This thread has been split from the Stanford Community Symposium 2018 thread. (Copied post) I watched Drs Fluge and Hanson with a rest between them. Utterly loving Dr Fluge’s talk where he moved between talk of the patients and the data. Didn’t understand a lot but someone?? talked of reducing carbs with benefits. I think it may have been Dr Fluge but he was not recommending it as a treatment because there was no data. I hope I’ve remembered that correctly. I’d like to hear Phair but that’s not till nearly midnight our time, so it may need to wait. If anyone hears it, please can you post something, a sentence or two. I shall look first thing in the morning. Eta: would also like to hear what Jared Younger has to say
They are only at the phase 2 open label trial stage. I think he said they are still assessing whether there is enough evidence to warrant going on to a full sized double blind trial.
The livestream recording of the whole Stanford community symposium is here. Oystein Fluge's talk starts at around the 37 minute mark. I believe the link will be removed once the separate Youtube videos are posted.
These are my notes from the first part of Oystein Fluge's talk covering the clinical trials. I need some more energy before tackling the part of the talk covering the lab work. It was encouraging to hear him say that the symposium had been very useful. The Norwegian group are collaborating with many researchers. They are combining clinical trials with lab work on the samples in their biobank. (As we know), the latest cyclophosphamide and rituximab clinical trials haven't been published yet. Cyclophosphamide Fluge noted that since 2004 8 patients with ME independently reported benefit from chemotherapy treatment. 7 of these had cyclophosphamide and 1 had iphosphamide. I felt that he may have been pointing out that the evidence for a response from cyclophosphamide has been there all along (whereas this kind of evidence was not so strong for rituximab). The cyclophosphamide trial is a Phase 2 open label study, 40 patients who have been followed for 30 months now. They can't give details yet. They don't know if it is the cytotoxic or immune modulatory properties of the drug that might be helping. Patients experienced quite a bit of discomfort, especially in the first 6 months. Rituximab Fluge talked about the Phase 2 trial results. The patients have been followed for 3 years now. There have been 14 major responders, 4 moderate responders and 10 non-responders. Gains have been maintained from the 6 infusions in the first 15 months. Problems with an open label trial with self-reported endpoints was noted. Was there something special about the people they put on this trial (a selection bias) that made this trial appear to find responders? Was it just the fluctuations of the disease? A placebo response is possible, but Fluge commented that having no response for the first 3 to 4 months makes it a very unusual placebo response. Fluge showed the results of the Phase 2 trial (screenshot below), and they do seem to indicate some people are responders - there is a low variability around each parameter once the participants are divided into the three groups and a very nice holding of gains in the major responder group. Details of the Phase 3 trial (151 patients) can't be given as the study hasn't been published yet. Disclaimer - I haven't double checked this, may well be errors.
If anyone wants to download it as a full talk here is the link http://pd vod.new.livestream.com/events/00000000007ec67b/cb7b1b79-beb9-44f8-a3a6-38a49863d19f_2128.mp4 It is 7.1GB
I have been wondering for some time - so just in case this might be relevant: I know from people with RA and MS treated with Rituximab that they get high dose cortisone and antihistamines immediately prior to the Rituximab infusion to reduce the risk of severe side effects. Does anybody know whether the participants of the Norwegian trials also got cortisone? And if they got, could this have any relevance, e.g. that some of the "responders" of the first trial phases benefited rather from the high dose cortisone than from Rituximab?
I get subcutaneous IGG (obviously not rituximab), and due to (well-known) side effects I took cortisone before the infusion, too. I realized combining that with anti-histamines works even better, and it seems to me, this time improvements set in faster than last time. So I find your remark quite interesting and I am curious to know, too. Edit: I didn't take cortisone with every infusion, only at the beginning. After some time, there were no side effects anymore, and I took the IGG alone. I still had improvements.
Thank you, @Inara . How high was the cortisone dosage you got? It still seems interesting to me to know the dosage the trial participants got. When I was suspected to have MS and got high dose cortisone, my neurologist tried to explain something about the blood-/brain barrier. I didn't understand this but among severel aspects the following seemed to be relevant: When the blood-/brain-barrier is not intact due to inflammation, cortisone will "shut" this barrier, but a certain, very high dosage is needed (and this only for 3 -5 days). I did not understand why other desired effects on the brain also would need a very high dosage and how high this dosage had to be. For my mobility related impairments, 1000mg methlyprednisolone/ day already showed clear improvement on the following day. I will write about my experience with high dose cortisone someday, but the story why and how I got this treatment (and continue to get it) contains so much weirdness that I don't know how to write it up without loosing trustworthiness. Perhaps we would benefit from a *good* neurologist considering all those aspects? Edit: In addition, as far as I know cortisone has a huge effect on metabolism. Even though I have no idea about the biomedical details, and don't know whether there might be some plausibility to the hypothesis that we just have to find the adequate substance to wake up from a hibernation-like state, with this regard, high dose cortisone might also have an effect? [Edited for clarity.] Edit: 1) Link to Andy's reply on an other thread: https://www.s4me.info/threads/me-conferences-in-sweden-oct-17th-and-18th.5436/page-2#post-112978 2) It's obvious from my other forum posts that my cognitive problems and other symptoms typical for ME haven't substantially improved with high dose cortisone until now. So I refrained from writing more about my cortisone story.
At the beginning it was 75mg Prednisone once or twice. Since I didn't feel too good with it, I reduced it to 50mg once or twice. I had to do this for ca. 3 months, with the higher dosage a bit longer. Now, 20-30mg of hydrocortisone are enough to help. (But at the very beginning, it had to be prednisone.) Oh, this "shutting" of the blood-brain-barrier with cortisone is interesting - one possible side effect of Igg is aseptic meningitis. Maybe that can happen if the blood-brain-barrier doesn't function 100%? What did your doctor say the dosage has to be? Cortisol certainly has an effect on metabolism. One of the better known effects is maybe the one on calcium metabolism.
(from the other thread - hope it's ok to quote it here) Indeed, I think this renders all my thinking with regrad to cortisone irrelevant.... Edit: But I didn't want to amputate Andy's reply, so here's the rest:
250 mg Prednisone or 40 mg Dexamethasone/ day for 3-5 days. (Standard dosage for MS is 1000 mg Methylprednislolone/day for 3-5 days). Interesting.
