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Gout can involve multiple joints. In my case, there is a numb feeling in my upper ball joint just under the toes. It is usually my small toes that hurt, especially if I walk too far. It is not just the big toe. It can also spread to the wrists, ankles, and other parts of the body. Doctors call it polyarticular gout.
It's great news that the pain is subsiding.
However I'm still confused about your diagnosis. Did your rheumatologist never suggest arthrocentesis (aka aspiration) to examine fluid from your affected joint(s)?
As far as I know, this is the only sure way to correctly identify joint disease, as symptoms are common between many diseases. Also, it is possible to suffer from more than one joint disease at the same time.
I've always thought that arthrocentesis was a fairly standard procedure amongst rheumatologists. Now, it seems that diagnosis amounts to almost guessing the disease, and hoping that the treatment will confirm the diagnosis.
Anyway, thank you for your interesting insight into magnesium deficiency. I'm struggling to understand exactly how this affects calcium in the body, so I'm researching the Food Standards Agency's Review of Magnesium, which seems to be a thorough investigation of magnesium, unless anyone knows of a better source.
I wrote a little about gout & heart disease last year.
Many researchers have reported links between high uric acid and heart disease, but nobody, as far as I am aware, knows what the link is.
The best source I know for keeping an eye on the latest gout research is Pubmed.
It makes sense to have your heart checked if you have gout.
Though incidence of gout in pre-menopausal females is lower than in men and post-menopusal females, it is by no means unknown.
Uric acid production and excretion is an extremely complex process, or rather series of processes. There are many reasons for excess uric acid leading to gout, and these are in no way restricted to the typical overweight middle aged male.
There are 2 other conditions that are commonly confused with gout, and also other rarer conditions. The two common ones are pseudo gout (calcium deposits rather than uric acid) and septic arthritis (infection in the joint). One or both of these can co-exist with gout.
The test for all three of these conditions is similar. Fluid from the joint must be analysed. This simple procedure is usually done by a rheumatologist who is the best type of doctor to consult with this type of problem. Joint diseases are notoriously difficult to diagnose properly, so it is best to seek expert advice.
Tophi will disappear eventually, but only if the treatment you are taking keeps your uric acid level below 6mg/dL
Uric acid testing is a vital part of any uric acid lowering therapy. If the dose of whatever uric acid lowering medication you take is insufficent, then you are wasting your time.
Voltaren is a brand name for diclofeenac – a Non-Steroidal Anti-Inflammatory Drug (NSAID). Though it will help ease the pain of gout, it does nothing to prevent it – i.e. it treats the symptoms, not the cause.
Though your symptoms sound very gout-like, it is a good idea to confirm the diagnosis with a rheumatologist, who should also be able to assess the seriousness of your gout and advise you if diet improvement is likely to be successful, or if you need medication to lower your uric acid.
I think the eyesight thing is probably an age related coincidence – there is no reason it should be linked to gout. However, are you sure it's short-sightedness? Vision deterioration is normally long-sighted. You need to see an optician – which is a good idea for anyone over 40. High uric acid is a recognised risk factor for diabetes, and I believe there is a vision issue with diabetes, though I'm not exactly sure what this is.
Normally, gout attacks go away after a few days, though there is little to stop them coming back if uric acid remains high. There is nothing intricsically wrong with spicy food, but too much meat may be an issue. Though it has long been suggested that high protein is the risk factor, I am now coming round to the view (thanks to Iron Brian) that it is probably too much iron.
There is a good reason for taking the kind of cherry juice that your mother took. (I'm not talking about the kind you get from the grocery store.) Cherries are high in anthocyanins which helps with inflammation but they are also high in perillyl alcohol. Perillyl alcohol has been shown in a number of studies to be an effective anti-cancer drug. Another good source of perillyl alcohol is celery seed extract which many gout sufferers swear by. Add to this that some gout sufferers have used poultices made of peppermint leaves (another good source of perillyl alcohol). The other two sources of perillyl alcohol are spearmint and lavender. Since inflammation is a major factor in cancer and perillyl alcohol suppresses many of the chemicals (interleukins) associated with it, you have to wonder if it suppresses the same chemicals that trigger gout attacks. With so many people swearing by cherries and celery seed extract, you have to wonder if perillyl alcohol is the phytonutrient responsible. Pure speculation.
