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ethanol-induced gastritis

Friday 24 February 2012

The extent of alcohol-induced injury results from the quantity of alcohol ingested as well as its mucosal contact time.

Injury usually requires gastric alcohol concentrations 10%.The presence of a concurrent HP infection may augment the alcohol-induced injury.

Alcohol contacting the superficial gastric mucosa impairs mucus synthesis and secretion and damages epithelial cells, causing them to become necrotic and slough, leaving the underlying mucosa exposedto the alcohol and to gastric luminal acid.

Acid back-diffusion increases mucosal blood flow, capillary permeability, and acid secretion.

Increased capillary permeability leads to interstitial edema.

Vasoactive mediator release from mastcells, endothelial cells, and neutrophils triggers venoconstriction and plasma transudation. The neutrophils generate superoxide anion and hyperchlorous acid in a manner similar to that seen in stress gastritis.

Arterial and arteriolar dilation rapidly follow, leading to marked congestion, edema, hemorrhage, cellular translocation, ischemia, and cell membrane damage sufficient to cause local edema, hypoxia, hemorrhage, and cellular necrosis.

Alcohol penetration into the congested tissues causes hemolysis, vascular congestion, protein precipitation, vascular stasis, thrombus formation, and capillary leakage.

Neuropeptides stimulated bythe alcohol affect blood vessels, leukocytes, and epithelium, and aid in activating inflammatory mediators.

Actively drinking alcoholics predominantly show multiple areas of subepithelial hemorrhage, prominent mucosal edema in the adjacent non-hemorrhagic mucosa, and onlymild inflammation.

The edema may be severe enough toextend into the submucosa.

The foveolar epithelium overlying the lamina propria hemorrhage may appear mucus depleted and show focal loss of nuclear polarity.

Tiny erosions may be present in some patients, especially those consuming large quantities of alcohol in a short period of time.

These resemble the lesions seen in stress gastritis and predominantly involve the proximal stomach.

In these patients there may be focal necrosis of the foveolar epithelium along with focal neutrophilic infiltrates in the gastric pits.

Chronic ethanol ingestion increases mucosal expression of EGF and other growth factors leading to increased cell proliferation.

Differentiation of cells in the proliferating mucous neck region replaces the damaged cells.

See also

- Gastritis

  • acute gastritis