Getting mobile fast during an acute flare.

[d q]

@Keith – How’s it going pal, hope your enjoying your weekend.

I remember a while back you were mentioning that it was important to get mobile as soon as possible during an accute gout flare. Generally I try to remain mobile during an acute flare by walking around as much as possible despite being in agony because I loathe just sitting around helplessly but I was wondering what those science findings that encourage this that I believe you said you had and will be publishing?

Cheers mate.

[Keith Taylor]

Yeah, good weekend thanks. But not so good as last weeks family garden party for my sisters birthday. These events get better as the generations grow. : grin:

Anyway, let me explain my thoughts and investigations so far about mobility during an acute gout flare.

Firstly, for the thousands of gout sufferers who will read this in future, let me summarize the background. Because this starts with my approach to acute gout pain management. Where I stated:

First and foremost I had an epiphany when I realized gout pain stems from an immune reaction. Prior to that, I had the more typical view that sharp uric acid crystals were forming. So, I understood the importance of getting mobile as soon as possible. Fortunately, prescription strength ibuprofen (Aleve) kept me going almost every time. But if it didn’t I supplemented with paracetamol (Tylenol).

So, I’m explaining my approach in an acute gout flare setting. But I also want to explain the science. Then gout patients can explain to their doctors why they need the right pain treatment to stay mobile during acute attacks. Because in my experience, you get a better response when you ask your doctors opinion about a specific medical study. Compared to “some bloke on the Internet says…”

Eventually, I want to incorporate this into the facts and templates on my main gout website. So, here’s some work-in-progress. But, please note this is not about the general benefits of exercise for gout sufferers. Because I should already have explained that at Gout & Exercise. Though, I can see that needs some updating after 6 years.

Acute gout pain is an inflammatory immune system response to uric acid crystals
I’m emphasizing this as my starting point. Because I still see references to uric acid crystals as “sharp needle-like”. But this is nonsense as it describes objects at a microscopic level which cannot be sharp. Also, to describe them as needle-like is like describing grains of soft sand as “craggy boulder-like”.

Unfortunately, this led me in the wrong direction as a newbie gout sufferer. Because I thought I should avoid more physical damage from these “sharp” crystals and rest as much as possible. But I couldn’t understand why attacks lasted more than a week in bed. Yet, if I had to force myself to work I was OK in 2-3 days.

Medical approach to inflammation
Before I get to the science of inflammation, I must point out I cannot find any specific investigations into the effect of mobility on gout flare duration. So, I have looked at inflammation in general. But, I’m aware that some aspects of specific diseases might mean we cannot apply certain findings to gout. Therefore, if you are looking for exact gout science about mobility during acute gout, please leave now. Perhaps you can raise funds for specific research. Or experiment on yourself. In any case, I can only give some strong pointers that remaining mobile is best.

Half a century ago, the attitude to inflammation was rest and immobilization. So Partridge’s 1963 arthritis study^[1] advocates

a period of complete immobilization can safely be used in the treatment of rheumatoid arthritis to control pain, muscle spasm, and disease activity.

But, this contrasts completely with Pinto’s 2017 investigation^[2]:

make the patients “sit less and move more”, particularly light-intensity activities and/or breaking-up sedentary time, is a simple and prudent therapeutic approach to minimize physical inactivity and sedentary behavior, which are overlooked yet modifiable risk factors in the field of autoimmune rheumatic diseases

So now, I’m trying to understand what are the specific inflammatory factors that mean mobility is beneficial during acute gout. Because I think there are specific gout-related factors behind Pinto’s recommendation.

Most recently, I’m looking at Wood’s 2009 investigation^[3]. In turn, that has me frying my brain with Bruunsgaard’s 2005 explanation of physical activity and inflammation^[4]. To explain “frying my brain”, I understand half the keywords: “myokines; TNF-alpha; IL-6; proinflammatory; antiinflammatory; exercise”. But, I think there’s real scope for a clear explanation. Because many of the terms in this study look like terms in complicated gout pain studies (which also fry my brain)

Practical Advice
Let’s assume I can convince the world that for acute gout flares, mobility is best. Then I hear the next question: “But I have a desk job, so I can’t stay active”. Well, I tripped over the answer in Bort-Roig’s 2014 study^[5]. “17 tips for mobilizing gout recovery” Coming Soon!

