Talk:Gout/Archive 1

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Video Talk:Gout/Archive 1

Indomethacin(idicin,microcid brandnames) and Allopurinol(Zyloric brandname)

I,after a pituitary tumour surgery(gland not removed) is experiencing gouts in my leg finger's junction.

as usual ,last week also a gout occured after almost 2-3 months gap.so took microcid and zyloric as per doctor's earlier prescription. next day ,I cannot breath!almost like asthma/suffocation.took asthalin inhaler to free.still ,I experience suffocation like a asthma patient. After visiting a Doctor ,He said microcid can be the reason.I am stopping both zyloric and Microcid and going to take Cherry fruits which many a times saved me from gout. Please add this sideeffects of Indomethacin to the wiki as well as doctor also said the same. 59.93.1.152 (talk) 08:30, 24 March 2009 (UTC)

Maps Talk:Gout/Archive 1

Purines vs proteins

The connection between high purine and high protein diets needs explanation, because purines are not proteins. Una Smith 20:50, 4 June 2007 (UTC)

This is an excellent if nonobvious question. For many years protein content in foods was used as a proxy for purine content; not because purines are a component of proteins (as you point out, they're not) but because the protein content of many foods was well-known and easy to measure, whereas the purine content was not as well-known; and because there was a general non-scientific association of certain high-protein foods like red meat and beans with gout. But in [5] "Purine-Rich Foods, Dairy and Protein Intake, and the Risk of Gout in Men" Choi et al. (cited in the main article) showed quite the opposite, as you surmise, namely:

These data support our findings that the consumption of protein does not increase the risk of gout but, rather, may actually decrease the risk and that the protein content of foods may not be a good surrogate for their purine content.

So, you are correct, but it was only recently that the protein-purine association was shown to be false.Derek Balsam^(talk) 21:17, 4 June 2007 (UTC)

Hm. A diet high in nitrogen (meaning high in purine and/or protein) was associated with improved excretion of uric acid as early as 1912. Una Smith 03:18, 5 June 2007 (UTC)

src: ard.bmj.com

Overconsumer vs underexcreter

The connection between normal serum urea and gout is poorly explained. Also, does diet modification help if the problem is underexcretion? Una Smith 20:50, 4 June 2007 (UTC)

This is important. Apparently a high percentage of new gout patients are prescribed Allopurinol but do not obtain sufficient relief. Physicians should switch them to Probenecid promptly in these cases, and gout sufferers need to understand the issues sufficiently to force the issue with their physicians. As many have noted, many doctors have little familiarity with gout and take a rather passive approach to treatment.Msml (talk) 15:06, 20 July 2009 (UTC)

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Bad sentence requires clarification

The following confusing sentence in the gout article needs work: "Avoiding alcohol, high-purine foods, such as meat, fish, dry beans (also lentils and peas), mushrooms, spinach, asparagus, and cauliflower can lower plasma urate levels." Is spinach, for instance, something for gout patients to avoid, or is it something that lowers plasma urate levels? You can't tell from the sentence. --Jim --The preceding unsigned comment was added by 64.58.2.30 (talk) 17:30, 18 February 2007 (UTC).

How about this one: (Under 'Prevention') In conjuction with the below some people may find that some food is a 'trigger food' some items include large amounts of vitamin C and oats (flapjacks). Two sentences in one? Nobody saw and corrected this one? Kortsleting 04:20, 27 May 2007 (UTC)

Also, it says "oats (flapjacks)". I know that in UK flapjacks are made of oats (what we in North America might call granola or oat bars). But in the US these are two entirely different foodstuffs, which could be confusing to North American readers. "Oats" alone would be much less ambiguous. Derek Balsam^(talk) 17:41, 27 May 2007 (UTC)

The following sentence is also confusing for someone who (like me) doesn't already know what it's trying to say: "Uric acid is more likely to form into crystals when there is a hyperuricemia, although it is 10 times more common without clinical gout than with it.[3]" What is the "it"? Is this sentence trying to say something along the lines of "Uric acid is more likely to form into crystals when there is hyperuricemia (although in nine out of ten cases, hyperuricemia does not involve gout)." I don't know anything about gout, so I don't feel comfortable actually editing the gout page myself--could someone who does please clarify this sentence? Thanks! 67.183.139.255 (talk) 19:41, 23 March 2008 (UTC)

src: www.clinsci.org

What about Water

Is a high ph or low ph better for gout? Is soft or hard water better for gout?(24.115.145.150 21:44, 10 March 2007 (UTC))3/10/2007

Metabolism works by active transport, which requires paired sets of chemical processes to adjust homeostasis. Gout is at its root a problem in purine metabolism. It can be altered by behavioral changes, but the small effects of water pH are swamped by other metabolic factors.Msml (talk) 15:11, 20 July 2009 (UTC)

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Weasel Words

This article has a Weasel Words tag on it. Thus the entire article is list as having weasel words. I'm removing that tag and adding a Weasel Words tag just to the sections that appear to have weasel words rather than letting the entire article be branded weasel. Fanra 13:35, 2 May 2007 (UTC)

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References to reference

One of the references in this article, Abrams B. Gout Is an Indicator of Sleep Apnea Journal SLEEP 28(2), Feb 2005, p. 275., is to an article that is not freely available on the web. That author has written two related articles that are freely available covering the same material. I am not certain if it would be appropriate to link to them in the main article or not. They are not as formal as the article in SLEEP. They Are: Curing Gout: a Personal Journey of Discovery and Burton Abrams Follows Up on Sleep Apnea and Gout

I have lifted the dietary recommendation from the page in French and translated them with a free translation service ( hence the poor grammar) but some recommendaitons clearly contradict the page in English. Particularly Tuna and salmon are recommended while the English version says to avoid fish. Does this imply the pysiologies of diefferent language speakers are different? What about bilingual people?

A useful article on gout is by Zina Kroner, D.O. Associate Medical Director, The Hoffman Center.LoopTel (talk) 23:26, 26 December 2007 (UTC)

"The dietary system is encouraged with a food poor in purines: --129.96.142.21 04:29, 26 June 2006 (UTC) Avoid the offals, the anchovies, the bouillons, the seafood, the asparagus, the spinach, the legumes. Consume preferably: cherries, celery, strawberries, cornflowers, weak dairy products in fat, bread (without white flour), tuna, salmon. An slimming is desirable as well as a significant decrease of the taken one of alcohol.

src: static.independent.co.uk

Diet Soda?

It says in the article diet soda should be avoided because it acts as a diuretic. But so does any drink that contains caffeine. And some diet sodas are caffeine-free. There's no citation for the claim that diet soda in particular is bad for gout, so unless one is added within the next few days (and not from some crackpot's (i.e. Joseph Mercola) web page, I'm removing the statement.

I haven't looked up a reference for you, but diet soda is a diuretic and can dehydrate you. As urine is how uric acid is expelled, being dehydrated can really hurt a gout sufferer. - JNighthawk 22:08, 15 July 2006 (UTC)

It is the caffeine in diet soda that makes it a diuretic. At the very least the article should be changed to specify all drinks containing caffine not just diet soda. I would also add that caffenines diuretic effects are relatively mild and to say that it is a cause of gout is proabbly pushing it a bit.Graemec2 09:48, 8 March 2007 (UTC)

Diet soda pop generally contains the sweetener Nutrisweet. This sweetener uses aspartame which converts into formaldehyde above 80 degrees F. This is then converted into uric acid.

