Gout Pal Interactive

It's a huge mistake to manage gout by simply controlling pain, or by using pain to assess the progress of gout.

3 attacks in 10 years does not sound much, but if uric acid levels are high, then crystals can still form slowly without a typical acute gout flare.

There are developing techniques in ultrasound and other non-invasive scanning technologies to assess joint damage. Unfortunately, these are not widespread, though it is always worth asking a local rheumatologist to see if you are lucky enough to have access.

Assuming, like most people, you cannot assess joint damage easily, the safest approach is to recognize that you are at risk of joint damage. Therefore you need to do something about it, now.

Your GP is doing you a huge disservice by waiting for more frequent attacks before doing something. The fact that you have had gout in the past puts you in a high risk group for joint damage. The only way to avoid such damage is to get uric acid below 6mg/dL, and keep it there.

Without proper monitoring and control of uric acid, you end up in the place where you worry about everything and how it might be affecting your gout. Your goal should be to lead a reasonably healthy life, without having to worry about the type of details you mention.

Exercise is certainly good for you. Whilst it can raise uric acid in the short term, regular exercise should lower uric acid in the long term. Your diet sounds healthy to me, so I would suggest keeping your healthy lifestyle, and managing your uric acid levels. Too much is made of individual food items, and other factors such as genetics and environment (especially temperature) play a much greater part.

No, nokka, you haven't missed anything. This is exactly the right thing to do, but it is rarely viewed that way.

Usual advice is to try diet & exercise, and if that doesn't work, start allopurinol. It makes much more sense to start allopurinol (or other uric acid lowering therapy) immediately, as this protects you from excess urate whilst you are improving your lifestyle.

If I were you, I'd get the uric acid lowered now. It takes a few months to dissolve old crystals, which can cause a gout flare. Get this out of the way before you travel.

I often find it difficult to know where to draw the line on diet for gout.

On the one hand, many people stress the importance of purine control. On several other hands there are arguments that calorie control, iron control, hydration, avoiding fasting or bingeing, and acid/alkali balance are equally, or more, important.

Much depends on the individual. Calorie control might be vital to one person, but not important to another. Purine control might be more important to a uric acid over-producer than it is to an under-excreter. Etcetera, etcetera.

A further complication is the contribution of anti-inflammatory foods. Lots of fruit and vegetables might have little effect on uric acid, but might make one naturally less resistant to inflammation, and thus less affected by accumulation of uric acid deposits.

We all come from different starting points. We all have different attitudes to the acceptability of daily medication. We all have different degrees of diet restriction that we find acceptable.

There is no “one size fits all” solution, except that, whatever you do, gout management only makes sense when you know your uric acid level, and do whatever suits you best to keep it under 6mg/dL.

Had Chilon of Sparta asked: “What is best for gout?” The Oracle's reply, “Know thyself,” is still completely appropriate.

We must remember that ALL the food proscriptions and prescriptions came from before the days of allopurinol and probenecid and they served to fill a need for doing SOMETHING even in the face of a nearly intractable disease with disfigurement and death as the common endpoint…that is human nature. Whether ANY of them works is subject to skeptical debate.

Look at it this way, would you today deny a teenage diabetic his daily insulin because long before insulin they practiced  the ketogenenic diet (all fat, little protein and NO carbohydrates) which kept the poor kid alive until he turned 20. Would you use talismans, prayers, and smoke to cure a modern case of bubonic plague, or copper bracelets to cure arthritis. Cherries, baking soda, no fish, no beer, no lentils or organ meats all fall close to the same kinds of treatments, they were better than nothing, but just barely, AND they got you to pay some quack, priest, or shaman some money.

noka,

Don't look at allopurinol as a temporizing measure to be used for trips abroad, or for a short time til LIFESTYLE kicks in. If you plan to use it that way it is better done without because going on an off is SURE to cause more problems than it helps.

On the matter of using it “until all the deposits are gone” I am reasonably convinced that after  several attacks the deposits will NEVER be completely gone. Eventually one of those colorful PET scans will prove this. THere will ALWAYS be residual crystals walled off by the body and invisible to the bloodstream…MOST of the time, but rest assured they will peak out occasionally and present a site for easy crystallization of new uric acid.

In your favor, 3 attacks in 10 years is something that shouuld be MONITORED, not treated. If they start increasing to 2 or 3 a year or even one crippling attack a year, then you'll need to reexamine allopurinol. For your months abroad, make sure you take a bottle of a good analgesic…colchicine if possible, although in truth Southeast Asian doctors might be more adept at dealing with gout than Western practitioners who are more impressed with the “machine that goes 'BING'!”

Is there any way I can tell if I am doing permanent joint damage ?

Be assured that EVERY attack causes scarring and some permanent joint damage; whether it is grossly obvious or not depends on the severity and length of the attack.

Hi, guys. I have been today for my blood test and have a doctors appointment for next monday for the results.

Couple of things: The slight inflammation and tenderness is continuing. In fact, over the weekend it got a bit worse. I woke in the middle of the night friday (quite usual these days with all the water being drunk ) and the toe felt pretty stiff and a bit fizzy. I lay there thinking 'Oh no, please don't let this be another full blown attack'. Anyway, it remained a a bit like that through saturday and sunday, though today its back to its normal low level tenderness. My understanding is that the blood test should only be done once the attack has stabilised (4 weeks since the attack now). Do you think the blood test could be affected by this ?

