**9. Treatment/management**

The management of patients with HGMP/CIP depends on the presence of symptoms or complications following the clinico-pathological classification proposed by von-Rahden. For the majority of patients, HGMP/CIP are detected incidentally (type I) and as such do not require any treatment, follow up or surveillance. For patients with acid related symptoms, treatment with acid suppression with or without pro-kinetic and antacid will suffice. For majority, a short course of treatment will be adequate. However, for a proportion, prolonged acid suppression similar to patients with significant gastro-esophageal reflux disorders may be required.


Table 3. Reported complications associated with HGMP/CIP based on literature search to 2010

Heterotopic Gastric Mucosal Patch of the Proximal Esophagus 139

Other reported modalities for treating symptomatic non neoplastic HGMP/CIP include argon plasma coagulation and endoscopic mucosal resection. However, these modalities

For those cases with complicated HGMP/CIP (type III), apart from acid suppressions, other

Type IV cases will require close follow up treatment may include argon plasma coagulation (Sauvé et al., 2001; Klaase et al., 2001), endoscopic mucosal resection (EMR) and endoscopic sub-mucosal dissection (ESD). For those with type V HGMP/CIP, treatment will depend on the stages of disease. Early adenocarcinoma can be treated with EMR or ESD. These can be resected after the creation of a polyp by rubber band ligation or with cap assisted EMR. For

It remains unknown whether patients detected to have HGMP/CIP requires to be followed up for future complications or progressions to types III to V. Patients found on biopsy to have dysplastic HGMP/CIP mucosa will require surveillance. It is unknown what time interval is recommended. Given that HGMP/CIP is gastric mucosa, following the

Currently, there are several controversies regarding HGMP/CIP. First, there is still dispute with regard to the origin of HGMP/CIP. However, it is widely believed to be congenital origin as result of remnant of columnar epithelium due to failure of complete squamization of the esophagus. There are several factors that favor the congenital origin hypothesis. The embryogenesis of esophagus can explain the profiles of HGMP/CIP; proximal location correlating with the last part of the esophagus, the proximal esophagus to transform to keratinized mucosa. Babies and children do not have sufficient duration of acid exposure to induce changes suggested by the acquired theory. Finally, although the staining pattern based on CK7 and CK20 are similar, staining with MUC protein shows differences between

An earlier study had also shown that the HGMP/CIP had cellular component different from

The proposed theory on acquired origin was based on similarities between histological findings of HGMP/CIP and Barrett's esophagus. Mucin protein (MUC) and CK7 and CK20 similarities suggested similar origin. Other study based on MUC also suggested HGMP/CIP being acquired in origin. In the future, other staining methods may be identified and may show clear differences between HGMP/CIP and Barrett's esophagus. Weak evidence come from higher incidence of Barrett's esophagus in patients found to have HGMP/CIP. However, the overall reported incidence rates are still too low to lend strong support for this

The latest theory proposed was based on findings of glandular cystic retentions secondary in the proximal esophagus. The evidence to support this theory are lacking given the very few reports of glandular retention cysts encountered in the clinical practice and reported in the literature. Furthermore, the absence of lesions found in the other part of esophagus makes the second and the third proposed theories less likely. Interestingly, it has also been proposed that the origin may be different, congenital in baby or children and acquired in

Barrett's esophagus, suggesting embryogenic in origin (Fuerle et al., 1990).

modalities such as dilatation for stricture and even surgery may be required.

have only been reported in small series.

other cases, surgical resections are indicated.

HGMP/CIP and Barrett's (Lauwers et al., 2005).

**10. Controversies** 

theory.

adult (Lauwers et al., 2005).

recommendations for stomach will probably be adequate.

Other reported modalities for treating symptomatic non neoplastic HGMP/CIP include argon plasma coagulation and endoscopic mucosal resection. However, these modalities have only been reported in small series.

For those cases with complicated HGMP/CIP (type III), apart from acid suppressions, other modalities such as dilatation for stricture and even surgery may be required.

Type IV cases will require close follow up treatment may include argon plasma coagulation (Sauvé et al., 2001; Klaase et al., 2001), endoscopic mucosal resection (EMR) and endoscopic sub-mucosal dissection (ESD). For those with type V HGMP/CIP, treatment will depend on the stages of disease. Early adenocarcinoma can be treated with EMR or ESD. These can be resected after the creation of a polyp by rubber band ligation or with cap assisted EMR. For other cases, surgical resections are indicated.

It remains unknown whether patients detected to have HGMP/CIP requires to be followed up for future complications or progressions to types III to V. Patients found on biopsy to have dysplastic HGMP/CIP mucosa will require surveillance. It is unknown what time interval is recommended. Given that HGMP/CIP is gastric mucosa, following the recommendations for stomach will probably be adequate.