No, formaldehyde is not converted to uric acid. Formaldehyde is converted to formate via aldehyde dehydrogenase, then the formic acid is converted to CO₂ by folate dependent pathways or excreted directly via renal mechanisms. Aspartame is nowhere on the urate pathway. See for example http://www.hpa.org.uk/chemicals/compendium/Methanol/kinetics.htm. Derek Balsam^(talk) 22:03, 2 July 2007 (UTC)

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Extra-articular effects

rstWhat about extra-articular effects of the deposition of uric acid crystals ? Soft tissue, kidneys etc
Kpjas 07:43, 8 Oct 2003 (UTC)

Why don't you add that in? --Alex.tan 07:06, 9 Oct 2003 (UTC)

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Overindulgence

Should not drinking alcohol to excess have been removed from the bulleted list? (as a method of avoiding dehydration)

And gout is commonly believed to be caused by overindulgence in rich food and alcohol... could someone debunk this if it's not true. fabiform 02:24, 11 Jan 2004

I was a vegetarian in my 20s when I had my first gout attack, and I hardly ever drink alcohol. -phma 14:50, 27 Jun 2004 (UTC)

There's also a genetic component to this condition. Gout sometimes runs in families. I have it, and so have others on both sides of my family. I'm pretty sure I've got a genetic predisposition towards gout.

JesseG 06:02, Jun 5, 2005 (UTC)

I recently had an attack of gout. My doctor decided to draw blood to do a test for uric acid. He said that the normal level was from about 3 to about 7 mg of the stuff, mine was up over 8.

JesseG 19:48, July 23, 2005 (UTC)

My first gout attack was after eating a lot of rich French goose liver spread Pate de foie gras. My second gout attack was triggered by a bottle of beer a couple years later. It was not necessarily the alcohol contents but the brewer's yeast that caused the on-set. Brewer's yeast is a rich source of purine. Alcohol is not the only cause, but it should be one of the major cause. The overindulgence theory had been around since Roman time. Removing an age old theory because one sufferer didn't drink alcohol is a bad move. Kowloonese 19:01, Jun 7, 2005 (UTC)

Perhaps there can be a cumulative effect. Being 63 years old I lead a fairly steady life, however we celebrated the end of term with a party last Sunday, and I spent the week eating up the left-overs - salmon, souvlaki and keftedes (meat balls)etc. I had a delicious "ladera" - olive oil based vegetable dish rich in tomatoes, onions, courgettes and aubergines - it is about 50% tomato sauce on Wednesday. Then a few glasses of wine and a couple of beers with friends on Thursday and I woke up yesterday morning with an agonising pain in my right big toe and aches in other joints. I tried drowning it in pain killers, but to no effect, so I went to the doctor this morning and he said "Gout". He has prescribed Colchichine as a short term remedy, 1 mg every two hours. I looked it up on the net, The effects are similar to Arsenic poison, ending with death from respiratory problems. I have supplemented it with cherries. If you do not hear from me again you can assume that this is a somewhat unwanted side effect. Otherwise, I will report progress. (please see warning at bottom of post) Sunday 16.15 GMT I have kept a log of the effects of the medication I have taken since starting to take Colchichine yesterday at 11.00 GMT. 13.00 GMT No noticeable effect. Went to bed, drank a lot of water, took 1 mg Colchicine,two ibuprofen tablets (400 mg) and one stilnox sleeping tablet. 15.00 GMT Woke up and took another 1 mg Colchicine. no change. 17.00 GMT Woke up. Noticeable improvement in condition generally, less pain but still acute. Took 1 mg Colchichine. No noticeable side effects. Practised the piano - feasible. Surfing the net I discovered that all the foods I had been eating(see above) were prime suspects in causing gout, but this seems to be true of almost everything with any flavour. 19.00 GMT Phoned my brother - a long time sufferer from gout. Told me he took colchichine. Said pain would go in a couple of days. Told me to stop taking tablets when side effects became noticeable - i.e diarrhea. Took 1 mg Colchichine. Drank plenty of water. Ate spaghetti with kefalotiri (cheese) topping. 21.00 GMT Took 1 mg Colchichine and one Ibuprofen. Definite improvement. No side effects noticed. Being 23.00 hours local time I took another stilnox tablet and went to bed. Drank some more water. 21.00 to 05.00 GMT today. Effects of drinking large quantities of water woke me about every two hours for trips to bathroom. Did not take any Colchichine until 05.00 GMT. 05.00 GMT (07.00 local time) Got up. definite improvement - only mild pain. Took 1 mg Colchichine. Drank 1/4 ltre low fat milk. 07.00 GMT Took 1 mg Colchichine and 1 Neurofen plus. Temporarily discontinued medication for High Blood pressure (Triatec and Tenoretic) as both of these are diuretics. Cannot decide whether possible stroke/heart attack is preferable to re-occurence of gout. 09.00 GMT Took 1 mg Colchichine. Mild attack of diarrhea. 13.00 GMT Took 1 Ibuprofen. Colchichine ended. Definite improvement, though still sore. Went swimming. 15.00 GMT Afternoon sleep. 16.45 GMT END OF CHRONOLOGY. I hope this may be of help if you suddenly get a first time attack of gout. Advice received tells me that Colchichine is now an old fashioned remedy with possible dangerous side effects, both long term and short term. "....stop using colchicine as it is very dangerous and causes chromosonal damage."

Glad to hear that you recovered. For me, a lot of fluid and elimination of high purine food from diet kept me gout free for couple of years now. Note that pure water is not as good a hydrating agent as electrolyte type of drinks. To me, my lowest moment was passing a kidney stone because of gout. When the uric acid is concentrate enough, it not only crystalizes into your toe joints, it deposits stones in your kidney too. If you think the gouty toe is agonising, think again for a passing kidney stone. I could tolerate the gout by sitting still. I had to go to the emergency room and asked the doctor to knock me out for the kidney stone. Anyway, keep watching that diet and beer. "May the gout be without you".  :-) Kowloonese 00:09, July 16, 2005 (UTC)

How to describe the pain? Saying it felt like someone doused the foot in gasoline, lit it on fire, dropped a semi on the foot, and drove rusty nails all at the same time to describe the pain doesn't feel to me to do justice to what the pain feels like.

JesseG 22:22, July 27, 2005 (UTC)

It feels like stabbing a blade of knife into the joint. Leave it there and wiggle it occasionally. That is the joint pain. Then for the swollen skin surface pain, your gasoline description seems appropriate. Kowloonese 23:47, September 1, 2005 (UTC)

I recently had one of those "get everything away from my foot" gout attacks a few months ago. I had to take my sock off and lay with it in a specific position to get to sleep. It was probably the most agonizing pain I've ever felt, whenever I moved it. I'm thinking it's right up there with kidney stones and child birth. - JNighthawk 22:15, 15 July 2006 (UTC)

Colchicine is rarely used, but its main side-effects are gastrointestinal upset. All those scary side-effects are rare. Its other main indication is FMF. JFW | T@lk 09:54, 17 July 2005 (UTC)

I don't think it's that rare; I and at least one friend of mine have both been prescribed colchicine - although in my case it was as an adjunct to probenecid. --moof 06:19, 2 September 2005 (UTC)

I've also been prescribed it. I believe doctors tend to use it in extreme cases that don't seem to respond to indomethacin right away. I had an attack that laid me up for almost 2 months and when I was originally in the hospital they said they'd never seen anyone in as much pain as I was in. I'd take some indomethacin for a couple days and no relief was forthcoming, they put me on colchicine and I took 11 doses of it in a single day and it finally broke the worst of it. --Crossmr 20:30, 13 May 2006 (UTC)

Colchicine has been prescribed by at least 5 doctors I've seen. It's very common for gout patients that I've spoken to and I know about 10 personally. Also, I disagree with the statement below stating 80% of patients experience GI upset. From what I've read 100% of patients will experience GI upset, it's just a matter of dose; you take it until that happens. Soporific (talk) 13:01, 9 July 2009 (UTC)Soporific

Drs prefer using NSAID such as indomethacin due to high risk of adverse effects from colchicine; up to 80% of patients on colchicine experience GI upsets (reference below). However, as a drug it is extremely effective, esp when administered early on (within 24h of symptom onset). May also prove beneficial for pts in whom NSAIDs are contraindicated (due to gastric reflux/ulcer, congestive heart failure, anticoagulant therapy). YC.

