Gastro-esophageal reflux disease and Barrett’s esophagus: an overview with an histologic diagnostic approach

Abstract

Summary The first part of this overview on non-neoplastic esophagus is focused on gastro-esophageal reflux disease (GERD) and Barrett’s esophagus. In the last 20 years much has changed in histological approach to biopsies of patients with gastro-esophageal reflux disease. In particular, elementary histologic lesions have been well defined and modality of evaluation and grade are detailed, their sensitivity and specificity has been evaluated and their use has been validated by several authors. Also if there is not a clinical indication to perform biopsies in patient with GERD, the diagnosis of microscopic esophagitis, when biopsies are provided, can be performed by following simple rules for evaluation which allow pathologists to make the diagnosis with confidence. On the other hand, biopsies are required for the diagnosis of Barrett’s esophagus. This diagnosis is the synthesis of endoscopic picture (which has to be provided with the proper description on extent and with adequate biopsies number) and histologic pattern. The current guidelines and expert opinions for the correct management of these diagnosis are detailed.

Expression of VEGF, EGF, and Their Receptors in Squamous Esophageal Mucosa, with Correlations to Histological Findings and Endoscopic Minimal Changes, in Patients with Different GERD Phenotypes

“…If no lesions were visible in magnification, biopsies from four quadrants of esophageal circumference were collected. After hematoxylin-eosin staining, all specimens were evaluated for the presence of typical GERD features in light microscopy: papillae elongation (feature expressed as papillae length as percent of epithelial thickness), basal cell layer hyperplasia (feature expressed as basal cell layer thickness as percent of whole epithelial thickness), and infiltrating inflammatory cells count, together making up histologic inflammation grade [5,27]. Moreover, the number of the papillae in large field of view, number of IPCLs per papilla, appearance of IPCLs (absent or normal versus enlarged), as well as the presence of DIS were assessed.…”

“…This group is classified as nonerosive reflux disease (NERD). In other patients GERD may proceed with esophageal injury endoscopically visible as erosions or ulcers (erosive esophagitis-EE) or may be complicated with Barrett's esophagus (BE), which is diagnosed in the presence of columnar or intestinal metaplasia in the esophagus [5][6][7]. EE may lead to serious complications such as gastrointestinal bleeding or esophageal stenosis.…”

“…Although the samples for histological examination are not taken routinely in GERD, they are helpful in discerning reflux esophagitis from esophagitis of other etiologies [16]. The typical histological changes found in GERD include elongation of the mucosal papillae exceeding 2/3 of epithelial thickness, basal cell hyperplasia exceeding 15% of epithelial thickness, inflammatory cells infiltration (more than 10 leukocytes per high power field), dilated intercellular spaces (DIS), and erosions [5,14,17].…”

Pathologist’s approach to paediatric and neonatal eosinophilic gastrointestinal disorders

“…The differential diagnosis of paediatric EoE, besides gastroesophageal reflux disease which more frequently affects adults 36 , includes: eosinophilic gastroenteritis, hyper-eosinophilic syndrome, Crohn’s disease, celiac disease, connective tissue disorders, achalasia, infections, GVHD reactions and causative drugs 37 . Rhinitis, asthma, eczema and both immediate and non-IgE-mediated food allergies are more common in EoE patients compared to the general population.…”

Local inflammatory response to gastroesophageal reflux: Association of gene expression of inflammatory cytokines with esophageal multichannel intraluminal impedance-pH data

“…Pathogenesis of GERD is complex, with a paramount role of impaired esophageal-gastric junction motility, delayed gastric emptying, and damage of the esophageal mucosa with aggressive content of the refluxate[ 2 ]. Traditionally, the grade of esophageal mucosa damage and intensity of symptoms were thought to be directly related to the acidity of the reflux content[ 3 ]. However, recent data suggest that this relationship is not linear, and the spectrum of manifestations may be genetically determined or be a result of a balance in factors responsible for a local inflammatory response in the esophageal mucosa, perception of refluxate, and processing of signals by the peripheral and central nervous systems[ 4 , 5 ].…”