Do Normal LFTs = PSC Remission?

Hi - My daughter is 16 and was diagnosed with PSC on the basis of elevated LFTs and a livery biopsy when she was 10. She also has mild UC. Over the past 5 years, her LFTs have been mostly within normal ranges with a few exceptions (mostly associated with stressful times at school). Does anyone know if normal LFTs is the same thing as having the disease “under control” or can PSC-related liver damage be taking place even though all LFTS are measuring normal? Thanks so much for your help!

Eric

Eric,
What form of PSC was your daughter diagnosed with? Large-duct PSC which is the most common, cannot be diagnosed by liver biopsy alone. You may want to consult with a hepatologist and have them do an MRCP which is an MRI of the liver and surrounding abdominal organs. This will give a more conclusive diagnosis of PSC when they can seeing narrowing of the ducts, beading, etc. I’m doubtful that biopsy alone can give you a full and total picture. I know that small-duct psc is localized to the smaller ducts of the actual liver itself and this may be what the biopsy revealed. Still I think imaging should be done to rule things out.
That being said, if she is conclusively diagnosed with PSC having normal LFT’s at this point may be an indication the disease is progressing very slowly, which is a good thing. My LFT’s would be way high and then I’d have an ERCP to clean out the hepatic and common bile ducts and then my numbers would normalize for a good long season. Things would then repeat and as I grew worse normalization was not possible.
I hope this helps, but I’d certainly inquire about getting that MRI, especially after 5 years just to be sure of where things stand. I’m glad to hear she is doing well.

Mark

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Thanks Mark! I believe she was diagnosed with the most common form. We have had 2 MRIs…one about 5 years ago that couldn’t detect any signs of PSC and one just a month ago that showed mild dilation of the intrahepatic ducts (up to 5mm) and common bile duct (7mm) along with mild hepatomelagy (17.7cm) and prominent peripancreatic lymph nodes. We’re not sure if the more recent MRI suggests disease progress or if the first MRI was just lower resolution as the technology seems to be improving quickly. In any event, do those more recent impressions mean anything to you? If we feel certain that she does have PSC then I am very inclined to pursue the Vanco treatment. Interestingly, this entire “ordeal” began with a massive c-diff infection when she was 10 years old and I’m suspicious that there is a connection between the c-diff and PSC/US in some patients. Thanks again!

Eric,
I’m going to send you a private message with some thoughts on the subject.

Mark

Hi Eric! Diseases act differently and PSC isn’t like UC. PSC doesn’t have remissions or flare ups. PSC is always ongoing (but it’s impossible to actually tell how much permanent liver damage that is happening). Some people refer to bacterial cholangitis as “flare ups”, but they are not actual flare ups. :slightly_smiling_face:

Hi Eric,

There is a connection between a dysbiotic gut and PSC. There is an interesting recent paper: “Gut pathobionts underlie intestinal barrier dysfunction and liver T helper 17 cell immune response in primary sclerosing cholangitis” by Nakamoto et.al. Basically, the findings of this paper are consistent with Ken Cox’s findings in his 2012 paper in which he found that vancomycin caused an increase in Treg cells and works as an immunomodulator.

Nakamoto et.al. found that Th17 promotes hepatobiliary injury. Th17 was induced by a cooperative mix of 3 bacteria, all 3 of which are necessary to cause Th17 induction. One of these bacteria is sensitive to vancomcyin. Vancomycin treatment thus decreased the Th17 response suggesting that therapeutic treatment of PSC is feasible. The induction of Th17 cells inhibits Treg cells, so Dr. Cox’s finding that Treg cells increased is consistent with the Nakamoto findings that vancomycin stopped the induction of Th17 cells.

Hope this makes sense.

Patients who have PSC and UC have one disease. When my daughter’s stools are not normal, we find that her liver enzymes are elevated.

That’s not actually true. PSC and UC are two completely separate diseases and they don’t affect each other.Just because your UC gets worse doesn’t mean that your PSC does so too. The reason for why the LFT’s go up when you have an UC flare up is because the same liver enzymes also exist in the gut.