And now you know why I never find time to answer forum questions promptly! 😮

High Fat Meals cause Gouty Inflammation – Physical Activity reduces it

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Mobility During Gout Flare References

1. Partridge, R. E. H., and J. J. R. Duthie. “Controlled trial of the effect of complete immobilization of the joints in rheumatoid arthritis.” Annals of the Rheumatic Diseases 22.2 (1963): 91.
2. Pinto, Ana Jéssica, et al. “Physical inactivity and sedentary behavior: Overlooked risk factors in autoimmune rheumatic diseases?.” Autoimmunity Reviews (2017). Ask if you need a PDF. Because I need to dive into my pocket for it.
3. Woods, Jeffrey A., Victoria J. Vieira, and K. Todd Keylock. “Exercise, inflammation, and innate immunity.” Immunology and allergy clinics of North America 29.2 (2009): 381-393.
4. Bruunsgaard, Helle. “Physical activity and modulation of systemic low-level inflammation.” Journal of leukocyte biology 78.4 (2005): 819-835.
5. Bort-Roig, Judit, et al. “Uptake and factors that influence the use of ‘sit less, move more’occupational intervention strategies in Spanish office employees.” International Journal of Behavioral Nutrition and Physical Activity 11.1 (2014): 152

[nobody]

I’m going to disobey Keith and decline to “leave now”. Sorry.

What I’m seeing here is confusion between different things:
-habitual exercise (that is, when you’re NOT having an acute attack… and I do mean “acute” as opposed to whatever you might have that lasts for months)
-exercise during an attack
-weight-bearing exercise involving a joint affected by an attack

Consensus is, habitual exercise is healthy.
There are conditions other than gout causing more or less constant joint pain or even inflammation and as far as I can tell, the recommendation is to keep exercising if you have that. Sometimes people confuse these conditions with gout but gout is different in that attacks typically stop and give you plenty of time for exercise before the next one starts.

Based on my experience, I do think exercise during attacks helps a bit. BUT. Not any exercise. In particular, you don’t have to be mobile to exercise. And I don’t think it needs to be actual exercise to help.
Being mobile has in my experience been most helpful for joint problems in the hands and arms. Let the painful joint rest and get your heart pumping my moving your legs. Easy.
Typical attacks involving feet are another matter. Staying immobile is fine for a while (I’ve used one of these things designed for people who have foot injuries for instance) and can bring some relief because part of the pain is due to muscular tension but I find remaining immobile for too long doesn’t help.
People find that bathing their foot in hot water helps. Hot showers work too. Even simply sitting before going back to elevating your foor helps a little bit. My working theory is that you need to get blood moving into and out of the affected area during attacks. Exercise obviously does that.

When your feet are OK, the simplest kind of exercise is walking, running and stuff. But if you’re having a acute attack in the foot, that’s a recipe for disaster. Trying to walk on an inflammed foot puts you at risk of debilitating ankle problems in particular. Protecting my foot by using crutches during attacks has consistently led to better outcomes. You can however exercise using weights and such without putting weight on the affected joint.

[d q]

@keith @nobody

I love a good debate. Anyway here is my two pence on this.

I have only ever had 3 attacks since August 2015 so cannot really give much independent experience. On the other hand I have dealt with the gout attacks in 3 different ways. One with no NSAID’s or Colchicine (I never knew about them during my first attack and just went to A+E) and the other 2 with Naproxen alone.

The second attack a year in August 2016 I used a strong course of Naproxen only as I was too worried about the side effects of Colchicine and what impact they may have on my condition. Regardless, the Naproxen helped significantly pain wise.

The third attack this March which has left me with constant residual pain due to commencing Allopurinol was also treated with Naproxen alone for fear of Colchicine however this time the Naproxen did next to nothing in helping me feel better. It may have been making things easier then what things may have been without but I certainly didn’t feel much relief whilst taking it. Maybe because I only took it for 10 days and not through the entire attack duration.

