Forum Replies Created
-
Posts
-
zip2play said:
Houston,
We've got a problem!
New York, I believe we've fixed it.
It was pants, but to be brief, the problem no longer has legs.
jp, 6 weeks is not a long time for most gouties, but it depends on:
- How long you had gout
- How high were uric acid levels before lowering treatment
- How low are uric acid levels with lowering treatment
The only way you can be certain of progress is the same way you can be certain of gout – get a joint fluid analysis, unless you have access to Siemens CAT scan gout detector (not the official name).
A very rough guide is one month for every year of gout, but that is so rough you could almost call it a guess. If you look at some research on urate deposits, you can see some of the factors that affect the timescale for getting rid of old uric acid crystals, and some of the timescales involved.
Frequent monitoring of uric acid levels is vital to assess progress.
Joe said:
One question I forgot to ask was since the drugs uloric and allopurinol prevent the purines in your blood from being turned into uric acid, what does your body do with all the extra purines? It seems like the body was turning the purines into uric acid for a reason, right? Now wouldn't the body have too much purines in the blood? Does anybody know about that.
Joe, I love that question.
I do not have a clue how to answer it, but that just makes me love the question even more.
Once I've worked it out, I'll let you know, but it won't be today – I'm planning my night of celebtation in honor of your latest results.
The gout pain lessening isn't coincidence, Linda. That usually happens, unless something triggers another attack.
The pain is caused when your immune system reacts to uric acid crystals. For most gouties, this is when crystals are forming. White blood cells attack the crystals and this leads to painful inflammation. They cannot kill the crystals in the same way that they kill an invading virus, so they coat the crystals, effectively hiding it. When you lower uric acid (through allopurinol, diet or some other means), previously hidden crystals can lose their protein shield as they dissolve. If they do not dissolve completely, the immune system attack occurs again. This process takes a few days, so that is almost certainly why your knee feels better now.
All that, is the reason I say gout must be managed by uric acid testing, as pain alone cannot tell you if your gout is getting better or worse.
Also see the links on https://gout-pal.com/gout-p…..rticipants
In that discussion, I had ideas about creating a better gout clinical trials update service (i.e. a single comprehensive list). There doesn't seem to be much interest in this (e.g. no reporting back from participants or organizers).
Are there enough people interested to make it worth the effort of a permanent feature? If so, is a page in the reference section enough, or would email notification for specific locations be required?
I've created this topic to draw attention to the debate on protein rich foods and gout.
That debate is heavily moderated on the specific topic of protein rich foods, especially the advice currently being given by professional advisors.
If you have received dietary advice for gout in the last twelve months from a professional advisor, please add your comments.
If you have related experiences or opinions to share, please start a new topic here, or on the Gout Cure forum, as appropriate.
Hi Lyndak,
Please listen to what zip2play and odo have said.
If your nephrologist is unsure about increasing your dose, point him at these articles on allopurinol & kidney issues.
To get rid of the old crystals in your body, and stop new ones forming, you must get uric acid levels below 6mg/dL. The sooner you do this, the quicker the old crystals will dissolve, but you may get joint swelling & pain until all have dissolved.
odo said:
Effectively controlling symptoms is all well and good, as I discovered is possible with Chinese herbs, but without knowing SUA levels this will simply be slowing down or masking the steady build up of urate and other long term implications of high uric acid. I think once the science and progression of the disease is understood it is not easy to ignore this fact and convince oneself the situation is under control.
The good news is that if one is prepared to continue with a healthy gout diet (plus whatever supplements) when starting Allopurinol, it should be possible to reduce SUA to safe levels on a low dose.
Wise words indeed, odo
Uric acid crystals tend to grow very slowly, and often go unnoticed. Unfortunately, without uric acid control, they will reach a level where:
- Acute gout flares become more frequent and more intense.
- Permanent damage to bones, ligaments & tendons from the corrosive effects of gouty tophi.
And this happens later in life when one is less able to cope.
Any form of gout treatment, whether medical, herbal, or dietary, MUST be accompanied by uric acid testing at least twice a year. Monthly is better.
Jean, I've just seen the irony of a meek and mild GoutPal offering aid to a lioness
lioness said:
Usually allopurinol or febuxostat is given after many many attacks.
Start attacking him now!