Reference Type: Journal Article Record Number: 105 Author: Wallace, S. L. Singer, J. Z. Year: 1988 Title: Review: systemic toxicity associated with the intravenous administration of colchicine - guidelines for use Journal: Journal of Rheumatology Volume: 15 Issue: 3 Pages: 495-9 --The preceding unsigned comment was added by 129.94.6.30 (talk o contribs) 01:43, 6 July 2006.

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Alcohol

Why is alcohol rich in purines? The claims seem unrealistic. In particular, brewer's yeast may be rich in purines (I don't know for sure), but there's no yeast in beer: with very few exceptions (cloudy beers), it's all filtered out before distribution. Also, the current page did not refer to red wine (or port), a classic substance to blame for gout. I've updated accordingly.

Purines are water soluble, so filtering doesn't help.Msml (talk) 15:21, 20 July 2009 (UTC)

I've suffered from gout for 9 years now, and my doctors have almost universally said "diet may help a little, but don't get your hopes up". One mentioned red wine; none have mentioned beer. --Groogle 04:12, 2 April 2006 (UTC)

It probably depends how you got it. Mine was caused by diet, and my doctor said diet and exercise would help the most.--Preceding unsigned comment added by JNighthawk (talk o contribs) 22:19, 15 July 2006

The author may have been misguided when linking alcohol to gout based on purine content alone. Rather, the mechanism of ethanol degradation may be the true culprit. Through a series of reactions, our bodies degrade ethanol to Acetyl CoA, an important metabolic substrate for the TCA cycle as well as the end product of fatty acid beta-oxidation. During this series of reactions, Adenosine Mono-Phosphate (AMP) is generated (specifically from the step that takes Acetyl-AMP to Acetyl CoA). Once generated, AMP can enter the Purine degradation cycle to ultimately produce Uric Acid and Urate. One key thing to note is that the increased AMP burden noted here is not unique to alcohol consumption and can be seen after any event that results in the rapid conversion of ATP to ADP & AMP, such as strenuous exercise. Thus, alcohol and exercise have synergistic effects on urate production.
Reference: Yamamoto et al, Clinica Chimica Acta 356 (2005) 35-57
RS52547 00:02, 26 March 2007 (UTC)RS52547

Alcohol is a misconception. While beer can slow progress of medication, only wheat beer can truly spur an attack.--69.62.180.166 01:03, 4 August 2007 (UTC)

No, not just wheat beer....but that's a real killer for me so I don't touch it. All GRAIN ALCOHOL is High in purines. My doctor told me that Gin, for example is made from a completely purine free substance and is gout safe. Except that as ststed above, alcohol can dehydrate and spur an attack.--Amadscientist (talk) 05:43, 22 July 2009 (UTC)

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Tea

It wasn't clear - is only green tea and caffinated tea contraindicated in cases of gout? Or herbal teas as well?

Hmmm. Caffeine is a xanthine derivative and hence a purine. I wonder if it really makes if difference. JFW | T@lk 15:29, 2 Jun 2005 (UTC)

Dehydration will cause the on-set of a gout attack. I guess you have to look at both aspects, 1. caffeine is a purine, 2. Tea and coffee are diuretic and hence increase purine concentration via dehydration. Kowloonese 19:16, Jun 2, 2005 (UTC)

Also can someone verify if all caffeine containing drinks increase the uric acid level or not? i would like to know if i can drink coffee or coke.

The article now specificly lists tea, under "Over the Counter Remedies", as GOOD for gout and, under "Other Approaches, Foods to Avoid", BAD for gout in different places. I'm sure that both statements are properly referenced, but the contradiction should at least be mentioned, it seems to me.75.83.0.34 (talk) 23:23, 21 May 2008 (UTC)

Genetics

I believe my problem with gout is partially due to genetics - there have been people on both sides of my family who've had gout. What I was wondering is how gout would work its way down a family tree. Would a person inhierit the condition from his mother's side, or his father's side? Or could it come from either side?
JesseG 02:43, August 11, 2005 (UTC)

My sister and I both suffer from gout, which suggests that any genetic influence is not on the Y chromosome. Also, my father does not suffer from gout, though he does have another arthritic condition. My guess would be that you could inherit from either side of the family, but that only inheriting from the paternal side is unlikely. --Groogle 04:17, 2 April 2006 (UTC)

My father has the gout. All but one of 5 children have now been diognosed with it. I was the first child at the age of 22 back in 1988 to be diognosed. At that time my age was considered very low for gout.--69.62.180.166 01:05, 4 August 2007 (UTC)

Great article but Needs image

This is a really good article. I'd put it up for peer review as the first step to featured status, but I'm pretty sure the response would be: needs a picture.

I had a picture of my feet taken during my second episode of gout outbreak. However, the swelling was not severe enough to be representative. Compared to my first outbreak (sorry, forgot to take picture), the picture is not really worth posting. I'll pass this to someone else and I wish I would never have another outbreak again. Kowloonese 23:43, September 1, 2005 (UTC)

I erased the request for photos, since all the specific photos (afected joints and microscopic urates) are in the article. Other photos can be added, such as medicines, foods, etc from commons to add more makeup to the article. Don't think it's now at a stage that a photo search is required. Bobjgalindo (talk) 12:06, 6 January 2009 (UTC)

Modern commonality

It seems that gout is relatively rare in the modern day but quite common throughout history. What accounts for this? What modern factors have decreased the prevalence of gout? --Lowellian (reply) 10:04, 22 December 2005 (UTC)

It is my opinion that the prevalence of gout is unchanged over the years. What has changed is the duration of an attack from weeks to hours due to modern medication. I can go from laying on the bathroom floor unable to move at 8:00 a.m. to teeing off for 18 holes at 11:00 a.m. Niloc--Niloc 11:43, 6 May 2006 (UTC)

How?! My gout attacks last days to a week or two. 25% of the time during an attack, I can't walk. What medications, life changes, etc. help?--Preceding unsigned comment added by JNighthawk (talk o contribs) 22:24, 15 July 2006

Indomethacin is the answer!--Niloc 02:57, 18 July 2006 (UTC)

Just FYI, Indomethacin seems to work well for me as well.--Randomthoughts 12:19, 9 September 2006 (UTC)

I suffer severe attacks. Incredible pain. Recommend to avoid alcohol / beef / spinach. On the other hand pure black cherry juice,(small amounts daily ), celery and milk have definitely helped. When I feel the "twinge" at the start of an attack ( regular sufferers will know what I mean )I can avoid full blown attack with over the counter Ibuprofen. -- Alan --Preceding unsigned comment added by 69.17.157.212 (talk) 18:30, 16 April 2008 (UTC)

