Hypothesis on Vancomycin 'brand' differences for PSC effectiveness

The vanco treatment for PSC is not really comparable to c-diff. C-diff infections are in the colon (and not in the small intestine). Also, c-diff is extremly sensitive to vancomycin (in theory, 500mg/day of vanco is 1000 times more than what’s needed to kill 90% of c-diff). We don’t know which bacteria we’re trying to kill when we take vanco for PSC, so it’s hard to compare doses. Furthermore, most bacteria aren’t known by man, so that doesn’t make it easier.

Upon advice from those with extensive experience, we use ANI brand capsules, which have worked very well for my son.

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Fecal concentrations of vancomycin are typically two orders of magnitude higher than what one would expect in the blood from IV administration. Taken orally, all but the most resistant organisms are eliminated, to include gram negative bacteria and even fungi, such as some candida albicans. In fact, at the phylum level the most sweeping change in the vanco gut is the complete elimination of gram-negative Bacteroidetes.

The gut pathobionts study is interesting. The idea is that if you can fix the problem if you cut off at least one of the three highlighted bacteria. Vanco won’t touch the klebsiella or proteus, but would take out the VRE-light E. gallinarum. The big caveat is that this study involves Japanese adults, a group that is unique in the overall PSC population (ex. IBD is rare). I don’t believe we’ve seen E. gallinarum in other PSC studies (with at least one looking at the biliary microbiome). We do see other species of enterococci, so what if we expand the study hypothesis to the whole genus and roll with the idea that vanco works by killing problem bacteria to include particular enterococci. Vanco users normalize over a wide spectrum of dosage, with a fairly specific breakpoint unique to each individual (eg. 2000mg normalizes, while 1750 does not). Enterococci vary from species susceptible to vanco to those with a wide range of vancomycin resistance (VRE). I’ve taken gut microbiome tests and compared results with other patients and controls. I get away with a low dose and don’t have any detectable enterococci in my gut. One treated patient, who needed a high level of vancomycin to normalize, showed trace amounts of enterococci. Was this VRE? Would VRE explain why some patients need high doses and others are unable to get the treatment to work?

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That’s a solid discussion! The conclusion is that it’s too advanced for us normal folkes to fully understand (at least for me haha). :sweat_smile:

Indeed, thanks JTB, I’m taking that information in as another puzzle piece - in a puzzle us patients should not have to solving for ourselves. But here we are - many of us here are at just that (a hobby?). Its self preservation, I need to be able to hold ground on hypothetical technical medical arguments against my continued script for Vanco - from Doctors or insurers. I also do failure investigation as part of my profession - and this is another such - only my experience is science and research applied to metal and equipment failure, not medical/bio. For each its like assembling a puzzle to try to see the whole picture with no photo on the box and no chance of all the pieces out there - for vanco/psc, each piece is knowledge provided by others. The microbiome - and it having any extended role in physiology - is even relatively new interest to the medical community, so it presents a challenge (quite a zoo down there). Grateful for your research on this. If I want to help understand the cause and effect here, I can no longer avoid those papers!.

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You need to read this paper. It will explain some of your questions about brand issues. Also understand that there are 6 sources for the API (active pharmaceutical ingredient). We do not know exactly what has the efficacy for PSC – certainly if we had funding we could do a study. I actually have the former MD, PhD CEO of a pharma company interested in doing this study. Buness2020_Article_SuccessfulResponseOfPrimaryScl.pdf (1.3 MB)

here is a link that combines the 3 YouTube links you posted: Vancomycin for Primary Sclerosing Cholangitis (PSC) Roundtable: Featuring Dr. Cox and Dr. El-Youssef - YouTube

Actually the original Vancocin capsules had a solid inside and they still do. But they too may need to be opened. Opening the capsules increases bioavailability. We are speculating that some capsules dissolve at different pHs causing them to not dissolve in the “right” part of the GI tract. Studies need to confirm this but we need money to do so. So in the interim, I recommend opening the capsules.
see Buness2020_Article_SuccessfulResponseOfPrimaryScl.pdf (1.3 MB)

Let me know if you need more information.

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No it is not likely VRE. As you stated, we have found that patients vary on their dosing needs. May be because of different phenotypes.

awesome info, thanks!

Thanks! I have been opening up my son’s hard vanco capsules since reading the original post… But his doctor just sent in a prescription for oral vanco, so we’ll be switching that that within the next couple days. I will report back on how things pan out with his labs… so we can keep the information flowing.

what do you mean “hard vanco capsules?” I am only aware of capsules that are openable. Also anything taken by mouth is “oral.”

My son’s current Vanco capsules are very hard, as in they feel hard & have a glassy sound when tapped, and the vancomycin inside is in the form of a hard clump. It’s difficult to remove the capsule covering the half that contains the medicine. On the other hand, his previous brand of oral Vanco also came in a capsule form, but they contained the powder form of the medicine inside, and the capsules were softer, as you could squish them from the outside. Both are oral capsules. We will be switching to the liquid form shortly. Make sense?

That was a typo. I know what oral means… just meant to write liquid.

I am not aware of capsules that have a powder inside unless they were constituted by a specialty pharmacy.

Cheers Cactusgirl !

You are - on this forum as well - what I described above as ‘a very helpful poster’ :wink: .Thanks for the work you do in this area and bringing it to these media. And a nod to others as well. Shared knowledge is our power :+1:. And now I have some more reading to do…

:grin:Let me know if you want additional papers. I actually put that Roundtable together and filmed it.

Cynthia

NO KIDDING! as a ‘wake up and smell the coffee’ piece of evidence - for good and well meaning institutional physicians who are torn between oath of ‘do no harm’ and a feeble and hasty policy of having to sell ‘not enough evidence’ - that particular video is enormously powerful in my opinion. As I mentioned above in this thread, its compelling and undeniable when a handful of the biggest players in the published realm on Vanco/PSC (I suspect you were off camera, and I also recognised Dr. Tabibian) from irrefutable research institutions, sit in a room and you can evesdrop on a candid unscripted off-the-cuff discussion … witnessing the stark sincerity of the very human discussion of there independant clinical experiences, I think really helps to break down the last of the lame-ass excuses I’ve heard for refuting the existing literature . My plan was to send this to my Tx nurse, who will pass it on to the Hepatologists and I will insist they watch it, and I will check back to see (note, I bring them the latest in Vanco research hardcopy papers with every appointment - like a tradition of bring them the newpaper). These Docs have traditionally have had a line to tow but struggle to medically explain my remission (they do not support Vanco for PSC) - not their fault and I know its troubling them. (I’ll point out to them there’s a Canadian at the table that they might recognize and put in a call to). Its fun fighting the good fight, I smile through my appointments, them not so much :laughing:.

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Have we emailed before?

no, we haven’t communicated other than another thread on this site I recall.

…and to complicate things more:). It seems that Vanco has an immunomodulatory effect as well. People with PSC+IBD might need a much higher level of Treg (approx. 2x higher) not to experience the PSC+IBD symptoms.
Below, (from the AASLD meeting posted earlier),
image,

at 9 months off Vanco, when the symptoms came back, Treg/Teff was at the same level as the Healthy control group, whereas on 1 year on Vanco (no symptoms) this level was twice than the Healthy control group. Also to be noted: the immune markers of the pediatric participants were positive (p-ANCA etc) and they become negative after OV treatment.

A question might arise though: would all the PSC patients (with or without IBD; pediatric or adults) present themselves with positive immune markers? If not, how would the Treg graphs on Vanco look like in this case?