It seems I can move from the toe being almost completely normal, to feeling it quite a lot – in quite a short space of time. Doesn't seem there is any rhyme nor reason to it – no obvious trigger. Is that the way it is ? Plus I think I get slight tingly, almost neuralgic tingling in my knee or sometimes elsewhere for a second or two sometimes. Its very slight and sometimes I wonder whether I've imagined it. Any thoughts ?

Finally, as regards allipurinol. My question above  regarding whether  I should take allipurinol for a time to get my uric levels down met with different responses. GoutPal thought that sounded a good idea; zip clearly felt that could be harmful. I'm interested in what way that could be considered a harmful thing to do ?

Thanks for any input.

Hi, got my blood test results today. The results weren't in mg/dl as I was expecting, but in umo/l.

The result was 467 umo/l, which the doctor said was just outside the normal range and were pretty good for someone who just had an acute attack. He has requested another blood test to be done in 3 to 4 weeks and to see how they are then.

He feels that as I've only had 3 attacks in 10 years and the levels aren't really high I needn't go on allipurinol as yet. He feels we need to continue to monitor levels. He feels that if the level remains a bit high we would still have few weeks to start allipurinol at 100mg before I go to South East Asia.

Any thoughts ?

The doctor I saw is the best in the practice, in my view. It transpires that his brother has gout, so he knows quite a bit about it.

His point is that from a clinical viewpoint you don't start to treat with allipurinol unless one of 3 things are in place: 1. the uric acid level is very high 2. you have had 2 or more gout attacks in last 12 months or 3. there is evidence of joint damage. In his view, none of those conditions are yet met, so he advises that I wait and see. He feels it could be another 5 years before I have another attack.

It is clear that I am susceptible to gout, but the attacks are rare. It may be that in normal circumstances my body can cope; it is only when a combination of factors come together that causes the trigger. To be honest, before this latest attack I had almost completely forgotten that I'd had gout in the past. I have never limited my diet or lifestyle in any way, sometimes having quite high levels of the things which are notorious for bringing on attacks – without any problem for at least 5 years.

So, for now, I think I'll take the Doc's advice and see what happens. I have another blood test in about 3 weeks, so we'll see what that says. I'm going to keep my fingers crossed and hope another attack doesn't happen soon. If it does, that's when I'll take the allipurinol route.

Wish me luck.

I firmly believe that non-invasive scanning methods will improve in sophistication and availability. I hope to see the day when an annual full body scan to check joints, heart, lungs, digestive tract etc is a standard routine.

When that time comes, and high uric acid gets treated at the first sign of tendon and cartilage damage, the medics will comment “Do you remember the time when they used to wait for the pain to get too bad before they treated this?”

In fact, we can see the results now from early DECT scans and it is clear that damage is being done much earlier than was previously the case:

In addition, the study also provided new information on the presence of subclinical tophi and the accumulation of monosodium urate crystal deposits in clinically challenging anatomic regions. “To our surprise, the study showed that uric acid can be  initially deposited in tendons and ligaments near and within the knee joint, ankle joint ,wrist , ie  in the collateral ligament / cruciate ligament and deep flexor tendons of the wrist”, says Dr. Nicolaou. “This is very important to know, since these deposits can increase the susceptibility of tendons and ligaments for tears. If we are able to detect the disease in an early stage, we can initiate a treatment to prevent destruction of the tendons and ligaments and joints where subclinical tophi are present.”

Science is moving on to help gout sufferers. Sadly, few doctors are keeping in step. My specific answer to point 3 of nokka's doctor is that it is now abundantly clear that one gout flare is evidence of joint damage. Not proof, I admit, but not statistical risk either. It is strong evidence.

Why, I wonder, do doctors spend so much time, effort and money addressing other preventative health issues, e.g. high blood pressure, where risk is statistical, yet insist on waiting for proof of joint damage before acting on gout.

In fact, the evidence has grown stronger this year. Dalbeth, as long ago as 2005, showed how tophi grow into the bone, causing permanent joint damage. Earlier this year, Carter and colleagues looked at seemingly unaffected joints of gout patients who had at least one clearly damaged joint (erosion detected by normal x-ray). Using MRI scans they found that as well as bone damage, there were problems with bone marrow, connective tissues and surrounding soft tissues. In seemingly unaffected joints they found similar problems, mainly with bone marrow and connective tissue. Note that these are the standard MRI scans, not the DECT scans that show urate deposits.

Gout is a progressive, debilitating disease. The sooner you get uric acid levels down, the less damage you cause.

Apologies – I actually googled 'umol/l gout'. It comes top.

Post edited 3:36 pm – October 4, 2009 by zip2play

'Although plasma is saturated with monosodium urate at a concentration of 7.0 mg/dl, higher concentrations of urate can remain in a stable supersaturated solution in plasma

The fly in the ointment is that supersaturation by definition is a solution that has more solute than can be normally held. It is “broken” when the first crystal forms…then the solution goes to normal saturation with the instantaneous release of crystals. Dropping the tiniest crystal into a supersaturated solution will INSTANTLY crystallize it.

 Thus supresaturation is only possible for a person who has NEVER had a gout attack. ONE attack and you have gout rendering supersaturation impossible. A person with gout CANNOT hold a 7 mg/dL UA in solution.

Too many doctors have forgotten their high school chem classes. Without rrealizing how stupid it is what they are actually saying is

” People wilthout gout do not have gout attacks.”