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ORIGINAL ARTICLE
Year : 2012  |  Volume : 7  |  Issue : 2  |  Page : 39-47

Cell proliferation of esophageal squamous epithelium in erosive and nonerosive gastroesophageal reflux disease


1 Department of Tropical Medicine, Assiut University, Assiut, Egypt
2 Department of Internal Medicine, Sohag University, Sohag, Egypt
3 Department of Tropical Medicine, Sohag University, Sohag, Egypt
4 Department of Pathology, Sohag University, Sohag, Egypt

Correspondence Address:
Medhat M Ali
Department of Internal Medicine, Sohag University, Sohag
Egypt
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Source of Support: None, Conflict of Interest: None


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Background/aim Gastroesophageal reflux disease (GERD) is a major public health problem that may cause erosive or nonerosive esophagitis in symptomatic patients. The severity of esophagitis in GERD seems to be correlated not only to the amount of reflux and altered motor activity but also to the ability of the mucosa to resist injury and repair the damage. This study aimed to evaluate the cell proliferation status of esophageal epithelium in both normal individuals and patients with GERD with or without erosions and its correlation with the degree of inflammation of the esophagus. Participants and methods This study was carried out on 33 individuals; their ages ranged between 17 and 74 years. All participants were subjected to a clinical assessment and an endoscopic evaluation. Four biopsies were taken using an endoscope at 5 cm from the Z-line; histological esophagitis was identified and graded. Cell proliferation was evaluated by Ki-67 immunostaining. Results The prevalence of GERD was the highest in the 15-29 years age group (46.43%) and decreased with age. Cell proliferation [estimated by the Ki-67-labeling index (Ki-67 LI)] was reduced in esophageal epithelium in erosive (13.44%) and nonerosive (36.83%) reflux disease in relation to normal individuals (68%). There was a statistically significant positive correlation between cell proliferation (Ki-67 LI) and the endoscopic grade of esophagitis among patients with erosive disease. However, there was no significant correlation between cell proliferation (Ki-67 LI) and the histological grade of esophagitis in both erosive and nonerosive reflux disease. Conclusion The ability of the mucosa to resist injury and to repair the damage should be considered a key factor in the development of GERD. Esophageal mucosa exposed to chronic acid insult show reduced cell replication, estimated by the Ki-67 LI. Erosive esophagitis in GERD seems to be related to a low cell proliferation rate of esophageal epithelium rather than the amount of reflux.


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