A Chronic Fatigue Syndrome/POTS Patient Responds to a Multiple Sclerosis Drug - What Does It Mean?

KME

Member
Thanks so much @Cort and @Rachel Riggs for sharing this story. (I don't think I'm doing this @ thing right but I'm sure I'll figure it out some day!) It’s hard to summarise such a complex story – you make it look easy, Cort! Rachel, wow, you’ve been through the mill. Sorry you’ve had such a rocky road.

I was fascinated on many levels, including similarities in our stories, but especially the B-cell altering nature of copaxone as a possible explanation for its dramatic effect in you. Last year I read an account of one of the people in Fluge and Melle’s rituximab trial in Norway who had had a major response, i.e. basically recovered. I was struck by how similar her description of how her major response started was to an experience I had for a couple of weeks in 2013. I was on week 9 of a tetracycline antibiotic (same family as doxycycline) when I started getting these brighter windows. Not a big change but a very significant one for me – less brain fog, a little more stamina. This continued for a couple of weeks but I stopped the antibiotic after 12 weeks (as the non-ME issue it was prescribed for had resolved) and two medical appointments then finished me off. At the time I had attributed these brighter windows to starting thyroid meds, but in hindsight this wasn’t the case: the brighter windows started just a week into a very low dose of thyroid meds, and I’ve continued to deteriorate over time despite remaining on thyroid meds and increasing dose.

Guess what my pharmacist figured out? Tetracylines, like doxycycline, have B-cell depleting effects. http://m.intimm.oxfordjournals.org/content/13/7/921.full The delayed response (i.e. starting in week 9 of the antibiotic) would match up with the delayed response seen in ME/CFS responders to rituximab.

I saw that @Issie saw benefits with 3 years of doxycycline.

Gulp. Might long-term tetracycline antibiotics be able to modulate our immune systems? Might people with chronic Lyme disease who benefit from doxycycline be benefitting from B-cell depletion as well as or instead of antibiotic action?

Has anyone been on long-term subantimicrobial doses of doxycycline (maybe for periodontitis or rosacea) and noticed an improvement in their ME/CFS and/or POTS or orthostatic intolerance?

@Rachel Riggs, you might like these posts by a blogger who has both ME and POTS if you haven’t come across them already.
https://tipsforme.wordpress.com/2014/10/18/am-i-pots-or-is-it-just-me/
https://tipsforme.wordpress.com/2015/04/29/i-am-pots-but-whats-me/

Would be fascinated to hear more stories like this about accidental improvements on immunomodulating meds.
 
Can you or she be more descriptive about this? I'm interested in what this might mean? So the lesions where there initially, went away, and then came back?

GG
When I checked one of the price comparison sites for the MS drug and it's generic equivalent, the price ranged from $1,800. to over $5,200. Yikes, no wonder the insurance companies don't want to pay for it. When I hear the word 'immune' being used in an article, I get a bit confused. I tend to think of 'immune' system as the thing that keeps me from catching a cold or flu or 'autoimmune' which, after so many different tests I don't test positive for on any level. I did have a huge problem in the beginning of my ME/CFS (14 years ago) with numerous virus' but over time that seems to not be an issue. Nor, do I have any typical joint 'inflammation'. So using the term 'immune' when talking about the reduction or cessation of all the overwhelming neurological symptoms of ME/CFS
disease and the disabling fatigue is confusing to me. Do they think these drugs work because one of the root issues is inflammation IN the nerves themselves? Anyone have an explanation in layman's terms I can wrap my addled brain around?
 