There are no good gout cases, but I have a miserable time; I react to beans, peas, beer, mushrooms, asparagus, plus all the usual suspects. I eat no meat at all, take Probenecid, and still have to resort to indomethicin, vicodin, celebrex, ibuprofen, and single malts to get relief. If I get restless and walk on the foot when the attack is 3+ on a 10 scale, I am laid up for two weeks. A tip: indomethicin is water soluble, so if you are 300 lbs like me, take 1.5 to 2x the dose (1 every 4 hours instead of six or eight).Msml (talk) 15:37, 20 July 2009 (UTC)

Galen

Not sure if citing the second most influential doctor (and perhaps most influential annatomist) in antiquity as a 'gladiatorial doctor' is something that I'd encounter in a reputable publication. But that might be my snobbery talking. Wilhelm Ritter 17:37, 12 August 2006 (UTC)

Fructose

Since high levels of fructose in diet is a cause of Hyperuricemia, how come this page didn't mention fructose at all ? --Preceding unsigned comment added by 38.113.177.205 (talk o contribs) 22:12, August 27, 2006

Not sure, its possible no one has gotten around to adding it yet. You can do so if you think it should be included.--Crossmr 22:21, 27 August 2006 (UTC)

Thanks for long overdue encouragement. I volunteered to add.LoopTel (talk) 14:19, 6 June 2008 (UTC)

Recent news reported on numerous studies that showed fructose is no worse than sugar as far as effect on obesity. However, the studies are silent on any new result about effect of fructose on gout.LoopTel (talk) 18:29, 9 December 2008 (UTC)

Fructose influences gout via hyperuricemia, and in that article I recently rewrote the explanation of the role of fructose. --Una Smith (talk) 15:46, 6 January 2009 (UTC)

Podagra?

I was taught that podagra was specifically gout of the first interphalangeal joint of either foot and does NOT refer to gout in general --Gak 21:28, 30 August 2006 (UTC)

Google doesn't exactly give much guidance on this. Its referred to on many sites in the same breath as gout, or qualified with "especially of the big toe" but not "exclusive" to that joint. You might have more luck looking at an actual medical dictionary to get a clearer definition.--Crossmr 02:10, 31 August 2006 (UTC)

My copy of Merck's agrees with User:Gak's assertion; however, it wouldn't surprise me if in antiquity 'podagra' referred to all types of gout. --moof 06:03, 4 September 2006 (UTC)

Inconsistency with regard to spinach

In the article, under the Prevention section, spinach is simultaneously recommended and avoided:

1) Avoiding alcohol, high-purine foods, such as meat, fish, dry beans (also lentils and peas), mushrooms, spinach,

2) juicing a combination of carrot and spinach can greatly reduce the pains of gout as well as lower euric acid levels.

I don't know which one is correct, though.

--Randomthoughts 17:34, 31 August 2006 (UTC)

Its quite possible that the juice of spinach helps it, but something in the leafy part makes it worse? Someone can possibly provide clarity on that, if none is forth coming we should probably remove it until its cleared up.--Crossmr 22:49, 31 August 2006 (UTC)

The Oxalic acid in spinach raises the blood pH and drives the uric acid into crystal form. Oxalic acid is harder to remove from the blood than other compounds, so it can be troublesome. I can't even glance at it in the vegetable aisle.Msml (talk) 15:42, 20 July 2009 (UTC)

Further research seems to indicate that spinach is a food to be avoided and that the compounds (oxalates) involved are soluble (not totally sure on that last point). I'm going to remove spinach juice from the remedy list. http://www.umm.edu/patiented/articles/what_lifestyle_measures_can_help_prevent_gout_000093_9.htm among many other articles--Randomthoughts 18:11, 6 September 2006 (UTC)

I may add my personal experience. Research data notwithstanding, after eating any of asparagus. cauliflower. mushrooms. or spinach, I am sure to develop gout. LoopTel (talk) 23:55, 3 June 2008 (UTC)

Added to Prevention

Under prevention, I added information from the 2004 study reported in the New England Journal of Medicine. It was very highly reported throughout the media and details that vegetable purines did not affect incidences of gout while confirming that animal flesh sources of purine did increase the incidence of gout. It also reported that low fat dairy products had some preventative effects.

The source was already cited in the references section.

Anecdotally, I'm currently trying to stave off the beginnings of an attack after a week of pork and steak. I stopped drinking milk in quantity years ago due to allergies and generally have a diet that is high in animal products. I'm slightly overweight but not close to clinically obese.--Randomthoughts 12:14, 9 September 2006 (UTC)

(I'm being utterly insensitive)... If it flares, could you take a picture??? Hope it doesn't though... -- Samir ???? 12:16, 9 September 2006 (UTC)

Haha. It's not much to see, just a bit of swelling and a bit red - not much compared to the last time when it was much worse (didn't have indomethacin). If I can get a good pic, I'll try to take one.--Randomthoughts 17:17, 11 September 2006 (UTC)

T-Rex with gout

I've added Sue, the T-Rex, to famous people with gout (I know T-Rexes are not people but Sue is really famous). I used the original Nature citation. However few WP readers have access to 1997 Nature so possibly we should change the citation to this Discovery feature about the paper. What do you think? Friendly Neighbour 12:49, 28 September 2006 (UTC)

Blood pH and bicarbonate as a remedy

I just wanted to mention sodium bicarbonate and its effects on raising blood pH for gout treatment. I'm pretty skeptical, and really don't think remedies such as this should be in the article until reliably sourced, but I've tried baking soda myself whenever I've found myself in the beginning stages of an attack, and I'll be damned if it doesn't work. It seems like such a hokey remedy, and I'm not too keen on the increased sodium consumption, but I've been using baking soda alone for gout treatment for nearly a year, and haven't refilled my indomethacin or painkiller prescriptons since last fall.

But realizing that my own example doesn't make for good science, and that baking soda is all over huckster, home-remedy websites, I'll just advise that people keep their eyes open for any legitimate gout-related studies involving pH.--Trypsin 15:11, 19 October 2006 (UTC)

It is an old remedy: http://www.henriettesherbal.com/eclectic/bpc1911/sodium.html . And perhaps this is a reliable source? Una Smith 02:51, 5 June 2007 (UTC)

Even if that site does accurately reproduce the British Pharmaceutical Codex of 1911, then all that means is that in 1911 pharmacists in Britain prescribed bicarb for gout, and apparently for just about everything else too. Given the age of the source, I'd be very hesitant to consider it as a reliable source for a current medical article; I think its very age makes it unreliable for anything except as a historical note.Derek Balsam^(talk) 02:59, 5 June 2007 (UTC)

Here [6] is a much more recent article reference about modern-day use of bicarbonate in gout treatment. Derek Balsam^(talk) 03:08, 5 June 2007 (UTC)

It is current standard therapy. So is potassium citrate. Both serve to make blood and urine more alkaline, which helps to dissolve uric acid crystals. So in the short term these agents may increase the uric acid in serum and urine, but without net precipitation. --Una Smith (talk) 06:48, 26 October 2008 (UTC)

Removed - probable vandalism

'Gout symptoms can be completely eradicated by simply mixing a flat teaspoon of baking soda in a glass of water. This stop the prurines from crystalizing in the joints. I am a twin. He suffers and takes medication. I simply brush my teeth with baking soda and that takes care of the problem.' I'm almost sure this is just plain vandalism. --204.155.226.2 17:20, 26 October 2006 (UTC)

If you look at the topic above about bicarbonate, you'll see that it might actually be legit. Still, it is unsupported and unencyclopedic. I fully support the removal. I just wouldn't strictly call it 'valdalism'. --Mdwyer 19:06, 26 October 2006 (UTC)

2006 (UTC)

Allopurinol

The decision to take allopurinol is a life long one. Then why has my doctor recommended this after the end of my gout attack? What other forms of treatment are there to prevent recurrence of gout? {{subst:unsignedIP|122.167.181.16|07:57, 20 June 2007}

Your choices are simple: Take the Allipurinol or never ever be further than 3 hours away from your Indomethacin! All of the homopathic remedies don't work other than to give you a great story to tell about the time you "drank pregnant monkey urine". I drank some "potion" made from the bark of a tree for 3 months straight, with no noticable difference. --Niloc 02:45, 21 June 2007 (UTC)

oh, thanks thats a great relief to know that i'm a slave for life...only problem is Indomethacin makes my stomach go bad and puke and what not...

