Alcohol and Gastritis

Ethyl alcohol

Ethyl alcohol is a NON-nutritional macro molecule that provides 7 kcal per gram; it is contained in alcoholic beverages obtained by fermentation (wine, beer, etc.) or distillation (grappa, whiskey, etc.) thanks to the degradation of carbohydrates (both simple and complex) by some microorganisms or yeasts, called saccharomyces.

Alcohol is a nerve and therefore acts toxic at the level of ALL body tissues, however, some districts are more vulnerable than others. The digestive mucosa cells are the first to suffer from the introduction of alcohol; in fact, ethanol absorption occurs by simple diffusion in the epithelium of the mouth, in the gastric mucosa and in the small intestine.

Once absorbed, ethyl alcohol enters the circulation and reaches all the suburbs, in which it shows its toxic function in a more or less evident way; the most easily identifiable effect is that on the central nervous system (CNS): sensation of heat, disinhibition, alteration of coordination and lengthening of reaction times to stimuli. However, although asymptomatic, cytolysis occurs in all the histological forms of the body: kidney cells, pancreas cells, liver cells, etc. Ethyl alcohol also causes a hormonal reaction very similar to the intake of a strong glycemic load with a surge of insulin, causing an increase in the adipose deposit fortified by its conversion to fatty acids since, NOT being a nutrient, its energetic oxidation It is never direct.

The disposal of ethanol occurs mainly in the liver thanks to specific enzymatic processes; however, following ethyl intoxication, also hepatocytes undergo cytolytic lesions identifiable with the blood detection of trans-aminases.

Frequent use of ethyl alcohol is a major risk factor for chronic abuse, which can lead to the onset of psychiatric ethylism syndrome.

Alcohol and gastritis

At the gastric level, ethyl alcohol has a markedly deleterious function; it can give rise to both acute and chronic complications, whose manifestation depends above all on the level of individual predisposition and on the presence of other inappropriate behaviors (poor diet, smoking, nervousness etc.). The most frequent clinical manifestations are:

• Acute gastritis
• Chronic superficial gastritis
• Chronic atrophic gastritis

The etiopathogenesis of gastritis - whether acute or chronic - depends on:

• Reduced mucus synthesis
• Alteration of submucosal blood flow
• Alteration of cellular permeability
• Blockade of the synthesis of cyclic Adenosine Monophosphate (AMPcyclic - messenger involved in signal transduction)
• Alteration of cell membrane potential

The most frequent complications of ethyl gastritis are acute and chronic; among the acute ones it is possible to find gastric haemorrhages identifiable with the onset of blood vomiting, while in the long term, the presence of mucosal pathologies can become chronic, facilitating the onset of gastric carcinoma.

Acute hemorrhagic gastritis

This kind of pathological manifestation is basically attributable (20-40% of cases) to two etiological causes: alcohol abuse and the use of gastrolesive drugs (anti-inflammatory NSAIDs); while it is rarer that it is caused by the ingestion of corrosive agents. The pathogenetic mechanisms associated with the onset of acute haemorrhagic gastritis are related to the direct damage to the mucosa epithelial action of alcohol, reflex gastric hyper-secretion and submucosal vasal congestion.

Acute haemorrhagic gastritis manifests itself with lesions of the gastric mucosa (which sometimes reach the perforation of the digestive tract) associated with erosions, ulcers and hemorrhagic extravasations, therefore with both occult and abundant bleeding; these organic alterations are related to symptoms such as epigastric pain, postprandial burning, nausea and blood vomiting. Sometimes systemic manifestations such as fever, tachycardia, pallor and sweating can be detected. The most serious forms of acute ulcerative gastritis evolve into electrolytic alterations (induced by vomiting) and in shock and / or cardio-circulatory collapse; in general the prognosis is benign and of short duration (about 2-7 days), but in the more serious forms complications of very serious entity are not excluded.

Bibliography:

• The Italian book of alcology. Volume 1 - A. Allamani, D. Orlandini, G. Bardazzi, A. Quartini, A. Morettini - SEE Florence - page 215
• Alcohol. Alcolismi. What changes? - B. Sanfilippo, GL Galimberti, A. Lucchini - FrancoAngeli - page 96