I can understand the reluctance to draw joint fluid.
To the patient, it sounds painful and intrusive. However, I can assure you, from personal experience, that there is no pain from the procedure. It is very similar to an innoculation, though obviously in reverse.
From the practitioners point of view, it may be an unfamiliar procedure, but if the doctor is unwilling to do it, referral to a rheumatologist is the obvious, and best, answer.
Though colchicine is widely considered to be a gout only pain reliever, PharmGKB lists several other conditions that respond to colchicine.
- [Calcium pyrophosphate deposition disease, acute (prophylaxis and treatment)] Colchicine is used for the symptomatic relief of acute attacks of calcium pyrophosphate deposition disease (chondrocalcinosis articularis; pseudogout; synovitis, crystal-induced). Intravenous administration of the medication is reported to be more consistently effective than oral administration for relief of an acute attack. However, the high risk of toxicity associated with intravenous administration of colchicine must be considered. Prophylactic use of oral colchicine may prevent repeat acute attacks.
- [Arthritis, sarcoid (treatment)] Colchicine is used to relieve acute arthritic symptoms associated with sarcoidosis.
- [Amyloidosis (treatment)] Colchicine is indicated to decrease amyloid deposition and resultant tissue damage in patients with primary amyloidosis or amyloidosis secondary to conditions such as psoriatic arthritis, ankylosing spondylitis, or familial Mediterranean fever. Colchicine has been used together with melphalan and prednisone for the treatment of primary amyloidosis.
- [Behçet's syndrome (treatment)] Colchicine is used in the treatment of patients with Behçet's syndrome. It relieves or prevents erythema nodosum and arthralgias and may also reduce the frequency or severity of oral and/or genital ulcerations in some patients. However, colchicine does not reduce the frequency or severity of ocular lesions associated with this disease or improve visual acuity in affected patients.
- [Cirrhosis, biliary (treatment)] Colchicine is used in the treatment of primary biliary cirrhosis. Biochemical indicators of disease activity (serum albumin, bilirubin, alkaline phosphatase, cholesterol, and aminotransferases) improve during treatment. Although colchicine may retard the development of fibrosis and hepatic failure in patients with biliary cirrhosis, it does not relieve symptoms, prevent or reverse histological changes characteristic of the disease, or decrease the need for hepatic transplantation. In a few studies colchicine-treated patients survived significantly longer than control patients. Colchicine may provide additional benefit when used concurrently with ursodiol for this indication. However, colchicine clearance is substantially reduced in patients with alcoholic cirrhosis. Caution and careful attention to dosage are recommended to prevent accumulation and toxicity if colchicine is administered to these patients.
- [Pericarditis, recurrent (treatment)] Limited data indicate that colchicine may be useful for preventing acute attacks of pericarditis that recur despite treatment with NSAIDs and/or corticosteroids. Colchicine has permitted withdrawal of corticosteroid therapy in some patients with this condition
Of these, clearly pseudogout (Calcium pyrophosphate deposition disease – CPDD) presents a real risk of misdiagnosis. That's not to say your doctor is wrong, just that it's better to be safe than sorry.
Diet drinks have the sugar replaced with artificial sweeteners.
In the case of Diet Red Bull, the sweeteners are Acesulfame K and Sucralose.
The only link to gout I can find with Acesulfame K and gout is an inconclusive report that it may reduce uric acid at certain dosages in rats. In “Studies on the effect of Acesulfame K on the Streptozotocin-diabetes in rats,” Meyer and colleagues state:
The concentration of the uric acid was significantly different in the mid-dose group … results are believed to have occurred fortuitously and are not related to treatment with the sweetener.