KME

Member
When I checked one of the price comparison sites for the MS drug and it's generic equivalent, the price ranged from $1,800. to over $5,200. Yikes, no wonder the insurance companies don't want to pay for it. When I hear the word 'immune' being used in an article, I get a bit confused. I tend to think of 'immune' system as the thing that keeps me from catching a cold or flu or 'autoimmune' which, after so many different tests I don't test positive for on any level. I did have a huge problem in the beginning of my ME/CFS (14 years ago) with numerous virus' but over time that seems to not be an issue. Nor, do I have any typical joint 'inflammation'. So using the term 'immune' when talking about the reduction or cessation of all the overwhelming neurological symptoms of ME/CFS
disease and the disabling fatigue is confusing to me. Do they think these drugs work because one of the root issues is inflammation IN the nerves themselves? Anyone have an explanation in layman's terms I can wrap my addled brain around?
@Stephanie ‘Stevie’ Stultz I think it is confusing – because we don’t understand what exactly is causing the immune problems in ME/CFS just yet. But we do know that the immune system is involved. We know that most (but by no means all) people’s ME/CFS is triggered by an infection, i.e. an insult to the immune system. We know that people’s immune systems get dysregulated/become dysfunctional, with some immune markers being upregulated and some downregulated, and that this changes over time. We know that some immune markers change when we do exercise. So you could think of post-exertional malaise as an immune reaction that manifests as fatigue, pain etc. In the same way, the fatigue normal people experience with flu, as in real flu with crushing, go-to-bed fatigue, is an immune response to the influenza virus. That fatigue tells you your immune system is activated, on it.

And we know that there are a number of features of ME/CFS that make it look very like autoimmune diseases, e.g. more females than males, familial patterns. The most convincing suggestion that ME/CFS is autoimmune is probably that we seem to react to immunomodulatory drugs the way people with autoimmune diseases do – this is what the initial rituximab research suggests.

This kind of reasoning backwards is really common in medicine. For example, a neurologist might think that a person might have Parkinson’s Disease but not be quite sure as in the early stages they won’t tick all the boxes. It can all look quite murky at the beginning of neurological disease, as Rachel’s story shows. So the neurologist might put the patient on levodopa, a Parkinson’s drug. If they respond, then that’s taken as confirmation that they have Parkinson’s. (If they don’t, they might still have Parkinson’s, and time will tell, so like Rachel going back for all those MRIs, this person will keep coming back until the pattern becomes clearer or symptoms resolve or are explained by another diagnosis.)

The reason you’re not testing positive for autoimmune disease is that those tests are looking for the markers that have been identified for other autoimmune diseases, e.g. for the antibodies common in people with Sjogren’s, or coeliac disease, or rheumatoid arthritis. But not everybody with autoimmune disease has antibodies. It may be that in the future we will find antibodies that are specific to ME/CFS, in which case finding those antibodies in your blood would confirm the diagnosis of ME/CFS alongside clinical picture and other biomarkers we may come up with. Some antibodies that are very specific for a particular autoimmune disease can confirm a diagnosis, but not having the antibodies doesn’t mean you don’t have the disease. They’re only a part of the picture.

Similarly you could have a brain MRI or EEG and be told that you’ve no evidence of inflammation in your brain. What they’re looking for there is something big and obvious like a frank encephalitis, i.e. a visibly significantly swollen brain. What we may be talking about in ME is a different kind of inflammation that we need different tools to measure e.g. SPECT.

So normal tests don’t mean there’s nothing wrong with you. They just mean you probably don’t have the diseases that we understand a lot better. Hopefully the research like the NIH study and Ron Davis’s study will point out where in the immune system our issue lies, and then there’ll be biomarkers and treatments and all kinds of fun stuff.

Did that make any sense? Hope so!
 

Ken Shield

New Member
Hi there - Rach here! :)

I first became sick in 2003 and received a diagnosis of MS in December 2009.

I had very few - maybe only one - lesion on my brain and it eventually went away. BTW - there is no definitive diagnosis for MS - just as with ME/CFS. There are a few more tools involved such as MRI's and spinal taps. Yet MS is treated as a legit disease, while ME/CFS is not....

As for the reactive hypoglycemia - I believe it's related to the lack of GI motility that can result from POTS. And also, as the newest criteria for a CFS diagnosis includes orthostatic intolerance - I feel it's safe to say CFS and POTS are either one and the same - or at least go hand in hand.
Hi there - Rach here! :)

I first became sick in 2003 and received a diagnosis of MS in December 2009.

I had very few - maybe only one - lesion on my brain and it eventually went away. BTW - there is no definitive diagnosis for MS - just as with ME/CFS. There are a few more tools involved such as MRI's and spinal taps. Yet MS is treated as a legit disease, while ME/CFS is not....