My offer still stands, but you might as well maul him into submission before I join the fray.
lioness said:
Well I'm a bit gobsmacked to tell the truth. Husband saw the doc today who said his serum urate level was not untowardly high and has put him back on prednisolone. He asked about febuxostat but was told that he is not bad enough for that yet. Usually allopurinol or febuxostat is given after many many attacks.
don't know what to think
Never ever, and by that, I mean not once, let any medic (or anyone else for that matter) tell you that uric acid is high / low / normal or any other label. It is a sure and certain sign that they do not know what they are talking about. It is the equivalent of the supermarket checkout saying that the price of your shopping is not untowardly high! I.e. it is totally ridiculous.
Uric acid levels have a number. It is absolutely vital that you know this number.
As limpy says, uric acid levels can be “close to normal” during an acute attack. But it is worse than this – the labels themselves are often pointless statistical averages.
Please ask your doctor to look at my article on the dangers of normal uric acid levels. I know we Brits tend to shy away from arguing with our doctors, but this looks like a clear cut case of a need for a second opinion. I'll come and hold your hand if you're anywhere near Yorkshire. I have an 80 year old friend who got similar, shoddy mistreatment. It gets a little personal with me now
.Adenuric and Uloric are both febuxostat. Uloric is Takeda's brand name in the States, Adenuric is for Europe (and I think rest of world, but happy to be corrected)
Yes, benzbromarone is approved for UK use by the NHS, but as a 'specialist medication.'
In practise, I think that means that your GP is highly unlikely to prescribe it, though I know that some GP's work with specialists to take on some of the routine monitoring work. I would imagine that, with the approval of febuxostat, the chances of a specialist wanting to use benzbromarone are reduced.
It definitely falls into the 'discuss with your doctor' category. There is no way, even where it has not been banned, that benzbromarone can be regarded as mainstream gout treatment.
toofast said:
I know it is a bit late in many places…but I found this forum recently and today finally got the nerve to start asking questions.
I have searched everywhere on this forum for a explanation as to why beer is so bad…if it is balanced against a good diet and you stay hydrated (lots of water).
Can someone point me to an explanation…sorry I've always wanted to know why since I was a kid.
Explanation of Father Christmas – easy. I'll even have a crack at explaining god. But beer and gout? Please give me something easier
Beer and gout is big league stuff. Every commentator, including myself, has opinions. Some are based on fact, most on dodgy science, and the rest don't care because they are in the middle of their own experiments.
As recent as 2009, we still have boffins reporting the purine content of beer (Determination of purine contents of alcoholic beverages using high performance liquid chromatography: PubMed ID:19353717). Yet we have known for years that relating purines to gout is too complex for simple analysis, as different purine bases have different effects. Also purines react differently according to other dietary factors. Dodgy science best ignored.
There is good statistical evidence to show that:
the effect of individual alcoholic beverages on serum uric acid levels varies substantially: beer confers a larger increase than liquor, whereas moderate wine drinking does not increase serum uric acid levels.
But statistics simply report the data according to the parameters of the study, and are almost the opposite of an explanation.
Then we have the anecdotal 'evidence' about twinges after beer. But twinges are no measure of uric acid control as you can see from the hundreds of debates on gout attacks during the early stages of allopurinol and other urate lowering treatments.
Until I finish my summary of the research (which is difficult as the scientists do not seem to want to investigate alcohol in any terms that relate to normal human consumption), I'll have to fall back on faith.
You must believe that beer is doing you good, and those twinges are old uric acid crystals being dissolved. You are certain to be consigned to gouty hell unless you worship beer on a daily basis.
But the big issue is why were you worrying about gout and beer as a kid?
I've found pain is easier to deal with when you know the cause.
Speaking of causes, gout has only one cause – uric acid crystals, but there are many reasons for excess uric acid and also mysteries why it crystallizes at different levels in different people.
First you need a proper diagnosis. A rheumatologist has been mentioned, and that is by far your best starting point. Family doctors are generally good at treatment (with many exceptions before somebody points out their own poor treatment), but less good at diagnosis. Gout can be mistaken for several conditions, and vice versa, so if there is any doubt, a rheumatologist is the way to go. Check that they specialize in gout, because general rheumatics are not specific enough to distinguish gout.
