Page 640 - Textbook of Pathology, 6th Edition

624 Post-necrotic Cirrhosis
forming regenerative nodules having disorganised masses
of hepatocytes. The hepatic parenchyma within the Post-necrotic cirrhosis, also termed post-hepatitic cirrhosis,
nodules shows extensive fatty change early in the disease. macronodular cirrhosis and coarsely nodular cirrhosis, is
But as the fibrous septa become more thick, the amount characterised by large and irregular nodules with broad
of fat in hepatocytes is reduced. Thus, there is an inverse bands of connective tissue and occurring most commonly
relationship between the amount of fat and the amount after previous viral hepatitis.
of fibrous scarring in the nodules. ETIOLOGY. Based on epidemiologic and serologic studies,
iv) Necrosis, inflammation and bile duct proliferation: the following factors have been implicated in the etiology of
The etiologic clue to diagnosis in the form of Mallory post-necrotic cirrhosis.
bodies is hard to find in a fully-developed alcoholic 1. Viral hepatitis. About 25% of patients give history of
cirrhosis. The fibrous septa usually contain sparse recent or remote attacks of acute viral hepatitis followed by
infiltrate of mononuclear cells with some bile duct chronic viral hepatitis. Most common association is with
proliferation. Bile stasis and increased cytoplasmic hepatitis B and C; hepatitis A is not known to evolve into
haemosiderin deposits due to enhanced iron absorption
in alcoholic cirrhosis are some other noticeable findings. cirrhosis. It is estimated that about 20% cases of HBV chronic
hepatitis and about 20-30% cases of HCV chronic hepatitis
LABORATORY DIAGNOSIS. The clinical manifestations go to develop cirrhosis over 20-30 years.
and complications of cirrhosis in general are described on 2. Drugs and chemical hepatotoxins. A small percentage
page 630. The laboratory findings in the course of alcoholic of cases may have origin from toxicity due to chemicals and
liver disease may be quite variable and liver biopsy is drugs such as phosphorus, carbon tetrachloride, mushroom
necessary in doubtful cases. Progressive form of the disease, poisoning, acetaminophen and α-methyl dopa.
however, generally presents the following biochemical and 3. Others. Certain infections (e.g. brucellosis), parasitic
haematological alterations: infestations (e.g. clonorchiasis), metabolic diseases (e.g.
1. Elevated transaminases: increase in SGOT (AST) is more Wilson’s disease or hepatolenticular degeneration) and
than that of SGPT (ALT). advanced alcoholic liver disease may produce a picture of
2. Rise in serum γ-glutamyl transpeptidase (γ-GT). post-necrotic cirrhosis.
3. Elevation in serum alkaline phosphatase. 4. Idiopathic. After all these causes have been excluded, a
4. Hyperbilirubinaemia. group of cases remain in which the etiology is unknown.
5. Hypoproteinaemia with reversal of albumin-globulin
SECTION III
ratio. MORPHOLOGIC FEATURES. Typically, post-necrotic
6. Prolonged prothrombin time and partial thromboplastin cirrhosis is macronodular type.
time. Grossly, the liver is usually small, weighing less than
7. Anaemia. 1 kg, having distorted shape with irregular and coarse
8. Neutrophilic leucocytosis in alcoholic hepatitis and in scars and nodules of varying size (Fig. 21.27). Sectioned
secondary infections.

Systemic Pathology

Figure 21.27 Post-necrotic cirrhosis, showing the typical irregular
macronodular pattern (nodules larger than 3 mm diameter). Externally
the liver is small, distorted and irregularly scarred.