How this relates to mobility is as follows;

The first attack I stayed in bed most of the time with no meds. The recovery time was approximately 12-14 days.

The second attack I took Naproxen thus I had pain relief and was able to walk around the house however the attack lasted 14-18 days. I tried to keep mobile where possible but did not exert force.

The third attack I took Naproxen and despite hardly any pain relief I kept pushing myself to walk around as best I can and although the ‘attack’ has passed residual pain still remains. That attack lasted over 18 days. Pain relief was next to minimal but I wanted to stay mobile.

So from my experience, resting is probably the better/faster option. Now had I not pushed myself when taking the Naproxen during the second attack maybe those 14-18 days would have been reduced by a further 3 or 4 days which would mean pain relief and a reduced length of attack.

Which ultimately begs 2 questions;

1. Can pushing yourself despite pain to get mobile asap actually cause irreversible damage as I am still dealing with residual pain today? Osteoarthritis as a result of a gout attack because of persistence to walk or was it just coincidence?

2. Even if one uses a combined aggressive pain relief course like mixing Colchicine with NSAID’s and Paracetamol to dampen pain who’s to say your joints are not taking a massive beating whilst you enjoy these mobile pain free periods? At the end of the day stopping inflammation is not your only issue when crystals break into synovial fluid or get stuck in soft bone.

[nobody]

You may have taken less Naproxen than (as Homer would put it) iron-stomached, steel-livered Keith would have used. I would certainly not take that much.
And if you take more NSAIDs in order to be mobile, it makes sense that inflammation is stopped quicker. That’s what taking a very strong NSAID dose is supposed to do.

About painkillers:
I think taking painkillers to be mobile is riskier than taking anti-inflammatories for the same purpose. Even considering that crystals can cause mechanical damage besides inflammation, anti-inflammatories do reduce the risk of damage. And crystals can cause damage outside of attacks.
Sorry if my insistence is annoying but effective doses of paracetamol are hard on the liver. If you’re already taking other medications which are known to cause liver problems, be careful. And if your liver function hasn’t been tested since you’ve started one such medication… well then, I would recommend not touching the stuff. There are other painkillers.

Now as to your questions:
I don’t know whether ignoring pain and walking during an attack might cause OA. What it definitively can cause is immediate and non-permanent problems. Slow damage is harder to understand, as are things like OA. There seems to be an interaction between OA and gout but I don’t know what processes are involved.
It stands to reason that abusing your joints, tendons and so forth could in some cases cause permanent damage. You also risk accidents when you push yourself.
But then, not being mobile for very long also involves a risk of long-lasting and possibly permanent damage, right? The same goes for not using the full range of movement of a joint, I guess.
My assumption is that minimizing risks is a balancing act. As far as attacks lasting a few days are concerned, the risks invovled in immobility seem very small compared to the risks involved in mobility. When you’re talking about symptoms lasting months however…

I’d be interesting in knowing the opinion of your current rheuma.

[Keith Taylor]

“I’d be interesting in knowing the opinion of your current rheuma.”
So would I. But, I’m looking for a specific opinion on whether mobility helps inflammation or not.

To explain, I’ve caused confusion between:

-habitual exercise (that is, when you’re NOT having an acute attack… and I do mean “acute” as opposed to whatever you might have that lasts for months)
-exercise during an attack
-weight-bearing exercise involving a joint affected by an attack

I believe habitual exercise is a separate topic. Specifically: “But, please note this is not about the general benefits of exercise for gout sufferers. Because I should already have explained that at Gout & Exercise.”

But, I do think I could have been clearer about the other points.

To explain, I do not want to encourage gout sufferers to risk further damage to joints that have already been weakened through gout. So, if you suspect this is the case, you should get imaging tests immediately. Certainly, standard X-rays and ultrasound are useful. But, if funding is available, then CAT scans or MRI scans reveal a better picture.

As an aside, let’s look at that damage for a moment. Because uric acid crystals cannot cause “mechanical damage” in the way I understand the meaning. Uric acid crystals cause tendinitis, osteoarthritis, and other damage through the immune response system. That is to say, when white blood cells (WBCs) attack uric acid crystals, all hell breaks loose. Because our bodies rely on many different types of WBCs. Some of which were destined to repair bone, cartilage, etc.

