|E-JCRT LETTERS TO THE EDITOR
|Year : 2015 | Volume
| Issue : 4 | Page : 1047
A case of heterotopic gastric patch of cervical esophagus: Cervical inlet patch
Sankalp Sancheti1, Indu Arun2, Suvadeep Chaterjee2, Shivani Jain3
1 Department of Pathology, Tata Memorial Hospital, Mumbai, Maharashtra, India
2 Tata Medical Center, Kolkata, West Bengal, India
3 Department of Oral Pathology, MP Dental College and Hospital, Vadodara, Gujarat, India
|Date of Web Publication||03-Nov-2015|
Department of Pathology, Tata Medical Center, Kolkata, West Bengal
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Sancheti S, Arun I, Chaterjee S, Jain S. A case of heterotopic gastric patch of cervical esophagus: Cervical inlet patch
. J Can Res Ther 2015;11:1047
We present a case of a 41-year-old male patient who presented with a 3 weeks history of progressive dysphagia and odynophagia. There was no significant medical history. Clinical examination of oral cavity, larynx, pharynx, neck, and abdomen were unremarkable. Laboratory studies showed hemoglobin of 12.1 g/dl, total leukocyte count of 10,000/cmm, and platelet count of 540,000/cmm. Serum creatinine and blood urea nitrogen were normal. An upper gastro-intestinal tract endoscopy showed three well-circumscribed erosive lesions with barrett's-like mucosa just distal to the upper esophageal sphincter [Figure 1]. Gastroesophageal junction was normal. A biopsy from the erosive lesion showed fragments of normal esophageal mucosa with stratified squamous epithelium and adjacent gastric oxyntic mucosal glands on microscopy. Intestinal metaplasia or H. Pylori-like organisms were not discerned in the oxyntic mucosa [Figure 2] and [Figure 3]. A diagnosis of heterotopic gastric mucosa (HGM)/cervical inlet patch with no evidence of dysplasia or malignancy was made. The patient was treated symptomatically with proton pump inhibitors, which controlled the symptoms, and the patient is currently asymptomatic and on regular follow-up.
|Figure 1: Endoscopic appearance of a typical cervical inlet patch showing well-circumscribed erosive lesion with pink colored mucosa resembling gastro-esophageal junction|
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|Figure 2: Photomicrograph showing a typical cervical inlet patch formed by esophageal mucosa lined with stratified squamous epithelium and adjacent heterotopic gastric oxyntic mucosal glands (H and E, ×40)|
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|Figure 3: Photomicrograph showing a typical cervical inlet patch in high power (H and E, ×400)|
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Heterotopias are defined as normal tissue occurring in sites not normal for that tissue. Gastric body type of mucosa has been described in upper one-third of the esophagus, usually within 3.0 cm of the upper esophageal sphincter and hence termed as "inlet patch."  The incidence of this anatomic structure varied from 1% to 13% in various endoscopic studies, whereas autopsy reports have reported the incidence of up to 70%.  Most cervical inlet patches are asymptomatic, but complications related to acid secretion such as esophagitis, ulcer, web, and stricture may produce the symptoms of chest and throat pain, dysphagia, globus sensation, and shortness of breath.  Grossly, they have pink to red appearance and its junction with esophageal squamous epithelium resembles gastroesophageal junction mucosa. Erosions and peptic ulcers are frequently identified in its vicinity. Microscopically, HGM contains a variable number of gastric parietal and chief cells with a mixed inflammatory infiltrate which may be associated with Helicobacter infection. Metaplasia may occur, but neoplastic transformation is rare.  The association with Barrett's esophagus is a debated area as both of them have been thought to be of congenital origin. The biopsy site is of paramount importance to the pathologist. A biopsy from proximal esophagus is likely to be HGM and should not be confused with Barrett's esophagus. It is not only significant for the clinicians but also for the pathologist to be aware of this entity as it presents with troublesome upper aerodigestive tract symptoms but rarely leads to neoplastic transformation. Symptomatic treatment with proton pump inhibitors along with assurance to the patient leads to a dramatic improvement. In our patient, there was no stricture or web formation, and the cause of his symptoms were thought to be secondary to esophageal irritation from acid secretion.  He responded well to treatment with a proton pump inhibitor. We expect that this report will play a role in increasing the awareness of this heterotopic structure, and an astute pathologist should always raise a possibility of HGM in proximal esophageal biopsies.
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[Figure 1], [Figure 2], [Figure 3]