Sucralose (also known as Splenda) is a trade name for trichlorogalactosucrose. I cannot find any research into the effects of this sweetener on uric acid or gout.
Other diet drinks may use various artificial sweeteners. Again, I can find little gout-related research. However in one report on aspartame (Aspartame: neuropsychologic and neurophysiologic evaluation of acute and chronic effects), Spiers and colleagues found that aspartame had no effect on uric acid and several other blood chemicals.
From this, I assume that diet drinks may be beneficial for gout if they reduce the amount of sugar in your diet and/or promote weight loss. Of course, an excess of any single food or drink will always run the risk of upsetting the metabolism and producing uric acid, so moderation remains important, as it does with most aspects of gout diet management.
Low fat foods are a very uncertain area. Naturally low fat foods, e.g. air-popped popcorn, are generally good for gout if they aid gradual weight loss.
Unfortunately, many low fat foods are highly processed, often highly sweetened, and generally unhealthy. It pays to read the labels, and gather specific nutritional information about all foods, especially processed foods. Very often they are packed with unnatural additives that will have your uric acid levels shooting up the scale.
Iron controls the enzyme xanthine oxidase which turns the purines into uric acid. The more iron that is available to the enzyme, the more uric acid is produced. The uric acid-iron coordination complex serves as the nucleus around which the urate crystals grow as more uric acid forms around the crystals. The more iron, the more crystals.
The Agricultural Research Service of the USDA and Michigan State University have both done studies on tart cherries and found that they help fight inflammation. Also, there are substances that block the absorption of iron which promotes inflammation.
marion lasher said:
I am under a doctors care and have been for quite a few month. I take a blood test every month to check my uric acid and it remains high. I have been on allopurinol for months and it is not helping.
This suggests to me that your allopurinol dose is not right, or you need an alternative drug for lowering uric acid. That is why it is so important to see a gout specialist, such as a rheumatologist. Most non-specialists do not seem to understand that, if uric acid levels are not coming down, both doctor and patient are wasting their time.
Have you been told to drink plenty of water?
I always find that I stay with a medicine better if I know what it does. Allopurinol lowers uric acid by removing an enzyme called “xanthine oxidase”. Xanthine oxidase is involved in a number of vital processes in your body. One of these processes, is the processing of purines, a vital part of your cells' genetic materials. Eventually, it creates the uric acid. The physician, by controlling the dose, could eliminate or severely reduce the enzyme from your body. This would get rid of your uric acid but it would impair the other processes with which the enzyme performs.
There is a genetic disorder called “xanthine oxidase deficiency” or “xanithuria” where the body has too little of this enzyme. People suffering from this disorder have a number of ailments which you want no part of. Too high a dosage of allopurinol, puts you at risk of the same disorder A good physician should know about this ailment and be alert to any of these symptoms of the disorder. If they develop, he may need to reduce the dosage.
Just as eliminating the enzyme is not a good idea, eliminating the uric acid is not the right goal either. Uric acid is not a waste product. It serves as an antioxidant and helps to improve the improve the immune system. (Don't confuse it with urea which is a waste product.) The goal of the physician is to provide a dosage that gets your serum uric acid level down to where the gout attacks are unlikely to occur. This may or may not be 300. A good physician will adjust the dosage to get it to what he/she thinks is a safe level of uric acid in your blood. First, decide the safe level of uric acid, and then decide on the dosage.
There are side effects. If these show up, he may switch you to oxypurinol. Oxypurinol is a modified form of allopurinol and some people tolerate better.
Allopurinol has problems other than the side effects. It has a poor rating in terms of people staying with the medication. As your physician has said, it is a long-term medication. You are subject to attacks while the medication is taking hold. After a couple of attacks, some people lose faith in the medication and stop taking it. Other people feel that they are cured and take themselves off of it. There is a temptation with any medication to feel safer and to endulge in foods you should stay off of. The medication is designed to work with the proper diet and lifestyle. If you do indulge and suffer a gout attack, don't lose faith in the medication.
