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Alcohol, commonly found in alcoholic beverages like wine, beer, and spirits, is a non-nutritional macro molecule that provides 7 kcal per gram. It is created through the fermentation or distillation of carbohydrates, both simple and complex, by microorganisms or yeasts known as saccharomyces. Although it may seem harmless in moderate quantities, alcohol is, in fact, a nerve agent that can have toxic effects on all tissues of the body, with some areas being more vulnerable than others.
When consumed, ethyl alcohol is first absorbed by the cells of the digestive mucosa, specifically in the mouth's epithelium, the gastric mucosa, and the small intestine. Once absorbed, it enters the circulation, reaching all peripheral areas, where it manifests its toxic function.
The most easily identifiable effect of alcohol is on the central nervous system (CNS), leading to sensations of heat, disinhibition, coordination alteration, and lengthened reaction times to stimuli. However, it also causes cytolysis in all histological forms of the body, including kidney cells, pancreas cells, liver cells, and others. Alcohol also triggers a hormonal reaction akin to the intake of a high glycemic load, resulting in an insulin surge and an increase in adipose deposit.
The disposal of ethanol mainly occurs in the liver, through specific enzymatic processes. However, following alcohol intoxication, hepatocytes may also undergo cytolytic lesions. Frequent use of alcohol represents a significant risk factor for chronic abuse, potentially leading to psychiatric alcoholism syndrome.
Gastrically, alcohol has a markedly deleterious function. It can lead to both acute and chronic complications, the manifestation of which largely depends on individual predisposition and the presence of other inadequate behaviors, such as poor diet, smoking, and stress. The most frequent clinical manifestations include acute gastritis, chronic superficial gastritis, and chronic atrophic gastritis.
The etiopathogenesis of gastritis, whether acute or chronic, can be attributed to:
The most frequent complications of gastritis from alcohol abuse are acute and chronic. Acute complications can include gastric hemorrhages, identifiable by the onset of bloody vomiting. In the long term, the presence of mucosal pathologies can become chronic, potentially facilitating the onset of gastric carcinoma.
Acute hemorrhagic gastritis is primarily attributable to two causes: alcohol abuse and the use of gastro-injurious drugs. It is less commonly caused by the ingestion of corrosive agents. The pathogenetic mechanisms linked to the onset of acute hemorrhagic gastritis are tied to the direct epithelial-damaging action of alcohol on the mucosa, reflex gastric hyper-secretion, and submucosal vessel congestion.
Acute hemorrhagic gastritis manifests with lesions of the gastric mucosa, sometimes reaching the perforation of the digestive tract, associated with erosions, ulcers, and hemorrhagic extravasations. These organic alterations are linked to symptoms such as epigastric pain, postprandial heartburn, nausea, and bloody vomiting. In severe cases, systemic manifestations such as fever, tachycardia, pallor, and sweating may occur.
The most serious forms of acute ulcerative gastritis can evolve into electrolyte alterations and potentially shock or cardiovascular collapse. While the prognosis is typically benign and short-lived, in the most serious forms, severe complications cannot be ruled out.
In conclusion, while alcohol may seem harmless in moderate quantities, its impact on the body, particularly the digestive system, can be severe. It is essential to understand the potential risks and complications associated with excessive alcohol consumption and to seek medical attention if any symptoms of gastritis or other alcohol-related health issues arise.