Me too, but Indomethacin + Symptoms (mine is just dizziness/diarrhea) is better than a lifelong decision of allopurinol. - JNighthawk 03:20, 24 July 2007 (UTC)

Is there any discussion about the effects of the over the counter drug "Aleave". I have had gout for 20 years and no longer have medical insurance and cannot get my Idonin any longer. I have been taking Aleave now, and it seems to work well and costs far less money!--Amadscientist 01:12, 4 August 2007 (UTC)

I presume you mean "indocin", a brand of Indomethacin and "Aleve", a brand of Naproxen. Both of these are NSAIDs. In general you can switch one for the other, but the dosage can be tough to figure out. For example Advil (another OTC NSAID, Ibuprophen) could also be used, but the dosage on the label may not provide enough anti-inflamatory effect. On the other hand, Advil can be just as bad -- or worse -- than indomethacin if the dosage is too high. All NSAIDs hurt the gut in some way or another. Although, as much as a gout attack hurts, I'd almost consider a bleeding ulcer an improvement...

Anyway, check out some of the pages that I linked above, but if you can, PLEASE go talk to your doctor. They will be able to tell you which OTC drugs will work safely for you. Besides, Wikipedia does not give medical advice! --Mdwyer 02:42, 4 August 2007 (UTC)

Unfortunately, I have received "antigout" diets from different rheumatologists and nutritionists with contradictory data. Gentlemen, you must face the situation: you are going to have to try everything for yourself to come up with a solution. Don't pass up that foaming mug of monkey urine; it alone may do the trick. In my case, allopurinal worked erratically and poorly. A high percentage of patients get poor relief from it, which none of my doctors bothered to tell me. A year later I was given Probenicid, works OK as long as I take it all the time. Which I hate. I have also put on 90 pounds since I can't follow a low-carb diet any more.Msml (talk) 15:51, 20 July 2009 (UTC)

Colchicum autumnale

I have removed this text below because it needs a citation.

The homeopathic preparation of the plant, Colchicum autumnale, from which Colchicine is derived, is a non-toxic alternative treatment.

I take great exception to the non-toxic claim in particualr, since the plant's article says the plant is poisonous due to its colchicine content. The line was reverted once before by an anon user with the edit summary of "fairies and unicorns cure gout". Amusing! --Mdwyer 04:39, 11 July 2007 (UTC)

While certainly not devoid of side effects, I highly doubt an actual homeopathic preparation of C. autumnale would contain any colchicine whatsoever. It would be interesting to find a reference to this effect. Fvasconcellos (t·c) 10:06, 11 July 2007 (UTC)

Question

I didn't go back far enough in the history to figure who added this, but this question was in the text of the article in chief:

What is the diagnosis code ICD for gout??

I moved it here. Perhaps someone has an answer? - Smerdis of Tlön 18:39, 2 August 2007 (UTC)

History--Bloodletting

Okay guys the history section is totally weak...especially considering the fact that in the quote from our doctor ahead of his time, he recommends blood letting. Come on, there's gotta be better historical information on a disease that's been around for sooooo long.

128.97.68.15 17:38, 23 August 2007 (UTC)

Age Claims?

Ok, the article claims that Gout affect people above 40; but i'm only 27, so either there is a wrong diagnosis or i'm an exception or age doesn't matter --Preceding unsigned comment added by 68.100.199.183 (talk) 03:27, August 26, 2007 (UTC)

It says mostly, not only.--Crossmr 03:32, 26 August 2007 (UTC)

Indeed I suspect most people who die in developed countries are above 40. This doesn't mean if you die at the age of 27 it's a wrong diagnosis or that the information is wrong Nil Einne (talk) 05:15, 29 August 2008 (UTC)

TOPHI, from GOUT

How do I get the swelling out of my elbows? I look like pop-eye. Please help, I'm taking celery seed and tart cherry and have no pain but the swelling is still there. My doctor used a needle once and drained some fulid out but it was still a large bump...Will the large bumps go away? or is surgery needed? Joejbryant 02:30, 23 October 2007 (UTC)

I'm only 26, and have had too many attacks to count. I've had it for over 6 years. The common age might be 40 to 50, but the article never metions anything about the higher levels of uric acid in younger people.

For your swelling try Indomethacin and ice. It will mess up your stomach, but you will feel alot of the pressure go away in hours. --Preceding unsigned comment added by 76.101.142.180 (talk) 02:52, 29 January 2008 (UTC)

Is Vitamin C good or bad

The page, under heading "Diet", list Vitamin C as a positive force in treating and preventing gout. Then it is later, under "Other Approaches, Foods to avoid", listed as something to avoid.Skafkas 03:42, 25 October 2007 (UTC)

Heh. Good catch. Actually, I think that should be read as "it is believed that diuretics might have a role in causing the disease, and so one should avoid the dehydrating effects of Vitamin C. Under the guidance of a doctor, Vitamin C might be an effective treatment, presumably along with a hydration therapy." I'm getting really close to weasel words and WP's prohibition on giving medical advice, though. Suffice to say that this page is difficult to maintain. --Mdwyer 14:44, 29 October 2007 (UTC)

Maintenance problems are not helped by the general perverseness of the disease and the medical establishment.Msml (talk) 15:57, 20 July 2009 (UTC)

A search of the combination "gout" and "vitamin C" on the web yielded mostly positive effects of vitamin C in preventing gout, though some include the weasel phrase "but not always".LoopTel (talk) 23:22, 11 October 2009 (UTC)

this article contains a lot of specious claims and misleading information

Such as it said gout is congenital- which I have removed. There may be increased risk to some people genetically but it is usually a result of lifestyle, or other diseases. Also a lot of flakey alternative medicine or anecdotal claims in here.Merkinsmum (talk) 23:10, 23 November 2007 (UTC)

Agree. Please remove whatever sounds doubtful, or copy it here for discussion. JFW | T@lk 23:37, 26 May 2008 (UTC)

Gout and CVD

Gout patients have a 35% higher risk of cardiovascular disease. Those with high uric acid but no gout had no significant association. http://archinte.ama-assn.org/cgi/content/abstract/168/10/1104 JFW | T@lk 23:37, 26 May 2008 (UTC)

There should be more

In my own personal opinion. there should be more content. substance to the overview of the topic. what is Gout i expect at least two to three pages, but i have searched various sites, and i only get a paragraph. The reason why this is an issue im a medical student writing a research paper for my english class. Also another suggestion use lamer terms for the reader. It is not going to be a problem when i do this paper for anatomy and physiology class but english I will need more understanble terms. Thanks:) --Preceding unsigned comment added by 75.37.93.93 (talk) 01:46, 12 June 2008 (UTC)