The reason that allopurinol is a long-term medication is that gout is a crystal arthritis. The uric acid forms crystals which become lodged in the synovial membrane of your joints. Your immune system reacts to these crystals creating inflammation and pain. Eventually, the attacks will abate either on their own or with the help of medication.
Part of the immune's system response is to cover the crystals with a protein coating. The crystals remain but as long as the coating is in place, the immune system ignores the crystals. Allopurinol, if it is in the correct dosage, prevents new crystals from forming but does nothing directly against the existing crystals. Over time the crystals dissolve but it may take months or years. Until the crystals dissolve, you are not safe from gout.
If you are taking allopurinol, it is vital that it is monitored properly. This is always best done by a rheumatologist, especially when you have complications like impaired kidney function.
If the dosage is not right, you are wasting your time. Regular uric acid tests are a must.
This won't help with the pain straight away, but you should be pain free in a few months if you take allopurinol every day.
The rheumatologist should be able to recommend a more effective pain killer until the allopurinol has got rid of the uric acid.
Allopurinol is not a medication that you can stop and start. It lasts for about a day in your body, so as soon as you stop taking it you are back where you started.
Also, it is vital that the dosage and your uric acid levels are monitored regularly. The dosage must be enough to lower your uric acid below 6mg/dL (approx 350 on the µmol scale). If it is not below 7, you are wasting your time.
Your high blood test levels (presumably for uric acid) are probably due to stopping taking the allopurinol.
Whenever you have a need for other medications, you must tell whoever is prescribing the medication that you take allopurinol every day. Penicillins like cloxacillin are excreted in urine through the kidneys. It is possible that the kidneys cannot handle both allopurinol and cloxacillin at the same time. Or, perhaps you are not drinking enough water. Only a proper medical examination can answer this.
There are many reports of skin rashes when allopurinol is taken with cloxacillin and other penicillins. Simply stopping and starting either or both of these drugs without proper medical advice and supervision is wrong.
If you stop taking antibiotics before you have finished the course of treatment, you weaken the bug causing the infection, but you do not kill it. It can then grow back stronger, and develop resistance to the drug you have misused – a process similar to the innoculation process that we humans use to develop resistance to diseases.
This is a very bad thing to do. At least when you misuse allopurinol you are only affecting yourself. Misusing antibiotics creates so-called “superbugs” – drug resistant diseases that affect all of us, often fatally.
It's time to stop messing about, and take your medications seriously.
Take the allopurinol every day. Test uric acid monthly or as advised by your doctor and adjust dosage to achieve normal uric acid levels. Never stop doing this.
If you need other medications, discuss possible interactions and different options before you start taking them.
There is some interesting research work that has been done by Andrew Ghio and others. One is a study titled “Iron regulates xanthine oxidase activity in the lung”. Xanthine oxidase is also the enzyme that converts purines into uric acid. The more iron, the more uric acid. The less iron, the less uric acid. Ghio has done other studies on the subject. The writeup was at address http://ajplung.physiology.org/cgi/content/full/283/3/L563. The significance is that there are foods that help the absorption of iron in the intestines and those that inhibit the absorption of iron. By including the foods that inhibit the absorption and avoiding the ones that promote the absortion, we can affect the amount of iron we take in. Unfortunately, the big food that promotes absorption is ethanol as in alcoholic beverages. The foods that inhibit absorption are dairy foods (particularly low-fat dairy), coffee, and foods high in phytic acid. Anyway, take a look at the research and see what you think.
Hi
My Doctor said that I might suffer a gout attack after I first start taking Allopurinol and so he told me that at the first sign of one I should take indometacin for the pain: 1 or 2 25mg pills 3 times a day.
