UDCA is on the more water soluble side of the spectrum when it comes to bile acids. The more water soluble, the less potentially destructive these acids are when they are stuck in place, as with PSC cholestasis. The thought here is to flood the system with less destructive UDCA to cut down on damage. The problem is that UDCA, as with the human body’s natural primary bile acids, can be converted to secondary bile acids by bacteria in the gut. These secondary bile acids are less water soluble and more potentially destructive. At high doses of UDCA, the secondary bile acid LCA is elevated as well and this is potentially what is leading to poorer outcomes. Notably, LCA is not elevated at more moderate doses of UDCA.
Both UDCA and oral vancomycin are FDA approved. Neither are approved specifically for PSC, so they are prescribed off label for the treatment of PSC.
The best indicator we have right now at improved outcome is near-normalization of ALKP/GGT.
The method doesn’t appear to matter, whether by UDCA, vanco, or even happening spontaneously.
If you can get your ALKP to <1.5 x normal, you are significantly less likely to reach an end point (transplant, cancer, death). UDCA often improves but infrequently near-normalizes ALKP/GGT. Moderate doses of UDCA probably won’t hurt anything, but likely won’t help a whole lot unless your numbers are really good on the treatment. How has your imaging changed over the last 25 years?
Another data point:
I’m 21 years into my PSC diagnosis. I took high-dose UDCA briefly back when that was the style, though it didn’t move my numbers significantly. At year 12 I became very sick and started oral vancomycin. It normalized my numbers/symptoms and I’ve stayed this way the last 9 years.