bridging fibrosis

MICROSCOPIC DESCRIPTION
the biopsy is adequate with over 10 portal tracts. The architecture is intact.  Thers is a moderate mononuclear inflammatory infiltrate in the portal areas with some interface activity and extension into the lobule.  Bile ducts are intact. No cholestaticplugs are identified. The lobules show mild disarray with significant inflammation, ballooning of hepatocytes and rare apoptotic bodies. Moderate macrovesicular steatosis is noted (involving 40-50% of hepatocytes) and prominent microvesicular steatosis is also present(60-70%).  No PAS-D globules are identified.  There is trace sstainable iron in Kupffer cells.  There is portal fibrosis and rare areas of pericellular fibrosis:  definate septa are not seen.

DIAGNOSIS
liver, percutaneous core biopsy:
-adequate biopsy showing moderate portal, interface and lobular chronic inflammation, with rare acidophil bodies, consistent with hepatisis C viral etiology.
-moderate steatosis, 40-50%
portal and early periportal fibrosis
-stainable iron is trace and there are no PAS-D positive globules.

COMMENT
grade &Ii stage, Batts and Ludwig, A.J.S.P. 1995 are 2-3 out of 4 and 2 out of 4 respectively.

The question:
Do I have bridging fibrosis demonstating fibrous tissue in the portal tracts of the liver with fibrous bands bridging to other portal areas or to central veins but without nodular formation or nodular regeneration.

Would you answer yes to this question?

[orleans]

sorry, over my head, jerry

[Trinity4]

"portal and early periportal fibrosis"

Don't know the exact extent the fibrosis has manifested, but that statesment indicated portal and periportal fibrosis.
Being a stage 2-3 you do have fibrosis - don't know enough about the other side of your question to answer correctly.

[HCA]

No-the bridging is the septa which according to the pathologist are not seen.

[jmjm530]

It appears you are stage 2 out of 4. Stage 2 is not bridging fibrosis, that would be stage 3. Of some concern would be the steatosis (fatty liver) especially if you're genotype 3.

How much concern I'm not qualified to say. In fact, none of here are doctors, so opinions in technical matters like these should be addressed by your doctor and/or pathologist.

Yes, pathologists frequently do speak to patients if you track them down and insist. I spoke to three of them during my treatment. One invited me over the lab and actually spent a half hour with me, allowing me to look at the slides. Another seemed pissed off I got his number and gave me a very curt answer.  The third fell somewhere inbetween.

[HCA]

Here is a fuller definition which confirms my earlier response;
''Portal fi brosis is a stellate enlargement of portal tracts without any bridging
fi brosis on the biopsy sample. Few septa mean at least one fi brous septa on
the core biopsy. Theoretically, a fi brous septa is a bridge of connective tissue
between two portal tracts, a portal tract and a centrolobular vein, or between
two centrolobular veins. Septal fi brosis means that the liver biopsy is crossed
by several septa; the transition between F2 and F3 begins when there is more
fi brous septa than portal tracts without septa on the biopsy. Cirrhosis means
that liver tissue is mutilated by nodular fi brosis that delineates hepatocytes nodules''

[princess514]

You seem well informed
Thank you