Actually on reflection he was a bit ambiguous and he may have meant that I should take it any way as a preventative measure but I think I'll wait and only take it if I need to!
My next appointment with my GP is in four weeks when he will “see hoe it's going” and increase my dosage.
Thanks again to you and everyone for the support and advice!
Good Luck, Rowland.
I'm particularly interested in the aftercare you receive – frequency of checkups, uric acid test results etc.
Has your doctor suggested what to do if you get a gout attack whilst you are taking allopurinol?
I look forward to your reports
Hi
I raised the original post and your replies have really eased my mind and helped me make my decision. I started taking yesterday – starting with 100mg and working my way up to 300mg after about a month. I'll let you know how I get on!
Rowland
The advice to see a rheumatologist is excellent. There are a number of ailments that mimic gout and aren't. To really be sure, the doctor needs to take a sample of fluid from the joint(s). They can then analyze the fluid sample to see if there are crystals and what kind. Too many family practicioners diagnose on the basis of the symptoms.
You MUST take her to a rheumatologist.
Today.
The body has no effective way of excreting iron. It guards its iron stores very jealously. Each day, we need only a trace amount of iron to replace the trace amount that we lose. Meat is the major source of iron for us because our bodies can readily absorb it. While vegetables and grain contain iron, we can only absorb two to three percent of that iron when these foods are eaten by themselves.
Excess iron does cause problems in the body. To protect itself, the body has a protection mechanism. The higher the body's iron stores, the less iron is absorbed from the food eaten. The problem is that that is only partially effective. If you are like me, you have been eatiing meat with every meal for decades. The result iis that iron has been building up for decades.
After you are fully grown, your need for iron drops dramatically for men. After menopause, women's need for iron drops dramatically. There are groups of people, like premenopausal women, who need more iron. For most of us, we don't need a multivitamin containing iron. Also, we do not need iron-enriched food. (Obviously, if your physician says that you need it, then follow his/her advice.)
I eat meat and seafood sparingly. I have switched to a multivitamin without iron. In addition, I check the foods I buy to see if they are iron-enriched. If so, I don't buy them. Also, I intend to start making regular blood donations. After I have made several donations, I will post a message about the impact. It may take a while since there is a period between donations. Is anyone out there who is already donating blood? If so, has it made a difference?
I've had a look at the research you mention.
The McGrath Rigby study is interesting, and available in full online. These reports often get moved or taken down, so I won't link to it directly. However it is easy to find by searching for “Hepcidin: inflammation's iron curtain”.
There is no abstract available. The most interesting part of it, for me, is:
A broader phlogistic potential of iron towards the joint comes from a recent report that iron depletion by serial phlebotomies diminishes recurrences of gouty arthritis
The report to which it refers is “Near-iron deficiency-induced remission of gouty arthritis”, a fascinating tale of blood-letting and gout remission.
The abstract is available:
Objectives. Previous evidence supports a role for iron in the pathogenesis of gout. For example, iron, when added to media containing urate crystals, stimulated oxidative stress with subsequent complement and neutrophil activation. Conversely, iron removal inhibited these responses as well as urate-crystal-induced foot pad inflammation in rats in-vivo. The objective of the present study was to investigate whether or not iron removal may improve the outcome of gouty arthritis in humans as well.
Methods. Quantitative phlebotomy was used to remove iron in 12 hyperuricaemic patients with gouty arthritis and maintain their body iron at near-iron deficiency (NID) level (i.e. the lowest body iron store compatible with normal erythropoiesis and therefore absence of anaemia).
Results. During maintenance of NID for 28 months, gouty attacks markedly diminished in every patient, from a cumulative amount of 48 and 53 attacks per year before (year –2, –1), to 32, 11 and 7 during induction (year 0) and maintenance (year +1, +2) of NID, respectively. During NID, attacks were also more often of milder severity.