For the second time today, I have seen mention of uric acid levels without numbers. Numbers, qualified by the measurement scale, are vital. Ranges like low, normal, or high are pointless. In fact they are worse – ranges are dangerous because they encourage misdiagnosis and promote the wrong treatment. Normal uric acid is the most pointless statement a gout suspect can hear.
In this context, the fact that uric acid in the blood can fall temporarily during a gout attack is a vital consideration.
zip2play said:
The download looks a bit risky ZIED.
Yup, definitely risky, but leaves me pondering the right thing to do.
OK, I know that the right thing to do is delete the link to a dodgy file.
On the other hand $31.50 from $ciencedirect for a 2 page report seems a bit $teep.
I've taken the cowards way out, and left the reference, but not as a clickable link.
If any members don't like, please report the item with the “Report Post” button, and I'll delete entirely. Note that you have to be logged on to use that button, even though it appears to non-logged on users. If you click it when not logged on, the message from the form goes absolutely nowhere. Bl**dy forum software.
In answer to your main question: How do you tell an old attack from a new attack, the answer is in your uric acid levels.
I recommend testing at two week intervals for the first few months of allopurinol treatment so that you can be sure that your uric acid is below 6mg/dL. This is also an opportunity to discuss allopurinol side-effects with your doctor.
Following the above, I just checked for more recent stuff, and see that Choi has published a review this year. His summary makes good reading:
Lifestyle and dietary recommendations for gout patients should consider overall health benefits and risk, since gout is often associated with the metabolic syndrome and an increased future risk of cardiovascular disease (CVD) and mortality. Weight reduction with daily exercise and limiting intake of red meat and sugary beverages would help reduce uric acid levels, the risk of gout, insulin resistance, and comorbidities. Heavy drinking should be avoided, whereas moderate drinking, sweet fruits, and seafood intake, particularly oily fish, should be tailored to the individual, considering their anticipated health benefits against CVD. Dairy products, vegetables, nuts, legumes, fruits (less sugary ones), and whole grains are healthy choices for the comorbidities of gout and may also help prevent gout by reducing insulin resistance. Coffee and vitamin C supplementation could be considered as preventive measures as these can lower urate levels, as well as the risk of gout and some of its comorbidities.
Thankfully this leaves me to apply my own interpretation of heavy and moderate.
hansinnm said:
“dried beans, pulses, spinach, mushrooms, cauliflower, asparagus, oatmeal…”
Are you still eating all those vegies without any “gout effects” ? Please, Utubelite, let me know. I am ready to ring all those people's neck who have kept me fom eating those healthy vegies.
I am not on Allo, but on Probenecid.
Get wringing Hans,
Choi exposed the vegetable purine myth in 2004. There are a couple of interesting purine studies related to gout. The earlier study is pretty deep, but explains that there are different types of purines. The Choi study failed to find any links between vegetables and gout, and from what I've seen, most professional advice has been updated on this. I guess I should check what my doctor is saying on this now, as I got similar advice to restrict those vegetables when first diagnosed about 10 years ago (i.e. 4 years Before Choi).
I still cannot find any studies explaining specifically why this is the case, though there are hints in the milk studies that protein intake might act like a natural probenecid, encouraging uric acid/purine excretion.
So there's mush room for improvement with your diet (sorry
)I've only just seen this, and I do not know why the search did not pick up my Devil's claw for gout review. Anyway, unless you really like the taste of this stuff, do not bother with it. It's unlikely to harm, but equally unlikely to help gout.
zip2play said:
If all else fails, perhaps you can get the uricase in some country that approves the drug even if it means you must administer it yourself…ugh!
I REALLY hate the fact that Savient isn't publishing these results.
I can't find pegloticase (Krystexxa) pricing, but rasburicase online from Canada is $500 for 3 doses.
Not sure if this means 3 days, 3 weeks or what, but it certainly aint cheap.
On the Krystexxa front, Savient have resubmitted their application for FDA approval. We will know one way or the other on 14th September 2010. 87 days to go.
The revised briefing material isn't available yet, but last years application is still on the FDA site (BLA 125293). As it's public domain, an email might get access sooner, but finding the right person might take longer than just waiting for the meeting notes!
Hi John,
I understand the zero now. Uricase converts uric acid to allantoin. I never realized it was so effective, but I've now seen (from rasburicase info in Australia) that conversion is dose dependent. Zero seems acheivable, but I'm at a loss to know if it is safe. I've also seen, in other studies, that uric acid test results have been unreliable as the enzymes continue converting uric acid after the blood is drawn, so can be artificially low unless precautions are taken.
