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Hi! I still have a few questions regarding small duct PSC. How exactly will

they be able to dx it-the ERCP have shown inconclusive. The liver biospy normal.

When they removed 's gallbladder hs liver has a white web casing over it.

Very Strange???? Should I ask for a test atha would show if he has

antimitochonial antibodies or does that show up in blood work? I read where

someone who posted was diagnosed with a Catscan and MRI I understand that it is

hard to dx small duct but how will it eventually be seen??? Still need a little

help understanding why they can't find anything except what appears to be

bacterial cholangitis attacks. He has had plenty of ERCP's as well, and

nothing. Is it a good thing that they can't see any evidence???? Sorry if

these questions sound basic???:) I have already learned so much for these post.

Thanks. I've changed the e-mail address to this one on Juno to keep the other

clear for work.

Pamela(wife of )

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Hi Pamela;

I'm presuming that since has had a number of ERCP's already,

the doctors involved must suspect a biliary disease, and this would

normally show up in serum blood tests as an elevated alkaline

phosphatase (ALP) and elevated gamma-glutamyltranspeptidase (GGT),

and perhaps also elevated alanine aminotransferase (ALT) and

aspartate aminotransferase (AST). Elevated ALP and GGT are almost

always diagnostic of bile-duct disease or blockages. Elevated ALT and

AST reflects damage to hepatocytes; this can occur together with bile-

duct disease. When ONLY AST and ALT are elevated (without elevated

ALP and GGT) this could suggest viral or autoimmune hepatitis. Does

have elevated ALP and GGT?

ALP can be elevated due to bone disease, and so a GGT test is often

done to confirm bile-duct involvement. If GGT was not elevated, then

an elevated ALP could possibly suggest bone disease rather than liver

disease.

Various antibody tests using blood samples can be used to look for

signs of autoimmune hepatitis. Smooth muscle antibodies (SMA) are

characteristic of autoimmune hepatitis (AIH) type 1. Liver/kidney

microsomal type 1 (anti-Lkm1) antibodies are characteristic of AIH

type 2. Soluble liver antigen/liver pancreas antigen (anti-SLA/LP)

are associated with AIH type 3.

If 's ALP and GGT are elevated, and if he does NOT have

ulcerative colitis or Crohn's disease, and no signs of autoimmune or

viral hepatitis, then the suspicion might be primary biliary

cirrhosis (PBC). PBC mostly affects women, but has been occassionally

found to occur in men. It affects the small bile ducts, and is rarely

associated with inflammatory bowel disease, and cannot be detected by

ERCP. PBC is characterized by elevated anti-mitochondrial antibodies

and so a simple AMA test using a blood sample can usually be used to

confirm or rule out PBC.

If the AMA test was negative, and since the ERCP's have not shown any

evidence of PSC, then the possibility would be small-duct PSC.

Suspiscion of PSC would be raised if ulcerative colitis or Crohn's

disease was present. But if small-duct PSC was in its early stages

and/or localized to only certain parts of the liver, then it might

not be readily detectable in a liver biopsy. Some centers are better

at detecting PSC in biopsies than others. In our son's case, one

center was unable to determine whether PSC was present in a liver

biospy sample, but when the sample was sent to Mayo Clinic,

Rochester, MN, they were able to detect PSC at stage 2.

I hope this helps?

Sorry but I don't have an answer for you on the white web casing over

the liver. This is a mystery to me.

Best regards,

Dave

(father of (23); PSC 07/03; UC 08/03)

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