So, there is no mechanical wearing down of joints. But, lack of maintenance because the janitors have been sacrificed to battle.

I think that this is a separate topic. Unless forced mobility of inflamed joints increases the chances of more specialist WBCs being sacrificed. Which means we have one meaningful question to ask a rheumatologist:

“Is there any evidence to support the notion that osteoblasts, tenocytes, and other specialized cells are at risk if mobility is increased during periods of inflammation” ❓

Finally, I return to my suggestion that mobility can reduce the duration of inflammation where there is no indication of joint damage. So, my second question for d_q’s rheumy is:
“Please can you explain Pinto’s reasons for recommending “sit less and move more”, particularly light-intensity activities and/or breaking-up sedentary time.” ❓

Because that is key to understanding mobility during gout attacks.

Of course, the real issue remains to get uric acid controlled. Then, gout stops and none of this matters. But like d_q, I love a good debate. Which is why I proposed the Mass Debating Society in high school. 😉

[nobody]

The thing is, your cites are about what I’d call habitual exercise, not about what you should do during brief acute episodes.
Obviously, it’s not somehow your fault or an argument against your experience that there seems to be little scientific reasearch into how best to deal with such episodes. Nevertheless, Pinto’s recommendations are as far as I can tell irrelevant to acute episodes.
Habitual mobility may prevent gout-related inflammation (or merely reduce it, which is good enough). It simply doesn’t follow that mobility would do much for acute episodes once they’ve started. If someone breaks a bone because of severe obesity, exercise may help address the cause in the long run but it obviously wouldn’t heal the bone. Likewise, it may be advisable to keep moving in the face of RA but it doesn’t follow that the same goes for acute gouty episodes.

More to the point considering DQ’s questions, how do you know that crystals cause no damage outside of inflammation or other things the immune system does or fails to do?
I’m not talking about crystals being “pointy” or anything like that. But if you have a sizable foreign growth in a weight-bearing joint, how could that not create a mechanical problem? Maybe I simply don’t understand where large amounts of uric acid are typically deposited.

[d q]

@nobody @Keith

This has kicked off into a brilliant debate. A great opportunity for us to brainstorm too.

“iron-stomached, steel-livered” – haha 🙂

Yes, from what I understand most of Keith comments were about habitual exercise whereas my findings were more concerned with what getting mobile asap can or can’t do to the acute flare. Despite uric acid forming microscopic crystals that are harmless in themselves the real issue is when they accumulate around the joints. From what I understand over time these crystals can mechanically intervene with the normal movement process of the joints. After all as nobody says there must be some sort of “additional friction or compensation for the foreign body” which I believe can cause some sort of bone erosion.

Whilst I most certainly believe that the real issue is addressing the underlining issue of lowering uric acid I also seem to have had better heating time results resting the joint longer. However on the flip side trying to keep mobile and use the joint during an acute flare caused me to almost become ‘aquatinted’ with the pain so somewhat more pain tolerant which I probably wouldn’t have been lying down resting. I definitely do not condone that as an advantage though. I think in future if an attack does strike I will take the more relaxed approach rather then express mobility.

Finally, I spoke to my rheumatologist about my ongoing pain and he’s response was quite simply you seem to have ongoing low grade inflammation which there is nothing we can really do about until you start febuxostat to begin to dissolving the crystals that are causing your immune response. I insisted and questioned if it could be permanent damage so he offered an ultrasound guided injection to remove the pain and check to see if there was damage but I rejected that route and explained that I would like to have a detailed MRI scan as I felt that they can better indicate damage. He wasn’t too pleased and explained that an injection would relieve the pain and that I could reject the needle at the time of the ultrasound however I said no. I want an MRI to give us CLARITY, ultrasounds are not as accurate. so I am now waiting for the scan date.

What do you think, can we get a clearer picture from that?

[nobody]

The injection wouldn’t have been only for the pain, right? I mean, you wouldn’t need to bother with this type of injection if that was the point. Pain management is routine.
What I suspect your rheuma had in mind was an injection that targets the inflammation. Not a permanent fix obviously but probably still worth trying since clearing crystals with febuxostat is going to take a while (assuming you tolerate the drug).

