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Volume 74 - 2011 - Fasc.2 - Symposium

Eosinophilic oesophagitis versus reflux oesophagitis

Reflux oesophagitis (RO) is defined as the inflammation of the lower oesophagus due to damage caused by acid reflux from the stomach. Histopathologic features of acid reflux include epithelial hyperplasia, baloon cells, basal cell hyperplasia, papillary elonga- tion, dilated intercellular spaces representing epithelial oedema, vascular congestion, and inflammatory cell infiltration comprising lymphocytes, neutrophils and eosinophils, most of which are non- specific. Eosinophils, on the other hand, are considered to be important in the differential diagnosis of RO and EoO which is a chronic inflammatory disorder characterized by eosinophil infil- tration of the oesophageal mucosa associated with a history of atopy or allergy. A cut off value of more than 15 eosinophils per high power field is suggestive of EoO with a tendency of eosinophils to concentrate in the superficial parts of squamous mucosa just below the luminal surface where they tend to form eosinophilic microabsesses. Dense fibrosis is seen in up to one-third of the patients with EoO together with an increase in the number of eosinophils in the lamina propria. In patients with intermediate levels of eosinophil counts (7-15 eos/hpf) immunohistochemistry for eosinophil secretory products could prove useful as it highlights degranulated eosinophils. In conclusion, distinguishing EoO from RO requires a thorough clinical, endoscopic and histologic evaluation of the patient which can only be achieved when close communication between pathologist and gastroenterologist is established. (Acta gastroenterol. belg., 2011, 74, 323-329).


Endoplasmic reticulum stress and inflammatory bowel disease

Endoplasmic reticulum (ER) stress arises from the accumulation of misfolded or unfolded proteins in the ER and elicits the unfold- ed protein response (UPR), an adaptive signalling pathway which aims at resolving ER stress. Genetic loci that confer risk for both forms of inflammatory bowel disease (IBD) include genes that are centrally involved in the UPR, including X-box binding protein-1 (XBP1), anterior gradient protein-2 (AGR2) and orosomucoid-1- like 3 (ORMDL3). The intestinal epithelium, in particular mucin- secreting goblet and antimicrobial peptide-secreting Paneth cells appear particularly sensitive towards disturbances of the UPR. Supportive of this view are mice with a genetic deletion of Xbp1 specifically in the intestinal epithelium, which develop spontaneous intestinal inflammation histologically remarkably similar to human IBD. Apart from such primary genetic factors that deter- mine the threshold of tolerable ER stress within the epithelium, secondary factors emanating from the environment might intersect with the UPR as well. These secondary factors might include microbial products, inflammatory mediators per se, hypoxia and glucose deprivation, pharmacological agents, and many others. Interaction of such secondary factors in a genetically susceptible host might provide the basis for intestinal inflammation and might provide a framework to investigate gene - environment interac- tions in human IBD, whereby a normally homeostatic adaptive response (i.e. the UPR) transforms into a potent pathomechanism of intestinal inflammation in the context of unresolved (i.e. unre- solvable) ER stress. (Acta gastroenterol. belg., 2011, 74, 330-333).