REFLUX ESOPHAGITIS
Reflux of stomach contents into the lower esophagus is the first and foremost cause of esophagitis. Many causative factors are involved, less well characterized than the name implies:

Decreased efficacy of esophageal antireflux mechanisms, particularly LES tone. Central nervous system depressants, hypothyroidism, pregnancy, systemic sclerosing disorders, alcohol or tobacco exposure, or the presence of a nasogastric tube may be contributing causes. In most instances, no antecedent cause is identified.

Presence of a sliding hiatal hernia.

Inadequate or slowed esophageal clearance of refluxed material.

Delayed stomach emptying and increased stomach volume, contributing to the volume of refluxed material.

Reduction in the reparative capacity of the esophageal mucosa by protracted exposure to stomach juices.
Any one of the aforementioned influences may assume primacy in an individual case, but more than one is likely to be involved in most instances. The acid-peptic action of stomach juices is critical to the development of esophageal mucosal injury; in severe cases, refluxed bile from the duodenum also may contribute to the mucosal disruption.

MORPHOLOGY.
The anatomic changes depend on the causative agent and on the duration and severity of the exposure. Simple hyperemia ( redness) may be the only alteration. In uncomplicated reflux esophagitis, three histologic features are characteristic
1. The presence of inflammatory cells, including eosinophils, neutrophils, and excessive numbers of lymphocytes, in the epithelial layer

2. Basal zone hyperplasia exceeding 20% of the epithelial thickness

3. Elongation of lamina propria papillae with congestion, extending into the top third of the epithelial layer
Infiltrates of intraepithelial eosinophils are believed to be an early histologic abnormality, since they occur even in the absence of basal zone hyperplasia. Intraepithelial neutrophils are markers of more severe injury, such as ulceration, rather than reflux esophagitis per se.

Clinical Features.
Although largely limited to adults over age 40, reflux esophagitis is occasionally seen in infants and children. The clinical manifestations consist principally of dysphagia; heartburn; and sometimes regurgitation of a sour brash, hematemesis, or melena. The severity of symptoms is not related closely to the presence or degree of histologic esophagitis; most people experience reflux symptoms without damage to the distal esophageal mucosa, owing to the short duration of the reflux. Anatomic damage appears best correlated with prolonged exposure of the lower esophagus to refluxed material. Rarely, chronic symptoms are punctuated by attacks of severe chest pain that may be mistaken for a heart attack. The potential consequences of severe reflux esophagitis are bleeding, development of stricture, and a tendency to develop Barrett esophagus, with its attendant risks.

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