Gastroesophageal reflux disease (GERD) is a common disease frequently encountered by surgical pathologists. Although the pathogenesis and clinical features of the disease have been studied for years, many unanswered questions remain. Typical clinical symptoms along with the endoscopic findings, pH monitoring, and biopsies, all support the diagnosis. However, these tests may yield conflicting findings, and at present there is no gold standard for the diagnosis of GERD. In patients with normal or nearly normal endoscopic findings (nonerosive reflux disease), the major diagnostic burden lies with the histology. The histologic diagnosis of GERD is based on a combination of findings, including basal cell hyperplasia, papilla elongation, inflammation, and dilatation of intercellular spaces. However, these features exhibit varying sensitivity and specificity, and minimal biopsy criteria for the diagnosis of reflux esophagitis have not been rigorously tested in well-characterized patient populations. However, given the high prevalence of GERD, pathologists face esophageal mucosal biopsies daily and must recognize the diagnostic strengths and limitations of histologic features of reflux esophagitis. Future studies and new techniques may improve the diagnostic strength of histology and establish meaningful minimal criteria for the diagnosis of reflux esophagitis.
"Although all patients were given trials of PPIs, minimal improvement was seen with these medications. The proximal nature of our findings also leads us away from a diagnosis of reflux esophagitis, as many of the typical histology findings for GERD are often found near the squamocolumnar junction.12 "
[Show abstract][Hide abstract] ABSTRACT: Esophageal lichen planus (LP) has been described as a cause of nonspecific esophagitis that may cause dysphagia, but its incidence is unknown. We aimed to estimate the incidence of esophageal LP in a defined geographic region and describe the clinical characteristics of affected patients.
A histopathology database for a population of 1 million people was searched for all esophageal mucosal biopsy results over an 8-year period. Cases showing inflammation or abnormalities without a diagnosis after three or more biopsies were reviewed for findings of LP.
Of 13,589 esophageal biopsies, only one received a diagnosis of LP. Seven patients (four male; mean age, 59 years; range, 39 to 76 years) were identified as having chronic dysphagia and nonspecific proximal esophagitis for which no diagnosis could be made. All patients had proximal inflammation, and six of seven had full-thickness lymphocytic infiltration. Elongation of the lamina propria papillae was noted in all patients, whereas six patients had parakeratosis and ballooning. Only one patient had findings potentially consistent with, but not sufficient for, a diagnosis of esophageal LP.
Esophageal LP appears to be extremely uncommon in this North American population, and esophageal biopsy alone is likely not sufficient to establish a diagnosis of LP.
Gut and liver 07/2013; 7(4):401-5. DOI:10.5009/gnl.2013.7.4.401 · 1.81 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The initial response of esophageal mucosa to gastroduodenal reflux is inflammation and hyperplasia. Secretory phospholipase A(2) (sPLA(2)) is a known mediator of gut inflammation, and its levels are increased in Barrett's esophagus. We hypothesized that the sPLA(2) gene is required to produce esophageal mucosal hyperplasia in response to gastroduodenal reflux.
C57BL/6 (n = 5) sPLA(2) (-/-) mice and C57BL/6( Cg-Tg(PLA2G2A)703N16 ) mice (n = 4) sPLA(2) (-/+) underwent a side-to-side surgical anastomosis between the duodenum and gastroesophageal junction (DGEA). Control animals [sPLA(2) (-/-) (n = 5), sPLA(2) (-/+) (n = 4)] underwent laparotomy with incision and repair of the esophagus. Tissue was harvested after 4 weeks, and H&E staining was performed to quantify esophageal mucosal thickness. Ki67 and sPLA(2) immunostaining were performed to quantitate differences in cell division and sPLA(2) expression.
Mice expressing human sPLA(2) had a 2.5-fold increase in thickness of the esophageal mucosa as compared to controls (p = 0.01). A 6.5-fold increase in proliferation (p = 0.02) and a twofold increase in sPLA(2) expression (p = 0.04) were demonstrated in animals exposed to gastroduodenal reflux.
The presence of sPLA(2) is necessary for early mucosal hyperplasia produced by exposure of the esophagus to gastroduodenal contents. sPLA(2) expression is upregulated by gastroduodenal reflux, strengthening its role as a critical mediator of early mucosal hyperplasia.
Journal of Gastrointestinal Surgery 09/2009; 13(12):2212-8. DOI:10.1007/s11605-009-0972-x · 2.80 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Esophagitis is essentially inflammation of the esophageal squamous mucosa. One of the major reasons for cause of Esophagitis is the acid reflux from the stomach. This condition is observed in the process of upper gastro-intestinal tract endoscopy and the diagnosis is arrived at by examining the images of the esophagus. The diagnosis is based on the observation of the lesions and coloration of the digestive mucosa. Our paper reports an implementation of Decision Support System (DSS) for diagnosis of Esophagitis based on the analysis of color and texture features of the images captured during the process of endoscopy. The Hue Saturation and Intensity color model is adapted. The statistical features of the Hue and Saturation form the color features and the texture features are determined by Discrete Cosine Transform coefficients of the image. The decision making structure is a feed forward neural network. The DSS has been tested and results are reported.
Journal of Mechanics in Medicine and Biology 12/2009; 09(04). DOI:10.1142/S0219519409003097 · 0.73 Impact Factor
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