As for the reactive hypoglycemia - I believe it's related to the lack of GI motility that can result from POTS. And also, as the newest criteria for a CFS diagnosis includes orthostatic intolerance - I feel it's safe to say CFS and POTS are either one and the same - or at least go hand in hand.
Thanks for sharing your story. Do you recall any relief from the numbness, tingling, and/or burning sensation in your feet during the 6 weeks?
 
@Stephanie ‘Stevie’ Stultz I think it is confusing – because we don’t understand what exactly is causing the immune problems in ME/CFS just yet. But we do know that the immune system is involved. We know that most (but by no means all) people’s ME/CFS is triggered by an infection, i.e. an insult to the immune system. We know that people’s immune systems get dysregulated/become dysfunctional, with some immune markers being upregulated and some downregulated, and that this changes over time. We know that some immune markers change when we do exercise. So you could think of post-exertional malaise as an immune reaction that manifests as fatigue, pain etc. In the same way, the fatigue normal people experience with flu, as in real flu with crushing, go-to-bed fatigue, is an immune response to the influenza virus. That fatigue tells you your immune system is activated, on it.

And we know that there are a number of features of ME/CFS that make it look very like autoimmune diseases, e.g. more females than males, familial patterns. The most convincing suggestion that ME/CFS is autoimmune is probably that we seem to react to immunomodulatory drugs the way people with autoimmune diseases do – this is what the initial rituximab research suggests.

This kind of reasoning backwards is really common in medicine. For example, a neurologist might think that a person might have Parkinson’s Disease but not be quite sure as in the early stages they won’t tick all the boxes. It can all look quite murky at the beginning of neurological disease, as Rachel’s story shows. So the neurologist might put the patient on levodopa, a Parkinson’s drug. If they respond, then that’s taken as confirmation that they have Parkinson’s. (If they don’t, they might still have Parkinson’s, and time will tell, so like Rachel going back for all those MRIs, this person will keep coming back until the pattern becomes clearer or symptoms resolve or are explained by another diagnosis.)

The reason you’re not testing positive for autoimmune disease is that those tests are looking for the markers that have been identified for other autoimmune diseases, e.g. for the antibodies common in people with Sjogren’s, or coeliac disease, or rheumatoid arthritis. But not everybody with autoimmune disease has antibodies. It may be that in the future we will find antibodies that are specific to ME/CFS, in which case finding those antibodies in your blood would confirm the diagnosis of ME/CFS alongside clinical picture and other biomarkers we may come up with. Some antibodies that are very specific for a particular autoimmune disease can confirm a diagnosis, but not having the antibodies doesn’t mean you don’t have the disease. They’re only a part of the picture.

Similarly you could have a brain MRI or EEG and be told that you’ve no evidence of inflammation in your brain. What they’re looking for there is something big and obvious like a frank encephalitis, i.e. a visibly significantly swollen brain. What we may be talking about in ME is a different kind of inflammation that we need different tools to measure e.g. SPECT.

So normal tests don’t mean there’s nothing wrong with you. They just mean you probably don’t have the diseases that we understand a lot better. Hopefully the research like the NIH study and Ron Davis’s study will point out where in the immune system our issue lies, and then there’ll be biomarkers and treatments and all kinds of fun stuff.

Did that make any sense? Hope so!
@KME What a great explanation. Thanks SO, SO much for taking the time to reply!! It made a lot of sense. When I think back to my early years with ME/CFS I recall that in several of the MRI's I had, the comments on the reports were "small, unexplained lesions in brain". There was no other follow up or comments by the doctors other than to say I didn't have MS. I saw 6 different Neurologists during that period, each one more dismissive than the previous one......It was maddening. The only other time I had 'antibodies' was when I was fighting Candida for about 2 years. In the beginning I tested positive for "Candida antibodies" and then later after going through a strict protocol it was at zero. And someone mentioned protozoas in this thread. I took 15 drops of Oil of Oregano (I put them in empty capsules) 3 x day for 6 weeks and was completely rid of a protozoa called Blastocytis Hominus. And, yes my ME/CFS was triggered by a virus, coupled with a near catastrophic reaction to Synthroid (because my adrenals were failing) and severe POTS. So, in that regard I'm a pretty typical patient.
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member

