Pathology of Reactive Gastropathy: Overview, Pathophysiology and Etiology, Epidemiology

The common fundamental causes of reactive gastropathy include chronic bile reflux and long-run intake of nonsteroid anti-inflammatory drugs ( NSAIDs ). Bile ebb normally occurs in patients who have undergone a Billroth II fond gastrectomy ; it is besides recognized to occur in intact stomachs in individuals with alcohol abuse, cigarette smoking, chronic respiratory disease, or duodenal ulcer, and even in healthy subjects. [ 8, 9 ]

The duodenogastric reflux results in break of the protective mucus barrier and direct wound to the gastric mucous membrane, causing backflow of hydrogen ions and epithelial damage. [ 10 ] The versatile bile acidic species differ in their capacitance to cause wound to the gastric mucous membrane. [ 4 ] The junior-grade ( deoxycholic and lithocholic ) and deconjugated bile acids are more deleterious to the gastric mucous membrane than the basal ( colic and chenodeoxycholic ) and conjugated bile acids .

In situations of upper gastrointestinal ( GI ) stasis, as is seen after gastric surgery, bacterial overgrowth occurs within the proximal modest intestine. This increase in intraluminal bacteria leads to subsequent genesis of relatively increase concentrations of deconjugated and secondary coil bile acids within the refluxate. The increased assiduity of the more toxic forms of bile acid, coupled with the decrease gastric emptying time of the refluxed bile, results in gastric mucosal injury and subsequent reactive gastropathy ( chemical gastropathy ) .

The prevailing mechanism of NSAID-induced gastric injury involves decreased synthesis of mucosal prostaglandins. [ 11, 12 ] Prostaglandins are derived from arachidonic acerb via the cyclooxygenase ( COX ) pathway. frankincense, inhibition of COX by NSAIDs reduces prostaglandin synthesis, thereby diminishing mucosal rake menstruation and decreasing mucus and bicarbonate secretion .

furthermore, NSAIDs, being weak constituent acids, can freely diffuse into the gastric epithelium. As a result of the neutral ph within the coat epithelial cells, the NSAID intensify dissociates into its ionized form, contributing to direct cell injury. [ 13 ]

Although it is known that NSAIDs that selectively inhibit cyclooxygenase-2 cause importantly fewer GI complications than nonselective COX inhibitors do, it is still ill-defined whether administration of selective inhibitors results in less austere reactive gastropathy ( chemical gastropathy ). [ 14 ] however, most of these COX-2 inhibitors have been withdrawn from the market or have had their indications drastically limited in see of their potential serious cardiovascular side effects. [ 15 ]

The epithelial injury results in excessive scale of the surface epithelial cells, which gives rise to a reactive foveolar hyperplasia. [ 2 ] The accompanying histamine-mediated vascular reaction leads to edema and hyperemia. Persistent epithelial damage may result in the handout of platelet-derived growth factor ( PDGF ), which stimulates legato muscle proliferation, followed by fibroblastic proliferation. [ 10 ]

The mucosal changes seen in reactive gastropathy are normally most outstanding in the antrum and prepyloric region. When associated with bile ebb secondary to partial derivative gastrectomy, the lesions develop near the surgical stoma, [ 16 ] but the more proximal oxyntic mucous membrane may besides be affected.

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To go steady, no specific familial predispose factors for the growth of reactive gastropathy have been identified .

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