**1. Introduction**

124 Gastrointestinal Endoscopy

[59] Kargar M, Baghernejad M and Doosti A. 2010. Comparison of three methods of

[60] Kargar M, Ghorbani-Dalini S, Doosti A, and Souod N. 2011. Real-Time PCR Assay

[61] Kargar M, Ghorbani-Dalini S, Doosti A, Souod N, and Abbasi P. Quantitation of

*Medical Sciences*. 11(3): 191-203. [Persian]

1-9. [Persian]

*infection*. 17 (Suppl. 4): S129.

polymerase chain reaction, culture and rapid urease test in diagnosis of helicobacter pylori in gastric biopsy specimen. *Journal of Semnan University of* 

Using Allele-Specific TaqMan probe for Detection of Clarithromycin Resistance and Its Point Mutations in *Helicobacter Pylori*. *Journal of Isfahan Medical School.* 29(126):

bacteria in gastric biopsy specimen from patients with gastrointestinal disorders: relationship between counts and 23S rRNA point mutations. *Clin. Microbial. and* 

> Heterotopic gastric mucosa (HGM) is abnormally placed gastric mucosa outside of the stomach and can be found almost anywhere within the gastrointestinal tract (von Rahden et al., 2004). HGM is most commonly found in the esophagus. The most widely known HGM in the gastrointestinal tract is in the Meckel's diverticulum. However, HGM is also found in the other part of the gastrointestinal tract including the tongue (Melato & Ferlito, 1975; Ortiz, 1982; Surana, 1993), duodenum (Kibria et al., 2009; Mann, 2000), gallbladder (Hayama et al., 2010; Popkharitoy et al., 2008), jejunum (Boybeyi et al., 2008; Nowak & Deppisch, 1998), ileum (Chan et al., 1999; Erez et al., 1991), rectum (Garmendia et al., 2007; Vieth et al., 2005) and anus (Steele et al., 2004). Interestingly, HGM of the umbilicus, a part of remnant alimentary tract has also been report (Heo et al., 2010).

> HGM patch (HGMP) of the proximal esophagus, also referred to as cervical inlet patch (CIP) is typically found in the proximal esophagus. It can also be found in the other part of the esophagus (Borhan-Manesh & Franum, 1991; Katsanos et al., 2010). On endoscopy, HGMP/CIP is clearly distinct from the esophageal squamous mucosa. HGMP/CIP is widely considered to be congenital in nature. However, it has also been proposed to be an acquired condition (Avidan et al., 2001; Meining & Baubouj, 2010). In clinical practice, HGMP/CIP is an under-recognized condition. The incidence reported in the literature varies with lower estimates in the earlier endoscopic studies (von Rahden et al., 2004). Later studies reported higher incidence (Ohara, 2010). The highest incidence was reported in an autopsy study (von Rahden et al., 2004). Use of newer endoscopic modalities has been reported to increase the pick up rates of HGMP/CIP.

> HGMP/CIP is largely asymptomatic and is incidental findings during endoscopy evaluations for other gastrointestinal complaints. Commonly reported symptoms are those symptoms complex referred to as extra-esophageal manifestations of gastro-esophagael reflux disorders. Other common upper aero-digestive disorders have also been linked to HGMP/CIP. Despite the benign nature of HGMP/CIP, serious and important complications have been reported (von Rahden et al., 2004). Furthermore, associations with higher frequencies of laryngopharyngeal malignancies have also been reported (Basseri et al., 2009). A clinico-pathologic classification has been proposed which categorized HGMP/CIP into five distinct groups based on clinical, endoscopic and histological findings (von Rahden et

Heterotopic Gastric Mucosal Patch of the Proximal Esophagus 127

Time line Tubular Solid Vacuolization Columnar Keratinizing HGMP

Fig. 1. Embryogenesis of the esophagus: solidification of the hollow tubular esophagus occur with rapid cellular proliferation followed by vacuoles formations (recanalization), columnarization (cilia phase shaded rippled pink) and the final stage of squamous cell mucosa formation (keratinizing followed by dekeratinizing phase-shaded gray). HGMP

Early Chronic HGMP/CIP

Gastroesophageal Esophagitis Established Barrett's

Fig. 2. Proposed acquired pathway through chronic reflux injury: Chronic acid (+/- pepsin and bile injury) leads to reflux esophagitis and reflux may reach the proximal esophagus resulting in similar changes. Chronic esophagitis leads to adaptive changes resulting in metaplasia metaplasia of the distal esophagus. Chronic injury in the proximal esophagus

lead to reactivation of buried columnar cells resulting in formation of HGMP

Reflux

form when the final phase is incomplete

al., 2004). The management strategies of HGMP/CIP are not well defined and are dependent on the severity of symptoms. However, other newer treatment modalities have also been reported.

This chapter discusses the pathogenesis, the endoscopic features, clinical symptoms and the management of HGMP/CIP, an entity that is still under-recognised and is frequently missed during upper gastrointestinal endoscopy examinations.