Some answers may be found in this lecture by Dr. Anne Louise Oaklander of Harvard and Mass General Hospital. Her work on Small Fiber Polyneuropathy shows how extensive the effects are from this type of nerve damage, which until recently was not studied, even though non-myelinated nerves are nearly everywhere and may make up over 80% of an axon which includes a myelinated fiber. POTS, autonomic dysfunction of every kind, aching, fatigue, cognitive issues, weakness light sensitivity, GI symptoms and most of the other symptoms of ME can be caused by this type of neuropathy. That is my memory of what she said. The effects of small fiber neuropathy go far beyond the conventional idea of numbness or burning in the feet. These nerve fibers are supposed to regulate blood vessels and service organs and tissues all over. When they do not, the affected organs and tissues cannot work properly. The causes for this type of nerve damage can be autoimmune illnesses, toxic exposure and many other known and unknown factors. She speculated that osteoarthritis too could get off to an early start with this type of nerve damage. Two effective treatments she referred to were corticosteroids and IVIG, but I expect others are applicable too.

Cort, it would be wonderful if you contacted her for an interview and shared some of our information too. She seems to be a pioneer, making discoveries which could be very useful to us.
I agree Cecelia. She is definitely a pioneer. I've covered hers and others studies in some blogs http://www.cortjohnson.org/?s=small+fiber+ and hope to interview her at some point. SFN is a fascinating topic!
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
I thought one of the keys to diagnosing fibro was that there supposedly was no inflamation? I'd appreciate if they'd make up their minds lol
Right not much swelling and few indicators of traditional inflammation but Montoya said what constitutes inflammation is changing as they find out more about the immune system...so it could be another kind of inflammation I suppose.
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
We figured out my POTS episodes are tied into my electrolyte balance, at first we thought it was just simple dehydration, because I have 2 doctors thinking maybe I am a low blood quantity creature. But if I drink a couple Gatorades my BP comes right up. And on the Pure Formula, vitamin site, Dr Ben has a "Ade" recipe for people like us. The ingredients are expensive because they come in bulk sizes so I am sure you can get them of great quality of other places reasonably. I know I will be checking Amazon.


. Is my body now mimicking pseudo CFS, if I go out and about have a good busy day, I will wake glands swollen, sore throat and so tired I can't get out of bed and sleep for a couple days. This started after a bad sore throat, glands swollen, armpits swollen and spleen tender. That lasted 10 weeks. They of course tested for Mono and Epstein Barr, both negative. But now pops up every time I overdue. I am the best hypochondriac in the world, I can make my glands swell, my pores bleed, and kidneys fail. Oh and BP drop to 60/40 or so low it won't register YOU get fast Service in ER then!
Interesting. They do say that POTS like ME/CFS is very variable. There are different kinds and it can be caused in quite a few ways. There is also the autoimmune subset of POTS patients where antibodies are attacking the receptors that control heart rate if I remember correctly.
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
Hey I'm not sure how your body would do with a little wellbutrin but if you can't get the naltrexone any other way you might beable to get contrave, 80mg welbutrin, 8 mg naltrexone and split it up. Some people have some more energy from wellbutrin but on label it is a atypical antidepressant, tho at that small of a dose its used for mild weight loss, energy, and sexual side effect reversal for other meds. Just a possibility to consider if you can't get the naltrexone any other way!


I gotta say I am very interested in hearing about this researcher's work as well. I have heard small fiver neuropathy is a possiblity for fibro too, I wonder if damage is being done there in all neuroimmune disorders?
About 40% of FM patients tested thus far have it.

Check out
and HR's Small Fiber Neuropathy Resource Page -
 

Rachel Riggs

Well-Known Member
Thanks for sharing your story. Do you recall any relief from the numbness, tingling, and/or burning sensation in your feet during the 6 weeks?
@Ken Shield I didn't, unfortunately. I noticed a dramatic improvement in my fatigue. But almost as soon as I was able to tie this improvement directly to Copaxone, I had the allergic reaction. It was so dramatic and I was so desperate to continue taking it that I even went to an allergist to confirm my allergy. It might have been a one time thing. But he did the standard skin tests and found me to be quite allergic. I have developed many allergies in recent years since I've been sick. I'm now allergic to penicillin and ginger - plus its relatives like turmeric.
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
I have this, I was in her study. I have done other studies in the Boston area, trying to advance the science!

