Classic histologic features of GERD-related esophagitis include which of the following?

Classic histologic features of GERD-related esophagitis include which of the following?

• A. Basal cell hyperplasia, elongation of lamina propria papillae, scattered eosinophils; may see neutrophils in acute exacerbations.
• B. Lymphoid aggregates with germinal centers.
• C. Goblet cell metaplasia.
• D. Severe necrosis of mucosa.

Answer: (A)

The key pattern in GERD-related esophagitis is how the squamous lining reacts to chronic acid exposure with regenerative changes. Basal cell hyperplasia reflects increased turnover of the deepest epithelial layer as the mucosa tries to repair itself, leading to a thicker basal zone. Elongation of the lamina propria papillae means the papillae extend upward into the upper portions of the epithelium, another sign of chronic irritation and המע as the tissue adapts to ongoing injury. In addition, inflammatory cells—classically eosinophils, and more so neutrophils during acute flares—can be present within the mucosa. This combination—basal cell hyperplasia, papillary elongation, and inflammatory infiltrates—is the classic histologic signature of reflux esophagitis. Goblet cell metaplasia would point toward Barrett esophagus, an intestinal metaplasia from long-standing GERD rather than the acute histology of reflux esophagitis itself. Lymphoid aggregates with germinal centers are not characteristic features of GERD-positive esophagitis, and severe necrosis of the mucosa is not typical of GERD unless there is an extreme, non-representative injury.

The key pattern in GERD-related esophagitis is how the squamous lining reacts to chronic acid exposure with regenerative changes. Basal cell hyperplasia reflects increased turnover of the deepest epithelial layer as the mucosa tries to repair itself, leading to a thicker basal zone. Elongation of the lamina propria papillae means the papillae extend upward into the upper portions of the epithelium, another sign of chronic irritation and המע as the tissue adapts to ongoing injury. In addition, inflammatory cells—classically eosinophils, and more so neutrophils during acute flares—can be present within the mucosa. This combination—basal cell hyperplasia, papillary elongation, and inflammatory infiltrates—is the classic histologic signature of reflux esophagitis.

Goblet cell metaplasia would point toward Barrett esophagus, an intestinal metaplasia from long-standing GERD rather than the acute histology of reflux esophagitis itself. Lymphoid aggregates with germinal centers are not characteristic features of GERD-positive esophagitis, and severe necrosis of the mucosa is not typical of GERD unless there is an extreme, non-representative injury.