Your situation is really frustrating, because rasburicase (sold as Elitek in the States, and Fasturtec elsewhere) looks like it could be an option, but it is restricted to patients on chemotherapy. I don't know if your doctors have any leeway on that, and it is very expensive.
Looking elsewhere, I see that BioCryst are recruiting for a new PNP inhibitor with the enchanting name of BCX4208. I know nothing of this drug, but there are trials in Dayton. If you follow the link on the Biocryst site you can see the recruiting criteria at clinicaltrials.gov. You can also search for other trials. There does not seem to be much else relevant in Ohio, but other nearby states may have something. Search for 'gout OR uric' for best results.
It is almost certainly gout. Almost every word of your description supports that.
There are some common misconceptions that cloud the issues.
- Diet often affects gout, but it is rarely a cause. The food & drink issues surrounding gout are always overplayed. It can be a factor, but hereditary issues with regard to kidney function and purine metabolism are the main causes of gout, together with medications for other conditions including high blood pressure and cancer..
- Uric acid levels often fall during an acute gout flare as uric acid moves from the blood into the joints and other tissues.
- Colchicine and prednisone are both painkillers. They should releive pain symptoms, but do nothing to get rid of the uric acid which is the root of gout pain. Colchicine is usually the best for gout.
- Untreated high uric acid leads to an increasing number of joints being affected. You do not always notice this build up, as pain does not always result immediately from slow build-up. The pain comes when the immune system sees uric acid crystals. Trauma can easily trigger this reaction, though it can also occur simply because a concentration threshold has passed. Your immine system often coats crystals without too much immediate reaction, but when a certain (unknown) amount of uncoated uric acid crystals are floating around, the immune system calls in reinforcements, and these signals are what cause the inflammation and pain.
The allopurinol approach suggested was the right one to take, and gets more and more urgent every day. However, keep getting tested even when on 300mg dose, as this is not always the final step. Dose can be up to a maximum of 900mg. The dose should be determined by your uric acid level, which needs to be lower than 6mg/dL. For the first few months of treatment, a level much below that (say 3 to 4 mg/dL) will ensure you dissolve existing urate crystals faster.
There are lots of studies showing low effectiveness rates, and many seemed to be published during the run up to febuxostat approval (or is that me being cynical?).
The answer seems to lie in the fact that Uloric (febuxostat) figures are based on the clinical trials where people are paid to take the drugs, and monitored on a regular basis. Also, many of these trials deliberately focused on gout patients who reported allopurinol intolerance.
This compares with most allopurinol effectiveness studies that are based on real-life effectiveness. Most of the ineffectiveness in these studies is either inadequate dosing or patients forgetting to take the pills. Once febuxostat is widely used, I'm certain that these factors will also render febuxostat 'ineffective'. Expect publicity on this when the next uric acid lowering treatment is nearing approval stage.
The other side to this story is that febuxostat trials were supported by comparitive studies of 40 or 80 mg febuxostat versus 300 mg allopurinol. Now, for many, 300 mg allopurinol is an OK dose, but many need up to the maximum of 900mg. This is like comparing different brands of pants without checking if they cover your butt
. Cheekily pointless.As ever, zip2play's advice is all you need. Go for allopurinol, and you are almost certain to find a cost-effective gout treatment that works. If you fall into the minority of people who are allopurinol-intolerant, then give febuxostat a try. Failing to lower high uric acid is not an option.
The studies produced to support febuxostat approval show many similar side-effects to allopurinol. Personally, I believe that many of these are simply due to our body's reaction to lower uric acid levels, and our mind's reaction to the stress of treatment. Dietary lowering of uric acid, in my experience, also causes tiredness, unfamiliar pains, feverishness etc. These are mostly cured with a determination to see the treatment through, and a pint.
Lickcheez said:
. Along with the results was a prescription for Allopurinol. Should i question this? I'm not 30 yet and don't really want to start taking pills everyday! Maybe try alternative diet and moderate drinking and such?
Very confusing stuff, some people swear by it, as others don't. Any help would be highly appreciated!!
zip2play gave the perfect answer.