Hot water

I removed the ref [7] for using hot water as it was a Rapid Response to a BMJ article. This is basically a feedback column/letters column similar to a paper except that it is on a journal website. [8] Hardly a reliable source and even the person suggesting it didn't exactly sound convincing and it appears to solely be 'theory' on his? part Nil Einne (talk) 05:45, 29 August 2008 (UTC)

I added a ref, a small study, that contradicts the hot water advice. --Una Smith (talk) 04:36, 25 October 2008 (UTC)

role of pH

This article needs to explain the roles of plasma pH and urine pH in gout. Especially before mentioning a diuretic drug that makes urine more alkaline while making plasma more acidic. Such a drug might help to dissolve uric acid kidney stones but if the problem is uric acid crystals in joints then making the plasma more acidic may do more harm than good. --Una Smith (talk) 06:40, 26 October 2008 (UTC)

Agreed, exceedingly important, but poorly communicated here and everywhere in the literature and with physicians as well. Msml (talk) 16:00, 20 July 2009 (UTC)

Removed pathophysiology speculation

I removed the following from the article, but am copying it here because there probably is something that can be said (and sourced) about kidney defects and genetics related to gout. --Una Smith (talk) 05:05, 27 October 2008 (UTC)

It may be possible that defects in the kidney that may be genetically determined are responsible for the predisposition of individuals for developing gout.

product placement?

In the main article it refers to "Tart cherry capsule and gout research.[2] " where [2] leads to an external source flogging its wares. I haven't removed it but could someone comment as I'm not familiar enough with wiki to rip it out. 78.146.17.36 (talk) 14:42, 23 January 2009 (UTC)

as heard no reply back, I removed it 89.242.126.76 (talk) 05:29, 25 January 2009 (UTC)

Medication section cleanup

The details of specific drugs belong on the articles about each of those drugs, not in this article. This article needs an overview paragraph about the role of each class of drug in the treatment of gout. I have started work on this. --Una Smith (talk) 15:24, 17 February 2009 (UTC)

Why is is considered an old disease?

This disease is for some reason considered an old disease. I even remember seeing everybody hates chris, and chris mentioned that his dad had gout and then followed by the fact that our generation probably doesnt even know what it is. Why is that? Is our generation not getting it for a reason and should we be more educated about this horrible disease. If anyone can please include this in the article. If not at least please answer in this discussion page. --Preceding unsigned comment added by 68.32.31.254 (talk) 04:33, 11 July 2009 (UTC)

You're just not aware of it, but this generation has been reported to have higher inncidents of Gout related illness. This is missing from the article but is true. However the article does go into detail about Gout being one of the oldest deseases known to man and was first mentioned in historic writings by the Egyptians in about 4000BC.--Amadscientist (talk) 02:07, 23 July 2009 (UTC)

Thanks For the info. It should be included more within this article --Preceding unsigned comment added by 68.32.31.254 (talk) 19:23, 27 August 2009 (UTC)

Image

Excellent photo! Damn these little pointed crystals!--Amadscientist (talk) 02:07, 23 July 2009 (UTC)

What's wrong with this article?

A couple of things. First the article is obviously edited by several well-meaning editors, but there is disputed information in several places. (see talk page above on Purine vs Protein - and the discussion about alcohol)

Also the article is written in many instances as if various assertions are facts.....when they are not. The article makes absolutely no mention of one major factor about Gout.....it is not fully understood by science and medicine. How Indocin works to actually eliminate an attack is also not clearly understood by medical professionals. There is also a section that makes claims about which medicine should be administered first. Let me be clear, any mention of medical care should be done with extreme caution and this article makes some very big mistakes, such as claiming gout had a singular cause in every individual (false) and that Gout is a symptom of obesity(false).

Gout is different in many individuals for a simple reason. Metabolism. The human body creates its own uric acid. In some people too much is created, in other people the precursor intake is too high, and with others (such as myself) the body is unable to excrete the acid fast enough. You can also have all three causes.

Also the hereditary factor is only barely mentioned and therefore misses facts about individual nationalities that are more inclined to develop Gout. For an example see the article on Lactose intolerance.

I believe any mention of what medication to take should be removed from the article unless it is fully referenced with a reliable source which conforms completely with policy and guidelines.--Amadscientist (talk) 02:21, 23 July 2009 (UTC)

The article should also mention that it is a known side-effect of certain drugs. (No, I don't remember which ones, nor do I know if the mechanism of action is through encouragement of nucleation or, more likely I suppose, increasing the levels of uric acid in the blood.) -Donal Fellows (talk) 16:15, 16 November 2009 (UTC)

Cherries

If anyone can find a good place (perhaps under "Lifestyle"?) in the article to mention cherries as a home remedy, here is a 2003 paper than may be appropriate to use as a citation: [9]

We should use primarily reviews. A study of ten healthy women says little. Doc James (talk · contribs · email) 17:29, 15 January 2010 (UTC)

When you say "we should use primarily reviews", I am not sure what you mean, do you mean reviews of the papers? Anyway, here's another paper from 2009, but this also has only 12 subjects so not statistically significant. [10]

A review is when some one takes all the papers on a topic looks at them and then publishes an overall conclusion rather than conducted a single experiement.Doc James (talk · contribs · email) 18:37, 17 January 2010 (UTC)

S-adenosylmethionine ("SAM-e")

S-Adenosyl methionine ("SAM-e supplement") has been recommended by some for treatment of arthritis in the feet, and other indications. However, the impact on gout would be far from benign: a 400-milligram supplement should be equivalent to about 130 milligrams of adenine, about equivalent to a serving of poultry (or the total recommended daily intake for a strict low-purine diet). But I haven't managed to dig up a reliable source that specifically counterindicates SAM-e for gout. Does someone know of one that they could add? Thanks. Wnt (talk) 06:05, 19 January 2010 (UTC)

Celery, cherries, strawberries, blueberries: citations

James A. Duke PHD, in The Green Pharmacy makes several comments:

• Some people recommend cherries but suggest a dose of 8 oz a day canned or fresh, these would be expensive and according to the writer its never been scientifically demonstrated but many people swear by it (so it's probably worth a try). The comment is followed by onbe that some people favor strawberries
• Celery: this is the suggestion for celery: tablets of celery seed or celery stalks. The author tried this so it has anecdotal support; he admits he was a skeptic but now believes.
• while clery has the highest recommendation there are also chiso, licorice, turmeric.

The Encyclopedia of Natural Medicine by Murray and Pizzorno lists cherries (again, at a does of half a pound per day) but states it has been shown to be effective in lowering uric acid levels and preventing attacks of gout. It mentions that Cherries, hawthorn berries, blueberries and other dark red-blue berries are rich sources of flavonoids remarkable in preventing collagen destruction and are good antioxidants and inhibit formation of leukotrienes.

I have used the black cherry syrup concentrate from Vitamin Shoppe with lemon juice and apple vinegar to good effect. The idea is to acidify the blood a little bit to get an overreaction that will drive the crystals back into solution. However, blood pH is one of the most rigidly controlled homeostatic systems in the body, because all chemical processes depend on oxidation/reduction. It may be a placebo effect, but at least it doesn't taste bad with a load of Splenda.

The Holistic Herbal by David Hoffamn recommends a tead of burdock root, celery seed and yarrow (not the celery seed, it seems to be common treatment-my comment RJFJR).This includes a note that diet is paramount; "Coffee and tea should be left alone and any over-indulgence in general is out" (I still find 'left alone' to be ambiguous-RJFJR) and "Alcohol has to be totally avoid".