Conclusions. During a 28-month follow-up, maintenance of NID was found to be safe and beneficial in all patients, with effects ranging from a complete remission to a marked reduction of incidence and severity of gouty attacks.
KEY WORDS: Gout, Arthritis, Hyperuricaemia, Oxidative stress, Near-iron deficiency.
Anybody know where I can get leeches?
Copyright is the same on websites as it is anywhere else – you must get the permission of the copyright owner before reproducing the work.
There is a “fair use” exception, whereby you may quote excerpts for review purposes. This area is very complicated, but generally, the limit is around 10%.
As far as I know, you are at liberty to describe the ideas in your own words. Similarly, I believe you may, for instance, present a chart of data in your own format.
Most scientific works produce an abstract which may be reproduced in full. Almost all of these are available on PubMed.
I have just read through the message that I posted earliier. The article that Janis Kelly wrote was on the subject of the work done by McGrath and Rigby. This might not have been clear. I have been reading some of the work done on Rheumatic Arthritis. These works take it for granted that iron is heavily involved in the inflammation process of arthritic diseases. Sure there are differences, but the inflammation processes work about the same. With a few exceptions, the feeling I get is that gout is the poor cousin of the other types of arthritis. I read several articles that speak of gout as “curable”. Somebody should spend some time going to the different gout websites and see how curable it is.
I believe hyperuricemia should be treated as a serious medical condition in its own right. I do believe that it contributes to renal disease, high blood pressure, cardiovascular disease, and adult onset diabetes. They reinforce each other. The medical profession calls it “metabolic syndrome”. The rest of us know it as “falling apart”. Most of the family physicians that I have seen are so focused on medicines and surgery that they are not as knowledgeable on two important areas that are critical to dealing with gout. One is in the area of sleep research and especially sleep apnea. The other is in nutrition. Nutrition is not considered as a legitimate field of medicine. It is as if the medical profession is waiting for the disease to happen so they can treat it with their medicines. The best defence is to keep the ailments from happening in the first place. This is why nutrition is the single most important field of medicine there is!
I'm new to blogging. Exactly, what are the copyright laws as to what is posted on internet sites? Does quoting a copyrighted work count as publication?
GoutPal said:
Medically, it is a real shame that doctors do not put more emphasis on the need for uric acid control. If they focused more on removing the cause of gout, and less on the masking of symptoms with pain-killers, we'd all be much better off.
The problem may be that there are just not enough of us out there to justify good research. Believe me I was shocked to find out that a new acid inhibitor had been developed and shown in trials to be more effective than allopurinol. That's another question I will have for my doctor. When fubuxostat is finally approved by the FDA, should I change over to that drug. I can hear the doctor now: “why rock the boat, if it works for you then why change”. Then I suppose I will have to consult a clinical pharmacologist. Does a new drug mean a better drug? What are the benefits of Fubuxostat over Allopurinol? How and why is it more effective? We know about Allopurinol in the long term but as with any new drug, we cannot possibly know if there are any long term negative effects from Fubuxostat, even though the trials have been very promising.
Wise words, Giovanni.
The “pill for life” objection is logically a weak one. It is one that I have felt, and probably ranks with my earlier objections (vanity this time) about wearing glasses for life. As we have the means to live a pain-free life through allopurinol, surely that is better than struggling for years just for sake of popping a pill. Just as wearing specs beats walking into lampposts.
Medically, it is a real shame that doctors do not put more emphasis on the need for uric acid control. If they focused more on removing the cause of gout, and less on the masking of symptoms with pain-killers, we'd all be much better off.
I have to tell you goutPal that I am so glad I found this forum to interact with fellow gout sufferers. I think it is safe to say that none of us wants to take a pill for life. When I was originally diagnosed with gout, my doctor told me that if I only suffered a few attacks per year, then why take a pill everyday. I was 21 years old at the time. The thought of taking a pill everyday at that age was never even a consideration.
