The Nonreflux Determinant of Esophagitis.

Am J Gastroenterol

Published: February 1975

Fifty randomly selected patients were examined clinically, esophagoscopically and biopsy specimens were taken transesophagoscopically from the lower third of the esophagus. In addition, upper gastrointestinal series and gastro-secretory studies were done in all subjects. In 15 cases, in vitro DNA synthesis using tritiated thymidine was measured. No clear correlation was found between clinical manifestations, esophagoscopic appearances and histopathologic findings (Table III). Eleven (27.5%) of the 40 patients with normal esophagoscopy showed abnormal histology, whereas two of the remaining 10 patients with esophagitis by esophagoscopic criteria showed normal histology. Thus, without biopsy about one-third of the cases of histologic esophagitis can be overlooked. In the over all series, there were 19 (38%) cases with histologic esophagitis. In eight (42%) of the 19 patients with histologic esophagitis, the lesion was confined to the lamina propria. In addition to inflammatory infiltrate and fibrosis, a thickened epithelial basal layer and relatively lengthened papillae were found to be important histological signs of esophagitis. Cases with thickened basal layer showed marked labeling with radioactive DNA precursor (H3 Thymidine) after two hours of incubation, compared with the other group of patients (normal esophageal mucosa histologically or histologic esophagitis without a thickened basal layer). This is thought to be a sign of increased regeneration and repair capacity. The lamina propria did not show any labeling in either group of patients at the end of two hours. Therefore, it is concluded that the esophageal epithelium has greater regenerative capacity and can repair itself and return to a normal appearance while the inflammatory process is ongoing in the lamina propria. Besides predisposing factors such as esophagogastric sphincter dysfunction and reflux of digestive enzymes, a local tissue reaction or cell proliferation and repair capacity of theesophageal epithelium must play an important role in the development of nonspecific "peptic" esophagitis.

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