Page 627 - Textbook of Pathology, 6th Edition

1. Hepatocellular injury: There may be variation in the and hepatitis D infection. However, some non-viral causes 611
degree of liver cell injury but it is most marked in zone 3 of chronic hepatitis include: Wilson’s disease, α-1-antitrypsin
(centrilobular zone): deficiency, chronic alcoholism, drug-induced injury and
i) Mildly injured hepatocytes appear swollen with autoimmune diseases. The last named gives rise to
granular cytoplasm which tends to condense around the autoimmune or lupoid hepatitis which is characterised by
nucleus (ballooning degeneration). positive serum autoantibodies (e.g. antinuclear, anti-smooth
muscle and anti-mitochondrial) and a positive LE cell test
ii) Others show acidophilic degeneration in which the but negative for serologic markers of viral hepatitis.
cytoplasm becomes intensely eosinophilic, the nucleus Until recent years, prediction of prognosis of chronic
becomes small and pyknotic and is eventually extruded hepatitis used to be made on the basis of morphology which
from the cell, leaving behind necrotic, acidophilic mass
called Councilman body or acidophil body by the process divided it into 2 main types—chronic persistent and chronic
known as apoptosis. active (aggressive) hepatitis. A third form, chronic lobular
hepatitis is distinguished separately by some as mild form of
iii) Another type of hepatocellular necrosis is dropout lobular inflammation without inflammation of portal tracts
necrosis in which isolated or small clusters of hepatocytes but these cases often recover completely. However,
undergo lysis. subsequent studies have revealed that morphologic subtypes
iv) Bridging necrosis is a more severe form of hepato- do not necessarily correlate with prognosis since the disease
cellular injury in acute viral hepatitis and may progress is not essentially static but may vary from mild form to severe
to fulminant hepatitis or chronic hepatitis (discussed and vice versa. Besides, two other factors which determine
below). Bridging necrosis is characterised by bands of the vulnerability of a patient of viral hepatitis to develop
necrosis linking portal tracts to central hepatic veins, one chronic hepatitis are: impaired immunity and extremes of age
central hepatic vein to another, or a portal tract to another at which the infection is first contracted. Currently, therefore,
tract. chronic hepatitis is classified on the basis of etiology and
2. Inflammatory infiltrate: There is infiltration by hepatitis activity score (described below). The frequency and
mononuclear inflammatory cells, usually in the portal severity with which hepatotropic viruses cause chronic
tracts, but may permeate into the lobules. hepatitis varies with the organisms as under: CHAPTER 21
3. Kupffer cell hyperplasia: There is reactive hyper- HCV infection accounts for 40-60% cases of chronicity in
plasia of Kupffer cells many of which contain phago- adults. HCV infection is particularly associated with
cytosed cellular debris, bile pigment and lipofuscin progressive form of chronic hepatitis that may evolve into
granules. cirrhosis.
4. Cholestasis: Biliary stasis is usually not severe in viral HBV causes chronic hepatitis in 90% of infected infants
hepatitis and may be present as intracytoplasmic bile and in about 5% adult cases of hepatitis B.
pigment granules. HDV superinfection on HBV carrier state may be
5. Regeneration: As a result of necrosis of hepatocytes, responsible for chronic hepatitis in 10-40% cases.
there is lobular disarray. Surviving adjacent hepatocytes HAV and HEV do not produce chronic hepatitis.
undergo regeneration and hyperplasia. If the necrosis
causes collapse of reticulin framework of the lobule, MORPHOLOGIC FEATURES. The pathologic features
healing by fibrosis follows, distorting the lobular are common to both HBV and HCV infection and include
architecture. the following lesions (Fig. 21.13).
1. Piecemeal necrosis. Piecemeal necrosis is defined as
The above histologic changes apply to viral hepatitis by periportal destruction of hepatocytes at the limiting plate
various types of hepatotropic viruses in general, and by HBV (piecemeal = piece by piece). Its features in chronic hepatitis The Liver, Biliary Tract and Exocrine Pancreas
in particular. It is usually not possible to distinguish are as under:
histologically between viral hepatitis of various etiologies, i) Necrosed hepatocytes at the limiting plate in
but the following morphologic features may help in giving periportal zone.
an etiologic clue: ii) Interface hepatitis due to expanded portal tract by
HAV hepatitis is a panlobular involvement by heavy infiltration of lymphocytes, plasma cells and
inflammatory infiltrate compared to other types. macrophages.
HCV hepatitis causes milder necrosis, with fatty change iii) Expanded portal tracts are often associated with
in hepatocytes, presence of lymphoid aggregates in the portal proliferating bile ductules as a response to liver cell injury.
triads and degeneration of bile duct epithelium.
2. Portal tract lesions. All forms of chronic hepatitis are
IV. Chronic Hepatitis characterised by variable degree of changes in the portal
tract.
Chronic hepatitis is defined as continuing or relapsing i) Inflammatory cell infiltration by lymphocytes, plasma
hepatic disease for more than 6 months with symptoms along cells and macrophages (triaditis).
with biochemical, serologic and histopathologic evidence of ii) Proliferated bile ductules in the expanded portal tracts.
inflammation and necrosis. Majority of cases of chronic iii) Additionally, chronic hepatitis C may show lymphoid
hepatitis are the result of infection with hepatotropic aggregates or follicles with reactive germinal centre and
viruses—hepatitis B, hepatitis C and combined hepatitis B