Stages and forms of the disease
Alcoholic liver injury represents a pathogenetic unity of three forms. They usually succeed each other sequentially, but can occur in isolation or coexist.
- Fatty liver (steatosis). The initial stage characterized by the accumulation of large fat droplets within hepatocytes. Inflammation is absent or minimal. The process is asymptomatic, with hepatomegaly being the only objective finding. Jaundice is uncharacteristic, though cholestasis is possible in rare cases. Lab tests show a moderate increase in aminotransferases. With complete alcohol cessation, the condition is 100% reversible.
Note: steatosis can also be non-alcoholic—occurring in the context of diabetes, obesity, pregnancy, protein deficiency, or medication use (glucocorticoids, amiodarone, methotrexate, estrogens, acetylsalicylic acid).
- Alcoholic hepatitis. A more severe stage featuring hepatocyte necrosis and active inflammation. Patients complain of fatigue, anorexia, fever, and pain in the right upper quadrant. Externally manifested by parenchymal jaundice. The acute process tends to become chronic. In one-third of patients, hepatitis transforms into cirrhosis within 1–2 years.
- Alcoholic cirrhosis. The terminal stage, occurring in 15–20% of individuals with chronic alcohol abuse. The risk depends on genetics and individual sensitivity to ethanol.
Pathogenesis of liver damage
Chronic ethanol intake triggers three interrelated mechanisms of tissue destruction:
- Autoimmune component. Lipid peroxidation is triggered, leading to the formation of aldehydes. Malondialdehyde-acetaldehyde (MAA) adducts are formed. The immune system produces autoantibodies against them, initiating an autoimmune attack on the body's own cells.
- Fibrogenesis. The toxic ethanol metabolite (acetaldehyde) binds to hepatocyte proteins. This stimulates collagen production, leading to fibrosis (scarring) of the parenchyma.
- Inflammatory reaction. Alcohol disrupts the intestinal barrier function. Endotoxins massively enter the bloodstream and activate liver macrophages—Kupffer cells. They release pro-inflammatory cytokines (IL-1, IL-6, TNF-α), causing potent inflammation.
Clinical presentation of cirrhosis
Cirrhosis decompensation is frequently triggered by new bouts of heavy drinking and the progression of hepatitis. The clinical picture consists of three main syndromes:
- Portal hypertension syndrome: characterized by increased collateral circulation, splenomegaly, development of ascites, and life-threatening bleeding from esophageal varices.
- Hepatocellular insufficiency.
- Hepatic encephalopathy.
Specific extramedullary/extraphepatic signs ("minor signs") are also detected: palmar erythema ("liver palms"), telangiectasias (spider angiomas), and gynecomastia in men.
Diagnostics and histology
Patients with alcohol dependence frequently resort to dissimulation (concealing the fact of abuse). The physician must look for objective signs of intoxication and use screening tools (CAGE questionnaire). The diagnosis cannot be ruled out solely based on the patient's denial of alcohol consumption.
Laboratory markers:
- Systemic inflammation: neutrophilic leukocytosis.
- Cytolysis: moderate increase in transaminases (AST predominance over ALT is specific).
- Cholestasis and immune inflammation: elevated alkaline phosphatase and IgA levels.
Biopsy data: Liver tissue reveals fatty degeneration (large fat droplets), infiltration by polymorphonuclear leukocytes, necrosis, and central vein sclerosis. A specific marker is alcoholic hyaline (Mallory bodies).
Management tactics
The key prognostic factor determining survival and disease progression is complete abstinence (cessation of alcohol intake). Without this, any therapeutic measures are ineffective.
Basic therapy includes:
- Adequate diet therapy focusing on vitamins and proteins.
- Correction of water and electrolyte balance.
- Treatment of complications, including infectious processes.
Briefly: answers to topical questions
What ratio is used to accurately assess the predominance of AST over ALT in alcoholic liver disease?
To assess the predominance of AST over ALT activity in alcoholic liver injury, the de Ritis ratio is used. This laboratory parameter is important for differential diagnosis.
- De Ritis ratio is the AST/ALT enzyme ratio, which is greater than 1 in alcoholic damage.
With the development of alcoholic liver disease, the value of this ratio usually exceeds 2. At the same time, in non-alcoholic fatty liver disease, this indicator generally does not exceed 1.3.
What pharmacological agents are used for specific pathogenetic therapy of severe alcoholic hepatitis?
Systemic corticosteroids are used to treat severe alcoholic hepatitis. Their administration aims to reduce short-term mortality, provided the patient has no active infection.
- Glucocorticosteroids are indicated as a short course during the acute period in severe disease.
- Severity criteria: Maddrey's discriminant function ≥ 32 and MELD score ≥ 20.
- Prednisolone is a drug from this group prescribed at a dose of 40 mg/day when Maddrey's score is > 32.
To remember the specific cytolysis marker in ALD, use the association: "Alcohol Shatters Tissue more than Alcohol Lesions Tissue" (AST predominates over ALT).
Class and exam questions
Can alcoholic liver disease be completely cured?
At the fatty liver (steatosis) stage, the disease is completely reversible provided there is absolute abstinence from alcoholic beverages.
How quickly does alcoholic hepatitis progress to cirrhosis?
If the patient does not stop drinking, alcoholic hepatitis transforms into irreversible cirrhosis within 1–2 years in 1/3 of patients.
Why does systemic inflammation occur with alcohol consumption?
Ethanol damages the intestinal barrier, endotoxins penetrate the bloodstream and force Kupffer cells to massively release cytokines (TNF-α, IL-1, IL-6).
What is dissimulation in the context of ALD?
This is the patient's deliberate concealment of alcohol abuse, which requires the physician to rely on objective laboratory and clinical markers.
What else to study on this topic
- CAGE questionnaire: methodology and interpretation of results
- Pathophysiology of portal hypertension in liver cirrhosis
- Differential diagnosis of alcoholic and non-alcoholic steatosis
- Hepatic encephalopathy: stages and mechanisms of CNS toxic injury
- Mallory bodies: morphology and diagnostic value
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