Thank you for your detailed response. I have had some urine work done already, and could provide some readings to it, but I didn't have significant protein in the urine, but that has varied on different tests. I'm sure you are referring to something more than what I have already had, though. What do you mean overtreat due to high value? High ANA or AMA? I assume I would begin Ursidol for the PBC, and then if overlap whatever treatment for that (meaning your comment on mild immunosuppressant therapy)?

I have an appointment with a gastroenterologist on March 18, since in my area liver specialists only are fairly rare. Do you suggest I see any other specialist?

Just one more question. My Igm was negative. I have read that almost everyone with PBC has a positive IGM. Is this something that would or could develop later? Also the SMA was negative. You also mentioned my LFT's were normal. My ALP is 500, not normal and my alt and ast are elevated (not over 2 x's though) Would IGM being negative mean anything? I know I will probably need a biopsy. I have an appointment with a specialist in a couple of weeks.

Hello! You mentioned you would like to see my liver biopsy results. I have those now. I am going to see my doctor tomorrow, but I would like another opinion before I see him. My biopsy says I have PBC with possible AIH overlap, though they can't determine that at this time without further testing. What I am confused about is the stage of my PBC. From what I am reading I think I know what the stage is, but not sure. the microscopic description is a follows.

H&E stained sections of the liver needle biopsy show preservation of the normal hepatic architecture. The needle core biopsies include parts approximately 31 portal tracts. The portal tracts show mild to moderate infiltration by lymphocytes along with a few plasma cells, neutrophils, and rare eosinophils. There are epitheloid granulomas in many of the portal tracts with some of the epithelioid granulomas occurring surround interlobular bile ducts. Interlobular bile ducts appear to absent in several of the portal tracts. Most of the portal tracts show mild interface hepatitis. There are scattered foci of lobular lymphocytic infilitration. Some of the lymphoctic infiltrates are associated with epitheliod hisiocytes or Kupffer cell proliferation. There are a few lobular epithelioid granulomas. There is no significant heptocelluar steatosis. No PAS positive diastase resistant intracytoplasmic globules are identified in PAS with diastase stained sections. There are rare sinusoidal PAS positive diastase resistant macrophages or Kupffer cells and a few PAS positive diastase resistant macrophages in several of the portal tracts. No hemosiderin is identified in hepatocytes of in Kupffer cells in section stained for iron. Reticulin stains show a normal pattern with plates of hepatocyts predominately a single cell in thickness. Trichrome stains show a focal portal and periportal fibrosis. No bridging fibrosis or cirrhosis is identified. Cytokeratin 7 stains show loss of interlobular or bile ducts in several portal tracts. Cytokeratin 7 stains highlight mild ductular proliferation in a few portal tracts. Cytokeratin 7 stains also show cytoplasmic and membranous staining of periportal hepatocytes around some but not all of the portal tracts consistent with chronic cholestasis. PAS with diastase, iron, trichrome, reticulin, and cytokeratin 7 controls stain appropriately.

I see my doctor at 1030 am EDT tomorrow, so if I could get an answer today that would be great.