Interpreting liver biopsy results

[hiddenorder]

Hi.  I was diagnosed with HVC last summer (Genotype 1).  Have probably had it for over 20 years but no notable symptoms.  Fortunately quit drinking almost 18 years ago.  My most recent hepatic function panel showed AST of 37 and ALT of 30.  These have consistently been pretty low since my diagnosis.  I was trying to decide whether or not to postpone treatment for a while to see what happens with the newer drugs in the pipeline and it was suggested that I have a liver biopsy to give me enough info to make an informed decision.  All my doc told me was that the necroinflammatory score was 3-4 of 18 and fibrosis stage 1 of 6 (HAI/KNODELL) and based on that I could wait but have monthly hepatic panels run to monitor.  I got a copy of the biopsy and would be interested to know if any of you have other thoughts.  Thank you so much.

Here's what it says:

Microscopic description:
Needle biopsy fragments of hepatocellular tissue show normal architecture and mild lymphocytic, portal and lobular inflammation with associated mild piecemeal necrosis.  Rare necrotic hepatocytes (acidophil bodies) are seen.  A trichrome stain demonstrates fibrous expansion of some portal areas without evidence of fibrous septa or cirrhosis.  A reticulin stain demonstrates normal hepatocellular cords and no significant reticulin fibrosis.  A Prussian blue iron stain is negative for intracellular iron accumulation.  A PAS stain with and without diastase does not show evidence of persistent PAS positive intracytoplasmic hepatocellular material following diastase digestion.  Persistent PAS positive Kupffer cells are present.  All of the special stains have adequate controls.

Modified histologic activity (HAI) index grading (necroinflammatory score):
a. Piecemeal necrosis: mild (score=1)
b. Confluent necrosis: absent (score=0)
c. Focal (spotty) lytic necrosis: one focus or ness per 10X objective (score=1)
d. Portal inflamation: Mild, all portal areas (score=1)

Modified staging:
Fibrous expansion of some portal areas without fibrous septa (score=1)

Additional features noted but not scored
Bile duct inflammation and damage: Not seen
Lymphoid follicles: Absent
Steatosis: Absent
Hepatocellular dysplasia: Absent
Iron overload: Absent
Intracellular inclusions: Absent

[friole]

http://library.med.utah.edu/WebPath/LIVEHTML/LIVER038.html

Here are some pictures of liver disease caused by hepatitis inclucing necrotic heptocyts and piecemeal necrosis.

In a nut shell, the hepatitis virus causes inflammation in the liver.  This inflammation starts out in the portal triads (where all the big veins come together in your liver) and gradually edges out of these portal triad areas into the lobules (the large areas of the liver surrounded by connective tissue).

http://www.vivo.colostate.edu/hbooks/pathphys/digestion/liver/histo_lobule.html

It is the inflammation that leads to scarring (fibrosis).  The scarriing then causes cell death (necrosis).  It sounds like the inflammation is just beginning to extend beyond the portal areas but there is not any fibrosis beyond the portals yet.

Acidophil bodies are single cell death. I tried to google the meaning of rare acidophil bodies but fell into the void (beyond my comprehension).


Like grandoak said -- you will get all kinds of opinions here.  All I know is that your inflammation is "on the move".  Your scarring is not yet bad.  You have no steatosis (fatty liver) and this is all good.  

Based on your liver biopsy I would probably treat, but there are new drugs coming. Threre are also a multitude of other reasons to treat or not.

Good luck with your hard decision
frijole

[GrandOak]

Basically it looks like your at the beginning of any damage being done to your liver.

There will probably be many who tell you to wait and others to treat now.  The fact is that one never knows if or when HCV might flare up and start inflicting damage.  More often than not it's a matter of when rather than if.  Also, no one can predict how fast damage will be inflicted when attacks upon the liver occur.

Also, the lower ones viral load when beginning treat can often times be an indicator on the chance for clearing the virus from the system.

Some folks clear spontaneously, but this seems to be rare.  Finally, for many treatment is no picnic and treating when younger and stronger may make enduring it easier, if there is such a thing as an easy treatment.

Bottomline is that treating always becomes a personal decision on how much risk they want to take on minimal damage occurring, how comfortable they are with knowing they are infected with the virus, how careful they want to be to not infect others if they don't treat, etc..