In incomplete<unk> , there are<unk> th foveolar cells and goblet cells, the latter (indicated by arrows) usually having a slightly bluish color compared to the apical cytoplasm of foveolar cells on H&E stain. An occasional but specific sign of goblet cells is crescent shaped nuclei (seen in middle one). Micrograph showing<unk>  - columnar epithelia with goblet cells - on the left side of image; and normal stratified squamous epithelium on the right side of image Alcian blue stain High-magnification micrograph of<unk>  showing the characteristic goblet cells, Alcian blue stain<unk> th macroscopic (from endoscopy) and microscopic positive findings are required to make a diagnosis.<unk>  is marked by the presence of columnar epithelia in the lower esophagus, replacing the normal squamous cell epithelium—an example of metaplasia. The secretory columnar epithelium may be more able to withstand the erosive action of the gastric secretions; however, this metaplasia confers an increased risk of adenocarcinoma. Screening Endoscopic view of<unk>  showing location of biopsies for screening using the Seattle protocol Screening endoscopy is recommended among males over the age of 60 who have reflux symptoms that are of long duration and not controllable with treatment. Among those not expected to live more than 5 years screening is not recommended. The Seattle protocol is used commonly in endoscopy to obtain endoscopic biopsies for screening, taken every 1 to 2 cm from the gastroesophageal junction. Since the COVID-19 pandemic In Scotland, the local NHS started using a swallowable sponge (Cytosponge) in hospitals to collect cell samples for diagnosis. Preliminary studies have shown this diagnostic test to be a useful tool for screening people with heartburn symptoms and improved diagnosis. Intestinal metaplasia The presence of goblet cells, called intestinal metaplasia, is necessary to make a diagnosis of<unk> . This frequently occurs in the presence of other metaplastic columnar cells, but only the presence of goblet cells is diagnostic. The metaplasia is grossly visible through a gastroscope, but biopsy specimens must be examined under a microscope to determine whether cells are gastric or colonic in nature. Colonic metaplasia is usually identified by finding goblet cells in the epithelium and is necessary for the true diagnosis. Many histologic mimics of<unk>  are known (i.e. goblet cells occurring in the transitional epithelium of normal esophageal submucosal gland ducts, "pseudogoblet cells" in which abundant foveolar gastric type mucin simulates the acid mucin true goblet cells). Assessment of relationship to submucosal glands and transitional-type epithelium with examination of multiple levels through the tissue may allow the pathologist to reliably distinguish between goblet cells of submucosal gland ducts and true<unk>  (specialized columnar metaplasia). The histochemical stain Alcian blue pH 2.5 is also frequently used to distinguish true intestinal-type mucins from their histologic mimics. Recently, immunohistochemical analysis with antibodies to CDX-2 (specific for mid and hindgut intestinal derivation) has also been used to identify true intestinal-type metaplastic cells. The protein AGR2 is elevated in<unk>  and can be used as a biomarker for distinguishing<unk>  epithelium from normal esophageal epithelium. The presence of intestinal metaplasia in<unk>  represents a marker for the progression of metaplasia towards dysplasia and eventually adenocarcinoma. This factor combined with two different immunohistochemical expression of p53, Her2 and p16 leads to two different genetic pathways that likely progress to dysplasia in<unk> . Also intestinal metaplastic cells can be positive for CK 7+/CK20-. Epithelial dysplasia After the initial diagnosis of<unk>  is rendered, affected persons undergo annual surveillance to detect changes that indicate higher risk to progression to cancer: development of epithelial dysplasia (or "intraepithelial neoplasia"). Among all metaplastic lesions, around 8% were associated with dysplasia. particularly a recent study demonstrated that dysplastic lesions were located mainly in the posterior wall of the esophagus. Considerable variability is seen in assessment for dysplasia among pathologists. Recently, gastroenterology and GI pathology societies have recommended that any diagnosis of high-grade dysplasia in<unk>  be confirmed by at least two fellowship-trained GI pathologists prior to definitive treatment for patients. For more accuracy and reproducibility, it is also recommended to follow international classification systems, such as the "Vienna classification" of gastrointestinal epithelial neoplasia (2000).
Barrett's esophagus
Nutcracker esophagus
Herpes esophagitis
Zenker's diverticulum
Esophageal candidiasis
Lymphocytic esophagitis
Esophageal achalasia
Eosinophilic esophagitis