1. Alcoholic Liver Disease
The Best Histopathology

2. Case Study Mr.T
• 56 year old Male presented to A&E with
Abdominal distension, somnolence and
haematemesis
• Orientated only to name
• Family members disclose a history of
alcohol abuse (100 units / wk)
• O/E: BP 90/60, Pulse 120. Jaundiced with
peripheral stigmata of liver disease and
shifting dullness

3. Mr.T Cont…
• Fluid resuscitation, abdominal
paracentesis and sclerosis of
oesophageal varices at endoscopy
• CT scan revealed 6.0 cm homogenous
liver mass with AFP level of 2500ng/ml
(>50ng/ml = abnormal)

4. Pathology Ladder
• Fatty liver (Alcoholic steatosis)
• Alcoholic hepatitis
• Fibrosis
• Cirrhosis
• Hepatocellular carcinoma

5. Steatosis
(Macrovesicular)
• 65% of chronic
drinkers
• Large sharp fat
droplets in
hepatocytes
• Accumulation due to
defect of secretion
of lipoprotein by
hepatocytes

6. Microvesicular (Foamy) Steatosis
• Much rarer – first stage
of hepatic
decompensation
• Groups of foamy
hepatocytes containing
small droplets
throughout cytoplasm
• Hepatocyte dropout due
to apoptosis and
pericellular fibrosis

7. Alcoholic Hepatitis
• Necroinflammatoy
lesion in centrolobular
area
• Characterised by -
Necrosis, Inflammation
and Fibrosis
• Infiltrate of neutrophil
polymorphs surrounding
Mallory bodies
• Acute alcoholic hepatitis
has a mortality rate of
20-50%

8. Mallory Bodies

9. Fibrosis
• Pericellular or “chicken wire” fibrosis in
hepatitis
• Venous lesions; sclerosing hyaline necrosis
portal hypertension
• Cytokine mediated transformation of Ito cells
into transitional cells, myofibroblasts and
fibroblasts
• Interference with O2 and nutrient exchange
between blood and hepatocyte = injury and
dysfunction

10. Pericellular (Chicken Wire) Fibrosis

11. Prognosis
• Initial fibrosis in steatosis will resolve with
abstinence
• Severe fibrosis may progress to cirrhosis
even without continuation of alcohol
consumption
• Factors affecting progression to cirrhosis
include; continued alcohol consumption,
severity of lesion and sex (F>M). There is
also thought to be a genetic component

12. Cirrhosis
• 10-20 % of chronic drinkers; irreversible
• Parenchymal necrosis, re-generation and
fibrosis resulting in disorganisation of the
acinar structure
• Usually micronodular, with uniform
regenerative nodules <3mm
• 60-70% 5yr survival in abstinence
• 40% in continued drinking
• 5 - 10% develop Hepatocellular carcinoma

13. Micronodular Cirrhosis

14. Microscopic Micronodular

15. Hepatocellular Carcinoma
• Progression of micro to
macronodular cirrhosis
(often after period of
abstinence)!
• Dysplasia in
regenerative nodules ->
Neoplasia
• Increased risk with
Hepatitis
• Fatal within 10 months

16. Conclusion
• Patient may present with a mixed
picture of pathology
• Important to remember that changes
are often reversible
• Serious consequences of continued
drinking – irreversible damage
• Cirrhosis and hepatocellular carcinoma

17. Questions?

18. References
• Alcoholic liver disease, Pathology and Pathogenesis,
2nd
Edition 1995 Ed. Pauline Hall
• Cpmenet.columbia.edu
• Gastroresource.com
• Lieben CS.Pathogenesis and treatment of alcoholic liver disease:
progress over the last 50 years.Rocz Akad Med Bialymst. 2005;50:7-
20.
• meddean.luc.edu
• merck.com
• Oxford Handbook Clinical Medicine
• Sougioultzis S, Dalakas E, Hayes PC, Plevris JN.
Alcoholic hepatitis: from pathogenesis to treatment.
Current Medical Research and Opinion, Volume 21, Number 9,
September 2005, pp. 1337-1346(10)