I'll just add that, everything you say points to hereditary gout, and no amount of miserable diet restrictions will change your parents. 70 years of pain-free pill taking is better than 50 years of intermittent agony.
Actually, I do not have the figures to justify a 20 year drop in life expectancy from high uric acid, but I DO have some figures to show increased mortality rates. I will summarize them soon.
odo said:
Where's the art?
I found some of Nick's art by googling zaleeu.
E.g. http://zaleeu.deviantart.com/a…..u-49451721
Zaleeu: “Someone once told me that artists create their best work when the are emotionally stressed.
Well, just lucky for me, I happen to be in agony.”
Oh what a dilemma – fix the gout but lose your art
I have a better life plan for you – fix your gout, but if you need inspiration, we'll come round and kick you.
hansinnm said:
Post edited 2:50 pm – May 26, 2010 by hansinnm
GoutPal said:
.. Great observations, Hans.
Thanks too to zip2play for observations on the urate pool …
vegetarianGuy [who] answered this much more eloquently in the first response
…[and there is poor] Nate, psychologically, at a loss to wonder why flares are still occuring…
Here we are, some of the most “informed” (at least more than most of the “medical profession”) and yet still almost as much staggering in the dark as before.
I'm certainly not staggering in the dark, though often struggling to find ways to explain why I will not switch the light on.
For anyone who seriously wants an accurate assessment of how long it takes for complete urate clearance, arrange constant urine analysis and regular DECT scans using Siemens SOMATOM Definition scanner and syngo DE Gout software. I'd happily work as a consultant for 10% of cost
.For the rest of us, “lowest uric acid, as soon as possible” is clearly best practice. If pushed for an answer on how long to clear urate deposits, I'd answer “reckon on 4 to 6 weeks for every year you have had gout, if you maintain uric acid in the 4 to 5 range.”
hansinnm said:
GoutPal said:
… but I've finished (for now) my review of the length of time for uric acid crystals to dissolve….
Thank you GP; most interesting.
However, I have some difficulty accepting the figures. How can any one set up a time schedule for dissolving of UA/MSU without knowing how much of that “schtuff” is in a person's body?
e.g. Let's say one person has 1,000 mg (I don't have the foggiest idea how much a person really has) and another one has 10,000 mg of UA/MSU in his/her blood and tophi combined, and the first one has a UA level of 5.2 mg/dl and the second one 8.5mg/dl, how can one predict how long it will take to lower the level where it is acceptable and no more tophi are present?
I am sure that the 18 guinea pigs did not have the same SUA level and the same length of time over which the SUA/MSU accumulated, nor the same “other” body “misgivings”, like high blood pressure, or diabetes, or arthritis, or liver/kidney irregularities, or whatever else is bugging us.
Besides, wouldn't the UA level be different for a person with little or no tophi and only SUA in the body vs. one who has egg-size amounts of tophi located at strategic points?
While I recognize that a low UA level will help reducing the existing amount of uric acid, I can’t help thinking that it will take a hell lot longer to get rid of tophi vs. serum uric acid in your blood.
I am looking at four different uric acid crystal configurations: 1) SUA/MSU in dissolved form in the blood; 2) uric acid crystals in some whitish “liquid” (referred to as: “schtuff”) right under my skin (not yet solidified to a tophus); 3) solid uric acid crystals in form of tophi, throughout my body, and 4) a solid blob of UA/MSU right on top of my toes and/or fingers.
I can't see, for life of me, how one can throw all that in one pot and come up with a good tasting dish to swallow.
Great observations, Hans. Thanks too to zip2play for observations on the urate pool – any definitive references?
I agree totally that the solution to how long the risk of gout flares lasts depends on the amount of schtuff (urate pool) and the rate at which we lower it. Unfortunately, precise answers are well nigh impossible, because both of these are difficult to measure. So what CAN we do?
In practical terms, the articles I refer to show that urate clearance improves with lower blood uric acid levels, and that it takes longer if you have suffered gout longer. Therefore getting the lowest achievable uric acid level (especially as zip2play suggests with combined XO inhibitor and uricosuric), and starting urate lowering therapy as soon as possible is the best way forward for anyone diagnosed with gout.
Psychologically, I sense Nate is at a loss to wonder why flares are still occuring despite his best efforts. These studies show that, statistically at least, he should be prepared for a few more months. Having said which, vegetarianGuy answered this much more eloquently in the first response
.
