Chronic hepatitis
–
Persistent, often progressive inflammatory process characterized by lymphocytic inflammation of portal tracts with varying degrees of parenchymal inflammation, hepatocellular injury, and fibrosis
Chronicity judged in several ways: Clinical, laboratory, morphologic
Practically defined as 6 months or more of elevated transaminases
Acute hepatitis
–
Active hepatocellular damage and necrosis
Usually of short &/or self-limited duration
Most often due to viral infection or adverse drug reaction
Infrequently biopsied because diagnosis usually made by clinical or laboratory data
ETIOLOGY/PATHOGENESIS
Viral Hepatitis
•
Hepatotropic viruses (A, B, C, E)
•
Other viruses, such as Epstein-Barr virus, CMV
Autoimmune Hepatitis
•
Type 1: ANA/SMA(+), hypergammaglobulinemia, concurrent autoimmune diseases
•
Type 2: Anti-LKM antibodies, more likely to develop cirrhosis
•
Type 3: Less well characterized; anti-SLA/LP antibodies; may have AMA(+)
Drug-Associated Hepatitis
•
Necroinflammatory
Acetaminophen, phenytoin, Macrodantin, sulphonamides
•
Cholestatic
Many antibiotics, steroids
•
Granulomatous
Allopurinol, many antibiotics, phenytoin
Other
•
Wilson disease
•
α-1-antitrypsin deficiency
•
Nonspecific reactive hepatitis
Reaction to extrahepatic infection or neoplasm, severe systemic illness, or to adjacent mass lesion in liver
CLINICAL IMPLICATIONS
Clinical Presentation
•
Signs and symptoms of liver failure
•
Many patients are asymptomatic
Laboratory Findings
•
Alkaline phosphatase may be mildly elevated
•
Viral serologies positive in viral hepatitis
•
Autoimmune serologies usually positive in autoimmune hepatitis
•
Other serologic tests, such as urinary copper, ceruloplasmin, serum α-1-antitrypsin, may be helpful
MICROSCOPIC
General Features
•
Broad range of histologic appearances with some features in common
Portal inflammation
–
Infiltrate consists primarily of lymphocytes
May have admixed plasma cells, histiocytes, and granulocytes
–
Lymphoid follicles common in hepatitis C
–
Nonspecific ductular reaction may be present at periphery of portal tract
Lobular inflammation/necrosis
–
Necrosis may be mild and spotty or confluent and bridging
–
May be accompanied by ballooning degeneration, reactive hepatocellular changes
Piecemeal necrosis (interface activity)
–
Defined as extension of inflammation into adjacent parenchyma with destruction of individual hepatocytes at interface
–
Results in ragged interface between portal tract and hepatic parenchyma
Fibrosis
•
Predominant pattern of inflammation in given case may be portal, periportal, lobular, or combination
Acute hepatitis usually diffusely involves lobule and is not confined to portal area
•
Inflammatory process may be sporadically distributed within liver, resulting in sampling bias
