Postnecrotic Liver Cirrhosis
Etiology and Pathogenesis. The process develops rapidly, sometimes within a matter of months. The primary triggers are fulminant viral hepatitis B (HBV) and massive parenchymal necrosis due to toxic injury.
Macroscopic Appearance. The organ is reduced in size and firm. The surface acquires a macronodular pattern: the nodule diameter exceeds 3 mm. On cross-section, these nodules are separated by broad, dense, grayish connective tissue bands.
Microscopic Appearance. The normal cord architecture is completely destroyed. Regenerative nodules of varying calibers form, completely surrounded by fibrosis. The radial arrangement of hepatic cords is lost, and the central vein is either absent or displaced to the periphery of the nodule. Wide connective tissue septa reveal approximated triads—a classic hallmark of stromal collapse following hepatocyte death. Lymphomacrophage infiltration and actively proliferating bile ducts are also visible within the septa. Hepatocytes themselves show hydropic or ballooning degeneration, with numerous regenerating cells present.
Clinicopathological Features. Early liver failure comes to the forefront, whereas portal hypertension develops only in the later stages.
Portal Liver Cirrhosis
Etiology and Pathogenesis. It forms slowly over several years, typically as the end-stage of chronic hepatitis (alcoholic or viral, most commonly HCV). The mechanism is based on the ingrowth of fibrous strands from portal tracts or central veins with their subsequent connection (septum formation). This gives rise to small pseudolobules (pseudolobuli).
Macroscopic Appearance. In early stages, the liver is enlarged, firm, with a micronodular surface (nodules do not exceed 3 mm). Due to concurrent fatty change, the nodules acquire a bright yellow color, separated by thin grayish septa. At end-stage disease, the organ may shrink, turn brownish-red, and nodule sizes begin to range from 3 to 10 mm.
Microscopic Appearance. It appears more uniform. The stroma is represented by a fine reticular network. Small monomorphic regenerative nodules separated by narrow septa are visible. Fatty and protein degeneration predominates in hepatocytes. The septa contain proliferating ducts and a cellular infiltrate determined by the etiology. Alcoholic cirrhosis is characterized by portal monolobular cirrhosis (connective tissue is clearly visualized with Van Gieson picrofuchsin staining).
Clinicopathological Features. Early portal hypertension is characteristic, while liver failure becomes a late complication. Primary biliary cholangitis (PBC) is classified separately—it is considered a "true" portal cirrhosis based on nonsuppurative destructive cholangitis and cholangiolitis.
Comparative Characteristics and Terminology
In addition to the two main forms, mixed liver cirrhosis exists, combining the morphological features of both postnecrotic and portal types.
Analogous terms are frequently found in medical literature, though it is important to understand the nuances:
- Macronodular cirrhosis closely correlates with postnecrotic cirrhosis.
- Micronodular cirrhosis correlates with portal cirrhosis.
Note: These pairs show a strong correlation, but are not exact synonyms.
| Feature | Postnecrotic Cirrhosis | Portal Cirrhosis |
|---|---|---|
| Rate of progression | Rapid (months) | Slow (years) |
| Common causes | Fulminant HBV, toxins | Chronic alcoholic hepatitis, HCV |
| Nodule size (macro) | Large (> 3 mm) | Small (up to 3 mm), up to 10 mm at end-stage |
| Septa | Broad, dense | Thin, narrow |
| Specific markers | Approximated triads in septa | Pseudolobules, monomorphic pattern |
| Early clinical syndrome | Liver failure | Portal hypertension |