My rheuma figures a well-done ultrasound is more informative than an MRI. Or maybe that depends on what you want to see. Based on SUA, physical exam and X-rays, serious permanent damage wasn’t expected in my case.
The advantage of MRIs is apparently that any qualified fool can do them. For the ultrasound though, I was to see a specific fellow.
In the end, if you’re 99% confident that the right course of action is going to be simple ULT whether or not a scan is done… well, in that case the cost/benefit of a scan is questionable.

[Keith Taylor]

It was certainly my intention to keep the focus of this on getting mobile quickly during acute inflammation. So, please accept my apologies if I’ve appeared to be talking about habitual exercise during inter-critical bouts.

Perhaps it’s best to add “woolly-brained and fuzzy-focused” to the list. Also, something about weak wanker humor as the “mass debate” joke never raised a trace of laughter.

Anyway, I think the perfect solution is d_q’s “I think in future if an attack does strike I will take the more relaxed approach rather than express mobility.”

I.e. it’s up to each individual to act according to their own beliefs. Now, I realize that’s not very scientific. But, I can now see that there is no reliable science to determine the best course of action. So, if you believe rest is the answer, then it probably is. And if you believe getting mobile as soon as possible is the answer, then it probably is.

Because until we have a proper medical study on human gout sufferers, we cannot say which is best. Also, I imagine that even if this is done, it will always depend on several complicated mitigating factors. For example, what if mobility increases immediate pain, with no lasting damage, but quicker recovery from the acute flare? Then that’s OK with me because I can tolerate that pain. But a different gout sufferer might not find this acceptable.

Finally, I can see the start of at least 2 more fascinating topics here.

First is d_q’s interesting way of getting what he wants from his rheumatologist and what happens next. The second, perhaps related, is the merits of MRI vs Ultrasound. Though returning to hedging my bets, I have to agree with nobody that it depends on what you are looking for.

[nobody]

I don’t understand enough about your high schools or debates to get a good joke, sorry.
I understand a little more about what people in the US call high school or debates… very perplexing things. Kind of like “country and western”.

[Keith Taylor]

Hey nobody, I never said it was a good joke! Also, I put high school to widen the audience. Because, of course, I went to grammar school – a haven for puerile humour. Just say “I like a mass debate” out loud. It was very funny when I was 13.

Granted, less funny now. 🙂

[d q]

@nobody – yes the injection was just for the pain and not for the inflammation. Even if you did take it for the inflammation it will ultimately solve nothing. Pain relief would come from it and ultimately it will come back unless we solve the UA crisis. Moving onto the MRI Ultrasound, the thing is I already had an ultrasound (twice in fact) once when I had my second attack to aspirate fluid which they couldn’t do and a second time long ago for pain. Fortunately returned a negative response for damage. Now an ultrasound wasn’t done for this particular situation however..! I have managed via my GP to arrange an ultrasound scan alongside the MRI. I agree about any fool can take an MRI however a qualified dude is required for an Ultrasound but the same analogy can be applied to a professional photographer with a rubbish camera or an amateur photographer with all the latest photo enhancing technologies camera. The point I’m making is the outcome of the MRI is simply more detail :). If ULT is 99% the right thing or not well I really have no idea? I mean you took febuxostat so you’ve got the best advice I can ever get about it. I mean I could potentially wait to see what both scans have to say but that would be another 3 week delay in starting febuxostat. The way I see it would be start ULT with febuxostat shortly after the Vitamin E test and then just take either colchicine or NSAID on the side which would ultimately protect me from acute attacks and maybe even solve the current pain.
How does that sound?

@Keith – I think your absolutely right on this point as I also forgot to mention that my rheumatologist suggested that gout pain control is very much down to the individual patient and how they find relief. So while one may find they get better or quicker relief resting another may find they get more faster relief by getting on their feet as quick as possible. Damage on the other hand is harder to predict. I would assume that how long you have had gout and what treatment was taken in the past will impact whenever or not forcing oneself to keep moving during an acute inflammation is actually counterproductive. I think the longer you have had untreated gout the more likely you might actually cause damage. But again, I am just drawing up scenarios in my head. The best way as you say would be to actually study it using a broad range of people over a period of time. 🙂

[nobody]

I have no useful advice to give you on this matter. Febuxostat is just another way to do ULT. We can talk side effects, pill-cutting and stuff but it should have the same effect as allopurinol on your inflammation.

