to decrease symptoms in addition to surveillance endoscopy and biopsy. Surgical resection, argon plasma coagulation, radiofrequency ablation, or other surgical interventions may be offered as primary management.4 Our patient had multiple lesions of gastric mucosa in her cervical esophagus, which likely contributed to her refractory gastroesophageal reflux disease and pharyngitis. Since diagnosis of her inlet patch, she has undergone radiofrequency abaltion of the heterotopic gastric mucosa, a Nissen fundiplication to reduce her reliance on pharmacological acid control, and a lingual tonsillectomy to treat her snoring and sore throat. She had a pronounced near resolution of globus sensation and has decreased her use of pharmacological acid control by more than 70%. Heterotopic gastric mucosa in the upper esophagus, or cervical inlet patch, may contribute to common symptoms such as globus sensation, pharyngitis, cough, and dysphagia. Otolaryngologists who encounter refractory cases should consider this clinical entity when such cases are referred for evaluation and treatment. Submissions Residents and fellows in otolaryngology are invited to submit quiz cases for this section and to write letters to the Archives commenting on cases presented. Quiz cases should follow the patterns established. See Instructions for Authors (http://archotol.ama-assn.org/misc/ifora.dtl). Material for CLINICAL PROBLEM SOLVING: PATHOLOGY should be submitted electronically via the online submission and review system at http://manuscripts.archoto.com. Reprints are not available from the authors. Return to Quiz Case 3. References 1. von Rahden BH, Stein HJ, Becker K, Liebermann-Meffert D, Siewert JR. Heterotopic gastric mucosa of the esophagus: literature-review and proposal of a clinicopathologic classification. Am J Gastroenterol. 2004;99(3):543-55115056100PubMedGoogle ScholarCrossref 2. Alaani A, Jassar P, Warfield AT, Gouldesbrough DR, Smith I. Heterotopic gastric mucosa in the cervical oesophagus (inlet patch) and globus pharyngeus—an under-recognised association. J Laryngol Otol. 2007;121(9):885-88817166326PubMedGoogle ScholarCrossref 3. Poyrazoglu OK, Bahcecioglu IH, Dagli AF, Ataseven H, Celebi S, Yalniz M. Heterotopic gastric mucosa (inlet patch): endoscopic prevalence, histopathological, demographical and clinical characteristics. Int J Clin Pract. 2009;63(2):287-29117535303PubMedGoogle ScholarCrossref 4. Yüksel I, Usküdar O, Köklü S, et al. Inlet patch: associations with endoscopic findings in the upper gastrointestinal system. Scand J Gastroenterol. 2008;43(8):910-91419086275PubMedGoogle ScholarCrossref 5. Wetmore RF, Bartlett SP, Papsin B, Todd NW. Heterotopic gastric mucosa of the oral cavity: a rare entity. Int J Pediatr Otorhinolaryngol. 2002;66(2):139-14212393247PubMedGoogle ScholarCrossref 6. Wacrenier A, Fayoux P, Augusto D, Laussel AC, Gosselin B, Leroy X. Gastric heterotopia in the nasopharynx. Int J Pediatr Otorhinolaryngol. 2002;64(1):65-6712020916PubMedGoogle ScholarCrossref 7. Lauwers GY, Mino M, Ban S, et al. Cytokeratins 7 and 20 and mucin core protein expression in esophageal cervical inlet patch. Am J Surg Pathol. 2005;29(4):437-44215767795PubMedGoogle ScholarCrossref 8. Basseri B, Conklin JL, Mertens RB, Lo SK, Bellack GS, Shaye OA. Heterotopic gastric mucosa (inlet patch) in a patient with laryngopharyngeal reflux (LPR) and laryngeal carcinoma: a case report and review of literature. Dis Esophagus. 2009;22(4):E1-E519473208PubMedGoogle ScholarCrossref 9. Akbayir N, Sökmen HM, Caliş AB, et al. Heterotopic gastric mucosa in the cervical esophagus: could this play a role in the pathogenesis of laryngopharyngeal reflux in a subgroup of patients with posterior laryngitis? Scand J Gastroenterol. 2005;40(10):1149-115616265772PubMedGoogle ScholarCrossref 10. Alagozlu H, Simsek Z, Unal S, Cindoruk M, Dumlu S, Dursun A. Is there an association between Helicobacter pylori in the inlet patch and globus sensation? World J Gastroenterol. 2010;16(1):42-4720039447PubMedGoogle Scholar
Archives of Otolaryngology - Head & Neck Surgery – American Medical Association
Published: Aug 15, 2011
Keywords: gastric mucosa,pharyngitis,esophagus,globus pharyngeus,gastric mucosal heterotopia,deglutition disorders,cough,endoscopy,mucous membrane,esophageal sphincter, upper,esophagus, cervical
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