GG
Good man! Is she doing anything else now that you know of?

Did you have SFN?
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
Thanks so much @Cort and @Rachel Riggs for sharing this story. (I don't think I'm doing this @ thing right but I'm sure I'll figure it out some day!) It’s hard to summarise such a complex story – you make it look easy, Cort! Rachel, wow, you’ve been through the mill. Sorry you’ve had such a rocky road.

I was fascinated on many levels, including similarities in our stories, but especially the B-cell altering nature of copaxone as a possible explanation for its dramatic effect in you. Last year I read an account of one of the people in Fluge and Melle’s rituximab trial in Norway who had had a major response, i.e. basically recovered. I was struck by how similar her description of how her major response started was to an experience I had for a couple of weeks in 2013. I was on week 9 of a tetracycline antibiotic (same family as doxycycline) when I started getting these brighter windows. Not a big change but a very significant one for me – less brain fog, a little more stamina. This continued for a couple of weeks but I stopped the antibiotic after 12 weeks (as the non-ME issue it was prescribed for had resolved) and two medical appointments then finished me off. At the time I had attributed these brighter windows to starting thyroid meds, but in hindsight this wasn’t the case: the brighter windows started just a week into a very low dose of thyroid meds, and I’ve continued to deteriorate over time despite remaining on thyroid meds and increasing dose.

Guess what my pharmacist figured out? Tetracylines, like doxycycline, have B-cell depleting effects. http://m.intimm.oxfordjournals.org/content/13/7/921.full The delayed response (i.e. starting in week 9 of the antibiotic) would match up with the delayed response seen in ME/CFS responders to rituximab.

I saw that @Issie saw benefits with 3 years of doxycycline.

Gulp. Might long-term tetracycline antibiotics be able to modulate our immune systems? Might people with chronic Lyme disease who benefit from doxycycline be benefitting from B-cell depletion as well as or instead of antibiotic action?

Has anyone been on long-term subantimicrobial doses of doxycycline (maybe for periodontitis or rosacea) and noticed an improvement in their ME/CFS and/or POTS or orthostatic intolerance?

@Rachel Riggs, you might like these posts by a blogger who has both ME and POTS if you haven’t come across them already.
https://tipsforme.wordpress.com/2014/10/18/am-i-pots-or-is-it-just-me/
https://tipsforme.wordpress.com/2015/04/29/i-am-pots-but-whats-me/

Would be fascinated to hear more stories like this about accidental improvements on immunomodulating meds.
Boy is that an interesting time-line......

Just to thicken the plot a bit more - Tetracycline antibiotics are also microglia inhibitors
 

GG

Well-Known Member
Good man! Is she doing anything else now that you know of?

Did you have SFN?
I wasn't clear, yeah, they diagnosed me with SFPN. did a tilt table test, which I passed at the time, but think I might not now. Having issues with my blood pressure, running high. No, nothing else going on that I know of.

I was looking to travel to DC area to be part of Dr Barniuk's study with the exercise, but I am stuck in a limbo while applying for disability now. Going to have to go see Drs for that, and not sure I have a solid ride for back and forth. Hope they recruited all the ME/CFIDS/CFSers they needed!

GG

Edit: Part of the reason I wanted to do the Barniuk study is I did the CPET test in 2010, so would be interested to see if things have changed in that area.
 
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Who Me?

Well-Known Member
I know someone had huge relief using a form of B bento something or other. Doctor's Best has it. She said it relieved a lot of her pain and numbness.
 

ShyestofFlies

Well-Known Member
thanks for the info above, never heard this before. Are you talking about 2 different drugs above? I was taking 4.5mg of compounded Naltrexone. So sounds like if it's a tablet I could split it in half perhaps? Would you take another antidepressant at bed? I currently take Remeron for sleep, but am getting to the top dosage (60mgs) practically every night now! So might need to find a new sleep med, maybe go back to trazadone, but Remeron was much better for me!

My Dr had me on Cymbalta (low serotonin), but I came off it, didn't feel it was helping my pain much anymore, but that has been months!