What I was trying to say is that if you’re confident ULT is what you need to do, what’s the point in trying to determine ahead of time what ULT would and wouldn’t solve? You’ll find out anyway.
I also assume you’d get a clearer pricture of the damage done by uric acid once it’s (mostly) gone than in the middle of the process (even if there was a point in having pre-ULT imaging, it’s too late for that now that you’ve spent quite a while under 400 umol/l).
Maybe I’m missing something.

About predicting damage, it seems we know one thing: the longer you’ve had untreated gout, the more damage there will be and the harder it will be to stop the damage from getting worse even with ULT. The relationship is going to hold regardless of exercise. Perhaps weight-bearing exercise could increase the amount of damage but I think that’s a separate issue from the matter of how you should behave during attacks.
About your assumption, the first times I got really serious attack, weight-bearing exercise involving the affected joint had disastrous effects. I very much doubt the problem was bone erosion or anything of the sort since no doctor noticed anything out of the ordinary, even on the MRI I had done back in the day. Granted, I saw a bunch of clueless doctors but that kind of damage can’t be easy to miss, right?

[d q]

if you’re confident ULT is what you need to do, what’s the point in trying to determine ahead of time what ULT would and wouldn’t solve? You’ll find out anyway.

This sir is indeed accurate and very true 🙂

I also assume you’d get a clearer pricture of the damage done by uric acid once it’s (mostly) gone than in the middle of the process (even if there was a point in having pre-ULT imaging, it’s too late for that now that you’ve spent quite a while under 400 umol/l).

True – to an extent. The reason for the imaging is to see if damage has already been done (I assume my doctor would know what damaged bone/tissue/muscle looks like [I hope]) and if he believes that ULT will actually repair anything that he finds. I assume if he spots a bone deformity then we know where we stand with pain relief right there. If anything its a way to get baseline images too. Ultimately I want to know if permanent damage has been done since the last attack. This constant low grade and occasionally high grade pain is debilitating.

Granted, I saw a bunch of clueless doctors but that kind of damage can’t be easy to miss, right?

Precisely why I forced the MRI on him. I mean if he or other doctors cannot interpret the ultrasound and the high resolution detailed images that will shortly be provided to him then what chance do we really have?

I know the attack was due to some Allopurinol induced ‘crystal dis-lodge or debulk’ or whatever but boy that crystal had a true field day and must have dis-lodged my whole foot with it.

My fault for not talking colchicine or NSAID with Allopurinol..? Probably.
My fault for even starting Allopurinol..? Who knows anymore.

Dissolving, Debulking, Dislodging, De-Whatever you call it.. Sometimes I think to myself this Allopurinol bulls*** really took me to the cleaners 🙂

Whoever is about to start Allopurinol please do not let the above deter you.

nobody – where are you based by the way..? 🙂

[Keith Taylor]

On the chances of repair d_q, it seems to depend on the type of damage caused. Because I found a relevant 2014 report below.

The report deals with extreme gout Uric Acid Arthritis, and extreme uric acid lowering. So, it doesn’t exactly match your situation. But I believe the principles still apply. So there’s strong evidence to suggest bone erosion will repair itself. Unfortunately, less chance of Joint Space Narrowing reversal, or cartilage repair.

Joint Repair after Uric Acid Lowering Reference
Dalbeth, Nicola, Anthony J. Doyle, Fiona M. McQueen, John Sundy, and Herbert SB Baraf. “Exploratory Study of Radiographic Change in Patients With Tophaceous Gout Uric Acid Arthritis Treated With Intensive Urate‐Lowering Therapy.” Arthritis care & research 66, no. 1 (2014): 82-85. Bone Erosion Reversed after Uric Acid Lowering PDF.