The above refernce also states: that the body metabolises purines into uric acid (which I'm not sure is stated in the article as why a low purine diet is recommended; if not I'll add it).

Can we make specific citations for any of the other statements in the article? If we get a picture I'd send it to peer-review but I suspect we'll be asked to cleanup the citations. (But looks like an excellent article to me!) RJFJR 14:30, September 11, 2005 (UTC)

Lancet

Review doi:10.1016/S0140-6736(09)60883-7 JFW | T@lk 23:07, 23 January 2010 (UTC)

Pathophysiology

Gout begins:

Gout is a medical condition that usually presents with recurrent attacks of acute inflammatory arthritis (red, tender, hot, swollen joint). It is caused by elevated levels of uric acid in the blood. The uric acid crystallizes and deposits in joints, tendons, and surrounding tissues

With due respect this is a little simplistic, perhaps even somewhat inaccurate.

There are number of theories, models and studies that shed some light on what causes acute inflammatory gouty arthritis .

I am prepared to enlarge on this aspect of Gout.

I would appreciate any comments, assistance or advice on how to achieve this goal. Is it possible to set up a page to collaborate on this idea? Once the page is in reasonable order thought can be given to how it should be used. Thank You--Nnoddy (talk) 01:35, 1 March 2010 (UTC)

What aspects are you referring too? The pathopysiology? Doc James (talk · contribs · email) 02:11, 1 March 2010 (UTC)

I don't know that I'd refer to it as pathophysiology. These ideas tend to separate the acute from the chronic or inter episodal stages of the disease. I trust I can put them here without inconveniencing anyone.

I find it hard to justify paraphrasing the carefully chosen words of professionals. I might need the permission of the authors.

You may have a few observations of your own. --Nnoddy (talk) 04:58, 2 March 2010 (UTC)

These ideas really seem to be attempts to explain intermittent acute symptoms. There is no explanation for the eventual resolution of an acute attack. The explanation for the sudden onset seems to be related to the crystals entering the synovial fluid. This does not explain why the phages do not attack crystals in other types of tissue does it?--Nnoddy (talk) 05:27, 2 March 2010 (UTC)

Yes this seems to be a discussion of potential pathophysiological mechanisms of the disease.--Doc James (talk · contribs · email) 06:21, 2 March 2010 (UTC)

Thanks I'll adopt that.--Nnoddy (talk) 08:48, 2 March 2010 (UTC)

We have a guideline at WP:MEDMOS which outlines what heading should be used. We do not need to say gout as that is what this page is about. That these are theories also does not need to be explicitly stated in the lead. Pathophysiology is all the is needed similar to what is used on many other pages.--Doc James (talk · contribs · email) 09:16, 2 March 2010 (UTC)

I've just come across this. Urate, sodium a crystalline compound deposited in tissues in persons with gout. Sodium urate crystals are capable of evoking an acute inflammatory response in the skin, subcutaneous tissues and joints.

I'm beginning to think that recurrent attacks of gout does not make sense! What does capable mean and then there is this little gem

The protein metabolic waste product Uric acid that is excreted by the kidney and gut has generally been viewed as relatively unimportant. Recently it has been discovered that uric acid is not biologically inert being both a pro- and anti-oxidant and may act as a neurostimulant, an activator of the innate immune responses and induce inflammation. --Nnoddy (talk) 12:03, 2 March 2010 (UTC)

My toe is still very sore.

---

Mechanisms

A Runaway Chemical Crystalisation

An acute attack occurs as a result of an inflammatory reaction to crystals of sodium urate that are deposited in the joint tissue. The inflammatory response involves the local infiltration of granulocytes which phagocytise the urate crystals. Lactate is high in synovial tissues and in the leucocytes that associated with the inflammatory process which also favours the deposition of uric acid.

B Kamikaze leucocytes

Self Perpetuating Fatal Phagocytosis

KT Rajan studied phagocytosis of urate crystals by polymorphonuclear leucocytes. From his investigations with specific reference to phagocytosis of urate crystals by polymorphonuclear leucocytes he proposed a sequence of events that may initiate the inflammatory reaction in acute gout. He concluded that :

(1) that neutrophil leucocytes avidly ingest microcrystals of sodium monourate

(2) that this causes the rapid degranulation and disintegration of the leucocytes

(3) that fresh leucocytes ingest the debris and crystals liberated by the dead cells, and in their turn degranulate and die, thus possibly establishing a vicious circle in the system.

In support of his theory Rajan quoted research in the 1960's where McCarty demonstrated that:

The severity of the inflammatory reaction is dependent on the number of neutrophils that are available at the time of invasion by the bacteria or toxic agent. In agranulocytosis the reaction to bacterial invaders by the host is functionally deficient and acute gouty effusions provoked by injecting crystals of uric acid into joints can be abolished by pretreating the host with drugs like vinblastine which reduce the total number of leucocytes available. (McCarty, 1965).

.

C Matchstick Model

Theodore Fields Director, Rheumatology Faculty Practice Plan, Hospital for Special Surgery New York suggests that

Whatever the cause of elevated uric acid levels, the key event in gout is the movement of uric acid crystals into the joint fluid. Inflammatory chemicals are released when the body's defense mechanisms, engulf the uric acid crystals. All the signs of inflammation, including heat, redness, swelling and pain are caused by these chemicals. (cytokines) The inflammation attracts more white blood cells to the joint, which increases the inflammation.

Theodore stated

"When thinking of gout, a useful model has been proposed by Wortmann. Uric acid crystals can be thought of like matches, which can sit quietly or can be ignited. Crystals can be present for years in the cartilage, or even in the joint fluid, without causing inflammation. Then, at some point, due to increasing number of crystals or other inciting factor, the matches are "struck" and the inflammation begins. This analogy is important both for conceptualizing the uric acid crystals in the joint and for understanding the various types of gout treatment (see below) - some of which attack the inflammation (pour water on the flaming matches) and some of which remove the uric acid crystals (take away the matches)."

--Nnoddy (talk) 02:45, 3 March 2010 (UTC)

---

MicroTophi Grenades

Urate Crystals in microtophi are normally covered with proteins that block the crystals from binding to cell receptors. When the coating is lost or the tophi burst the crystals suddenly bind to cells suddenly causing the inflammation.

Crystalisation from Supersaturated Fluid

Damaged cells release sodium urate resulting in a supersaturated microenvironment and crystalisation of sodium urate triggering the innate immune response.[11]

What Could End the Attack?

Humans lack the uricase enzyme that converts urate to the more soluble and easily excreted compound allantoin in most mammals. The tangible presence of tophi is a fair indication that the human body does not have an effective means of eliminating monosodium urate monhydrate crystals once they have formed. The body's visible solution is to encapsulate the crystals and prevent interaction with the immune system.(hide the matches)

Anti-inflammatory drugs are effective in acute epsiodes and the body has a range of anti-inflammatory cytokines including, IL-1RA, IL-10, and transforming growth factor (TGF)-beta that are produced.[12](pour water on the flaming matches) --Preceding unsigned comment added by Nnoddy (talk o contribs) 03:08, 3 March 2010 (UTC)

References are a little old. It is better to use stuff in the last ten years. Pubmed is a good source for finding review papers.Doc James (talk · contribs · email) 05:50, 8 March 2010 (UTC)

Sustainable v Unsustainable statements

Pathophysiology

Will someone please suggest some meaninful headings on this section?