My Drs response verbatim, except for his name in regards to getting 50 mg dosage: "Dr said all the studies he know are based on the formulation he uses. He’s not comfortable with this, and doesn’t know how accurate this would be due to fillers." Comfortable is another word for NO! FYI Thought he was open to idea, but it's a no.

GG
Contrave is the name of the drug I mentioned: it is a compound of 80mg wellbutrin the antidepressant and 8 mg naltrexone. Naltrexone is usually used at doses 50+ for addiction. Contrave is a weight loss drug, if you are under weight or anorexic/afflicted with an eating disorder it would not be advisable to even consider.

I brought it up as an alternative to research more into for those who cannot get naltrexone any other way or who are not comfortable dealing with overseas pharmacies or measuring out their own dosage. If you happen to be overweight, have depression, and have cfs symptoms like I do it might be worth asking your doctor about. My theory was you just cut one of the 80w/8n in half and you basically have a very very mild dose of wellbutrin and about 4mg ldn.

From what I can tell the only contraindications are these:
  • Currently taking an MAOI or have taken an MAOI in the last 14 days
As far as I know, these are no more extreme than taking naltrexone and wellbutrin seperately.
The opiod part is from the naltrexone.
The bulimia/anorexia is for both parts of contrave as it is a weight loss drug primary approval by the FDA.
The maoi is from any anti depressant and most drugs... maois are pretty hardcore in terms of interactions so I can't imagine many cfs/me patients would use them anyway.

I'm not honestly sure what if any effect the wellbutrin part of this drug would have on sleep, wellbutrin for me worked very well for somethings like reversing sexual side effects of ssris and combating the weight gain I had from taking Abilify. Wellbutrin has been known to increase energy levels in some patients and is used as a booster compliment med to ssris or stand alone as what is called an atypical antidepressant.

I have taken Wellbutrin successfully, but those who have medication sensitivities, bad interactions with anti depressants, etc. obviously should not try to go on this med with or without a doctors approval.

When I started taking it I was on 100, 200, then 300 mg. It was the most successful of the ADs I have tried, in that it relieved the side effects from Zoloft, and provided the benefit of weight loss and possibly helped with my depression anxiety and other mental health issues. But alone it would not be able to be my primary anti depressant.

It does not relieve pain as far as I know like cymbalta and other SNRIs can possibly do. For me SNRI's have never relieved any pain, and in fact often make it worse by adding the lovely withdrawl side effect of brain shocks, but I know some people are greatly helped and swear by them.

Anyway I mentioned it simply as something to look into if you have no other way to get doctor observed naltrexone. I'm curious @Who Me? What indicates this drug would be unsafe for everyone?
 

Katie

Active Member
Many people, especially as they get older do get white areas on their brain that can look like MS lesions. Look it up on the 'net. People who develop Alzheimer's have whitish plaque on their brain. That does not mean everyone with white spots (seen through a brain scan-CT) will develop MS or ME or Alzheimer's Disease.
I've had a brain scan and their are white areas seen but not quite consistent with MS. I do have POTS, leaky gut syndrome, IBS, FM and ME. Now I suppose you could say I have multiple diagnosis but not if you understand ME/CFS (read the Canadian Consensus) there are many, many symptoms when taken individually can be labelled as individual diseases or syndromes. Put them together and you have what is, at least now, called ME/CFS.
Maybe I'm missing what some of the other members were trying to say???

The good news of this article is that there may be hope for a disease, that nobody seems to be able to figure out, that is somewhat similar to MS, Polio etc and the drugs used for these conditions may in fact help ME/CFS. Yes, there may be millions of people dx with MS when indeed they have ME or vs vs. And yes, sometimes the drugs that help these conditions are very powerful and can cause severe side effects, damaged liver etc. Think about cancer drugs. One would have to make a choice when offered such a drug, weigh the options. The lessor of two evils.
 

Who Me?

Well-Known Member
@GG to make LDN get a glass bottle and fill it with 50 ML water. Drop the pill in and let it sit for an hour or so. Get a 5 ml irrigation syringe and you're set.

@ShyestofFlies Many people have issues with AD, I can't take them, their horrible. My impression was it was tossed out with no thought about other medications someone might be on or their history with AD's. IMO it is not a good substitute all because it has naltrexone in it.
 
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