[nobody]

Your main problem I think has been not getting enough blood tests and being too slow to adjust your medications. This hemoglobin thing should have been detected much quicker and you’ve spent way too much time with above-target SUA since starting your ULT.

Based near a border in Europe, I am. Sometimes we have to shop for health care for the other side of the border so as not to be limited by the regulations of any single country.

[d q]

@Keith – Thanks for that interesting article Keith. Gives me some hope!
Funny actually, my foot has been quite well today. Loving the Uric Acid Arthritis approach by the way.

@nobody – near a border in Europe.. Well well Jason Bourne 🙂

brother I had more blood tests since starting allopurinol then I have in the last 10 years so it definitely wasn’t a blood test thing. With regards to haemoglobin, well that doesn’t change in a week or two. Haemoglobin changes need a minimum of 3 weeks between tests to notice, aggregate, and finally create trends. The only delay I see was Colchicine but thats tried and tested now. Way too much time after stopping Allopurinol? It will only be 3 months tomorrow. I’m sure 3 months won’t cause any major changes. Anyway as explained I’m doing my trial Vitamin E blood test to check if there’s been any impact in a week and will be starting febuxostat after my visit with the professor mid-September. I remember you mentioned something about your haemoglobin dropping by 1.0 when you started febuxostat. Do you recall it returning to usual levels a while after starting? I’d really appreciate if you could let me know. Cheers.

[nobody]

I knew you’d appreciate it so I got it tested again: no change, still a touch lower than it used to be but not weird. Could be a random variation… not the most likely explanation perhaps but at least my hemo didn’t keep dropping. That would have been more significant. As it stands, it’s nowhere near my one clearly anomalous hemo test result (that was after a surgery).

Yes, you are finally getting adequate testing. But I was commenting on your infrequent tests before we even knew about the hemo issue. That leisurely testing pace didn’t just make it harder than necessary to detect and pin down your hemo problem but also led to a slow dose increase. As a result, you had already spent too long with an above-target SUA before you stopped allo. And then your break between drugs kept getting extended… all in all, not the best way to prevent or stop chronic inflammation, I’d say. If the reason for such a long break was a course of colchicine, presdnisone or something, OK. But simply waiting?
The reason I’m being a bit of an asshole right now isn’t that I want to dwell on the past but that I think you could benefit for expediting the next steps, especially in case it turns out febuxostat doesn’t work for you either.

[d q]

I knew you’d appreciate it so I got it tested again: no change, still a touch lower than it used to be but not weird.
Thanks mate, I do really appreciate it yes. Just out of interest it was a touch lower then your original levels prior to starting febuxostat right, not lower then it was when it originally made its first drop after starting?

I think it just came at a wrong time, starting allopurinol then going through an attack then inflammation (which can cause hg drop too). It all happened so abruptly in some accelerated mess. I mean even today some doctors are not entirely convinced it even was allopurinol and still think it was just some internal multifactorial infection/inflammation (not me though).

I would have to agree with you on certain aspects like trying febuxostat and colchicine a little quicker but bare in mind my haemoglobin only really recovered in mid-July or so. Still, as you say thats a month and a half too late. Anyway, I’ve got a blood test coming up to see where we stand. I also silently started vitamin E to see if that makes a difference.

p.s. How are you doing on febuxostat these days? Your previous unexpected attack gone?

[nobody]

Yes, my two hemo test results since starting febuxostat were basically identical. In the last few years, all my other hemo test results have been a bit higher.

I haven’t had a very long attacks since I started using colchicine. Of course that attack is gone. But I got three other attacks on the same foot since then. This is very unusual for me but not a huge surprise considering my ULT. And these attacks seem to be getting milder.
The main problem is that my liver is struggling, probably more because of the anti-inflammatories and stuff than because of febuxostat. But of course it contributes to the problem. And it’s most likely the reason I’ve been taking so much colchicine and stuff in the first place.
I knew going into this than my liver was likely to be the limiting factor in addressing gout. You’ll probably be fine.

[d q]

@nobody (aka Jason Bourne) – Well your hgb stabilising is certainly a relief as it gives me some hope.

Forgive me if I already asked this but how long have you been taking febuxostat and at what dose?