I did not have another attack until I was 27. Fine I said, I can deal with this right. My next attack happened when I was 31. Good I said. I have only had 3 attacks in ten years no big deal. That is when the trouble started. I began getting more frequent and disabling attacks. More protracted and more painful. They would come at the worst possible times. On vacation, at weddings etc. I took my son to College in August. Guess who was limping around like an old man. Trips to the ER became more frequent. I remember getting shots of the drug Toradol for the pain. So I did begin to take allopurinol in my mid 30's. However, I never intended to stay on the drug and I ceased the therapy after several months. I have been off and on the drug many times even though it works perfectly for me.
My concern has always been liver damage and other possible side effects that I was not prepared to deal with in the least. Now, at 45, I have thrown in the towel. I thought I could beat the gout, but the gout beat me. So now I am back on the allopurinol after my latest attack. I am actually taking the brand name, Zyloprim. I intend to stay on this drug for the forseeable future. I am not prepared to endure permanent joint damage. I have no tophi thank God, but why risk it at this point. I am just tired of the whole routine. Indocin makes me very sick and I cannot take it as prescribed. Colchicine works, but if I take too much, it also makes me sick. I find that gout takes a physical and mental toll at this stage of my life that I am just not prepared to deal with any longer.
Thank you for the welcome and the response. Given this latest gout attack, I have concluded that I must take the medication in order to return to normal. As I have aged, the attacks have become prolonged. This latest is not the worst attack I have ever suffered, but the 3 week period in dealing with it was quite taxing on my nerves and my body. I have concluded that once an attack arrives, my entire body is affected. I do not feel well and I cannot think clearly because of the combinationof the pain, elevated uric acid levels, and the treatment to attack the problem. I am just now, nearly a week after restarting the allopurinol, starting to feel like myself. Therefore I have finally given up and decided to take the medicine in the long term unless my doctor tells me otherwise. My concern has always been residual damage to the body because of the allopurinol. But, I have done enough research on the drug which indicates to me that it is very safe and effective, unless one has a allergic reaction to the medication. Even then, once the medicine is stopped, you should feel fine. Allopurinol has been around for nearly half a century and if there were any significant affects, we would know about it after all of this time. I no people who take one cochicine tablet along with their daily dose of Allopurinol. I do that for the first several weeks after going back on the medicine to prevent an attack while my uric acid levels are being reduced.
Thank again. I look forward to further discussions.
Welcome Giovanni,
I understand the reluctance of taking a pill everyday just to ward off infrequent attacks, but the real issue is not whether you have a painful gout attack.
Gout pain is due to your immune system responding to the presence of uric acid crystals. It attacks these in the same way as a virus, but cannot kill them – they merely get hidden.
The uric acid crystals, coated with proteins from your immune system build up slowly. They do not always produce the severe painful gout reaction. Often you simply experience a little tingling, numbness or other slight discomfort. But the crystals are still building up.
They are the fuel for more intense gout flares in future. But, worse still, they are the building blocks of tophi that can damage your joints, causing the worst gout pain imaginable.
The reasons for taking allopurinol are twofold. Firstly, to get rid of existing uric acid crystal deposits. Secondly to prevent new crystals forming.
It is for the second reason that you must continue with allopurinol even when the gout pain stops. More importantly, you must keep monitoring uric acid levels.
You might find that a lower dosage or allopurinol “holiday” is feasible, as long as your uric acid level has kept below 7mg/dL for a year or so. But you must continue to be tested as advised by your doctor, even if you are showing no symptoms. If uric acid starts to rise again above 7mg/dL (or you show any other gouty symptoms, as uric acid levels are notoriously difficult to measure consistently), get back on the allopurinol.
Thank you for your kind comments about my website.
I have mentioned febuxostat before. You can see references by searching for febuxostat in the search box near the top of this page. The fullest account was in my December 2006 newsletter, so an update is long overdue.
I'll add a febuxostat review to my list of things to do. I'd love to hear of personal experiences or views of this new gout medication.