For example, ALP exist in ALL tissues in the body, but is mostly concentrated in the liver, bile ducts, bones, intestines, bones and kidneys. An inflammation in any of these organs might cause elevated ALP. :slight_smile:

PSC and UC are not completely separate diseases. You should read these papers —

…[T]he strong comorbidity between primary sclerosing cholangitis and inflammatory bowel disease is likely the result of a unique disease, which is genetically distinct from classical inflammatory bowel disease phenotypes…At present, our findings are most consistent with the hypothesis that PSC-IBD is a unique disease that shares some genetic factors with ulcerative colitis but is distinct from classical IBD phenotypes4,34. This hypothesis is further supported by the observa- tion that PSC-IBD shows clinical differences from classical IBD and requires specialized management; in comparison to IBD, PSC-IBD has a higher rate of pancolitis with ileitis and rectal sparing, as well as a higher incidence of colorectal cancer. https://www.ncbi.nlm.nih.gov/pubmed/26974007

“Analysis of five chronic inflammatory diseases identifies new associations and highlights disease-specific patterns at shared loci”
by Ellinghaus et. al

“Distinct gut microbiota profiles in patients with primary sclerosing cholangitis and ulcerative colitis” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5504370/

by Lukas Bajer, Miloslav Kverka, Martin Kostovcik, Peter Macinga, Jiri Dvorak, Zuzana Stehlikova, Jan Brezina, Pavel Wohl, Julius Spicak, Pavel Drastich

I think I need to step in here on this conversation. This discussion is not helpful to the original posters question. We can give our opinions and we are fine with sharing medical journal findings, but we are not doctors here on this forum and our opinions in serving one another here are based on our life experiences with PSC and UC. We must each seek the advice of our hepatologists and make the decision that is best for us individually. I too find it troubling to state that the two are one disease as well, but again that is my opinion on the matter but we must not have this back and forth conversation. If we need to get into something deeper between one another take it to a private message.

Thanks,

Mark Wilson, Moderator

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FYI, my post is an exact quote from a paper in a medical journal. I edited my post to add the link to the paper.

It’s not so much the article you shared but the tone of the conversation between you and the other poster. We just need to avoid any type of argumentative discussion. It helps no one, and keep in mind, not everything you read in articles even from medical journals are conclusive or accurate. I think instead of stating “that’s not actually true” or “you are actually incorrect”, I think a calmer approach to something two might disagree with would be something along these lines. “It may be worth reading this article and consider what these doctors came up with. It may be a help in understanding the correlation between psc and uc.” This approach doesn’t put the original poster on defense, but gives them a second opinion on what may be the problem or something they had not considered. Remember this is a peer to peer forum and we are not to present ourselves as medical experts, that’s what we go to our doctors for. I hope this helps explain our concerns a little better.

Mark

Your daughters symptoms mimic mine in many ways. I don’t have hepatomelagy and my ALP stays now mildly elevated. AST and ALT both ok normal range for last couple of years. My CBD went to 10mm for a couple years and now I think back at 6. But now my hepatic duct is dilated to 9mm. I have mild beading in my right and left hepatic ducts, not in my CBD. I don’t have UC, but I had a wild bout of IBS 2015-Q1 2016. Came on and stopped.

I asked my hepatologist about the ducts changing as they have. Her Response: “Things are stable. With PSC, we will see changes in the bile duct caliber even without any procedures or progression
But over all your bile ducts look stable”

So although my ALP is slightly elevated due to beading (schlerosing), overall the disease itself is quiet. But I also know my disease is still at work. How I feel is what is most important to me. I too find that stress is a huge trigger. For me I believe I can become more symptomatic due to stress. I also believe that the insane stress I was under in 2014… is what triggered it’s awakening. I felt pretty crummy for 3-4 years before diagnosis, Jan. 2018. During those 3-4 years my LFT’s remained normal.

PSC presents so differently for everyone. I have D3 and B12 issues which we find coordinate with having PSC. Energy is everything. I am fortunate to have a forward thinking ND. I’ve never seen much of a consistent pattern of what remission means. Overall, I think your daughter is doing well. And you are right on top of the details that help all of us try to make more sense out of PSC.

I’m sorry too, I’m still not fully on board 2.5 years later. Your Warrior is not alone. :slight_smile:

Jennifer