From my understanding your not a great fan of using NSAIDs so why are you currently taking them? If I remember you were mainly a colchicine only approach? Or are you using combination therapy for these milder attacks? Not so sure I understand “unusual considering your ULT” What are your latest liver tests? Out of curiosity do you have any general liver problems?

Gosh I just realised I asked you about 20 questions! I’m just learning (and teaching in some threads) Sorry bro 🙂

I’m still struggling with this painful foot and I really hope febuxostat works for me. It’s been a nightmare these last few months. I just want to complete this Vit E trial first.

[nobody]

I mean I’m not used to having so many attacks of this type. They had become quite rare and now I’m basically getting one every other week more or less at the same location.
I was saying that’s not a big surprise on account of my ongoing ULT.

My hemo tests didn’t seem to be affected by febuxostat dosage but n=2. Meaning that the lack of change in observed hemo values could easily be a coincidence. Either way, I don’t have enough data to conclude anything other than what I’ve already told you.

I’m not currently taking NSAIDs. But it takes a while for the liver to recover. I guess taking something like febuxostat every day doesn’t help.
Like I told you, I tried mild “combination therapy” for one of these recent attacks, in part because you had asked about it and I had never tried that on top of febuxostat. Normally I would only use colchicine.
I don’t know if colchicine is technically an NSAID but I don’t call it that though we use it as an anti-inflammatory. I think paracetamol is technically an NSAID but we generally don’t call it that, do we? I used the phrase “and stuff” in case there was any doubt regarding the semantics, hoping that it would make clear that all drugs used in the face of gout symptoms were included. But since I’m only playing an English speaker on the Internet, I guess my shorthands must sometimes be opaque. And jokes about how words sound will be lost on me.

In case you’re wondering why I’m not getting yet another joke, I don’t know this Bourne fellow. No matter.

[d q]

Oh nobody you do make me laugh.. I think its just we share similar situations here and there that makes our cases unique in their own right.

Well firstly I’d like to thank you for trying the combination therapy, your a true ‘internet friend’ speaking in your words, how did it work for you?

I know everyone reacts differently to medications but the haematology results are encouraging as I need that little bit of assurance with this ongoing pain right now.

I asked my first rheumatologist if it was OK to use NSAIDs with Colchicine and he said it was fine whereas the second rheumatologist said not to. So I guess that means Colchicine isn’t really an anti-inflammatory because they couldn’t be used together otherwise one could use Diclofenac with Naproxen.
I’m not sure if Paracetamol is an anti-inflammatory but I guess a little research answer that for us.

I’ve got my ultrasound coming up and am extremely anxious for the results.

But going back to two questions, how long have you been taking febuxostat and at what dose? Cheers buddy.

p.s. Jason Bourne is an actor in a famous movie called The Bourne Supremacy.
He is a secret agent hence ‘near a border in europe’
(http://www.imdb.com/title/tt0372183/?ref_=tt_rec_tti)

[nobody]

My rheuma did call colchicine an anti-inflammatory. And it’s not a steroid so…
I guess NSAID is a bit of a misnomer and that what’s really meant is peripherally-acting COX-1 or COX-2 inhibitor.

I had told you about my little “combination” trial in another thread.
Briefly, it seemed to work. I didn’t notice any drug interaction. But n=1…

I’ve tried different febuxostat doses and went on and off the drug. Sorry but I’m not going to sift through old notes to provide useless details. Suffice it to say that after decades of hyperuricemia, my SUA has consistently tested in the safe zone for the better part of the year. I went into some of the details in other threads when they were relevant.

[d q]

@nobody

hello mate. Yep I agree you have answered combination therapy somewhere in our comprehensive threads. I too believe Colchicine is some sort of anti-inflamotory for the very same reasons you mentioned. In any case, being told you can use them together obviously means they work in their own unique ways without ‘major’ contraindications outside of general side effects.

Bro it was a simple answer of “I’m currently taking 20mgs/40/80 right now”
It really didn’t require the ‘go check other threads for your answer’

Relax my brother we’re in the same boat.. 🙂

[nobody]

It’s not that simple actually.

[d q]

Ok.

[Author]

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