Gout occurs when crystals of uric acid, in the form of monosodium urate, precipitate on the articular cartilage of joints, on tendons, and in the surrounding tissues.

Surely this statement needs a reference. This is certainly one possible mode of a gout attack that is in any case subsequentially covered in the article. Perhaps it should go. The interesting but unreferenced information is the "possibly accurate" extent of the alleged precipitation. Just what is the limitation on urate precipitation?

"Paradoxically, acute attacks of gout can occur together with a sudden decrease in serum uric acid, such as due to use of drugs (uricosurics, xanthine oxidase inhibitors), or total parenteral nutrition.[21] However, the sudden decrease may be a consequence of abrupt formation of crystals (removing uric acid from the serum), rather than a cause."

This appears odd to me because the cause of the sudden decrease in uric acid would appear to be the desired result of the administered medications which either slow the re-uptake of uric acid or reduce its production.

Why then attribute this reduction in uric acid to the abrupt formation of crystals? What if the real mode of operation of these drugs is the formation of sodium urate crystals? Tophi heaven!

This undoubted clinical observation is not explained by the preceding statement. Why? How does starvation fit in with the pharmaceutical reaction? The statement is correct but the explanation needs clarification and reference.

Regardless of the serum concentration of uric acid, precipitation of uric acid is markedly enhanced when the blood pH is low (acidosis).

The first problem with this statement is that uric acid precipitates as monosodium urate. It appears that the solubility of uric acid and monosodium urate differ in relation to pH. The solubility of uric acid increases with alkalinity whereas the minimum solubility of sodium urate is about pH 7.7 This must be a remarkable phase diagram. The second problem is no refereces.

A similar pH-sensitive effect occurs in urine,[22] contributing to uric acid nephrolithiasis (kidney stones).

A rather long bow to draw but hopefully its correct.

Uric acid is a product of purine metabolism, and in humans is normally excreted in the urine.------- The kidneys are responsible for approximately two-thirds of uric acid excretion, with the liver responsible for the rest.

Statements need to be merged.

Purines are generated by the body via breakdown of cells in normal cellular turnover, and also are ingested as part of a normal diet. The key issue seems to me to be that purines are predominately the metabolites of guanine & adenine. As such they are produced by the body with every cellullar division. Unless the article makes it understood that consuming DNA & RNA is consuming purines the dietary component of uric acid plasma levles makes no sense. Basically a low purine diet avoids cells.ie milk - protein & fat! One can't avoid purines by eating vegetable DNA.

Please help if the inclination strikes. --Preceding unsigned comment added by Nnoddy (talk o contribs) 12:38, 8 March 2010 (UTC)

Epidemiology

Where in the world is the epidemiology? There needs to be a section near the beginning that tells how common the disease is, what ages, genders, etc. are commonly involved.

Diagnostic Confusion

Yes, jdwolff, it is the most common mistake made in the mis-diagnosis of gout .. in my experience. However, I can not point to any references, only my experience.

Famous people

Perhaps it's because it is the only mention of gout in the mainstream media, but the mention of king of the hill seems rather incongrous. I'd say either remove it or add more modern-day references if possible.

Harvard Researcher Hyon Choi

Althouh Choi's research is cited in "Food's to Avoid" (references 27 and 28) it isn't very well represented. He followed 47,000 men for 12 years and concluded that purine rich vegetables such as peas, mushrooms, spinach, do not cause gout. I believe also that his work implicates beer, but not red wine, as a cause of gout.

In a recent publication discussed here: http://www.scientificblogging.com/news/coffee_prevents_gout Choi concludes:

Their findings, featured in the June 2007 issue of Arthritis & Rheumatism (http://www.interscience.wiley.com/journal/arthritis), provide compelling evidence that drinking 4 or more cups of coffee a day dramatically reduces the risk of gout for men.

A lot of the stuff in the main article seems out of date and/or fallacious in light of Choi's work.

Gout - Kilkenny Punk Rock Band

For the greater interest, GOUT (Gareth Sweeney, Morris Deegan, Mickey Burgan) were also an incredibly talented punk rock band, who created great interest in Ireland, the US and in Italy, during late 1990's and the early noughties. They were spotted by Winston Smith, the famed Dead Kennedy's artist, who quicly offered to paint their album cover FOR FREE for them. Having turned down a Sony contract, unfortunately each went their way. Among lesser claims, the drummer has so far unanimoyusly been defined "the loudest man in Ireland".

Foods To Avoid

Missing yeast extracts from the list.

Gout Gripes

Quotes from the famous and the less than famous about their experineces with gout.

I've observed that sufferers complain about the technical nature of discussions here.

The real point of Wiki is that individuals can contribute. There is very little in the world that is not directly experienced by someone. Wiki is not a chat page but when suffering is involved it is perhaps appropriate for a little relaxing of standards and levity. Personal experiences are valuable to fellow suffers. Is this a Wiki task?

Interesting bit about human physiology

Uptodate says "Noninflamed synovial fluid is significantly cooler than serum, being 90 to 91ºF (32ºC) in the knee". I never knew that. The ref they use however is from 1949.Doc James (talk · contribs · email) 01:23, 9 June 2010 (UTC)

This ref however says 35.2

Doc James (talk · contribs · email) 01:33, 9 June 2010 (UTC)

Article order

Sorry, this article's prevention/management is a "choppy" mess to quote from the GA review. The problems:

1. I don't think lifelong treatment with allopurinol is prevention (perhaps "Prevention of further acute attacks"), anymore than giving statins after a heart attach is primary prevention (this is secondary prevention, but that is not what most people would initially infer from just an unqualified "Prevention")
2. no patient ends up on allopurinol, until they have had at least 2 acute attacks, so Prevention#Medications should come after current list of drugs in Management
3. Prevention#Medications states "Urate lowering measures should be increased until serum uric acid levels are below 360 µmol/L (6.0 mg/dL)" - yet not the usual approach taken (if my patients get to maximum 300mg allopurinol and stop having further attacks, I'm uninterested in the precise urate levels)
4. "Management" seems imply an overall logical sequence of managing acute attacks and then preventing repeated occurances if required. Term feels awkward compared to "Treatment", especially if lifestyle approaches are not to be included here but left in a prevention section... and the prevention section has the subheading of "Medication".

I've done some reordering (keeping all the original material).[13] David Ruben ^Talk 01:52, 10 June 2010 (UTC)

and then some citration details tidy up. Finally the External link is to an abstract, and seems wrongly placed - can it be worked into the Prevention section ? David Ruben ^Talk 02:05, 10 June 2010 (UTC)

Removed the external link. This content is already discussed in the article.Doc James (talk · contribs · email) 04:05, 10 June 2010 (UTC)

Gosh, I'd forgotten about not using regular preventative med until two attacks. My below-neck medicine is rusty...we don't really do gout in psychiatry :/ Casliber (talk · contribs) 02:13, 10 June 2010 (UTC)

I do not know. Most people think of gout as the acute attack. They say I have had gout not I have gout when they speak of health problems. Thus in this situation I think secondary prevention should remain under the prevention section.Doc James (talk · contribs · email) 03:36, 10 June 2010 (UTC)

new med for gout

I have had gout on and off for thiry years. On one trip to the ER I met a Dr who told me he had just finishe working on a new medicine that will virtually remove all the uric acid from your blood. I thought it was paraclease but I can't find anything about it. The DR had told me it should be on the market within six months and that was at least two years ago. Anyone heard anything about it.----Terry A --Preceding unsigned comment added by 74.4.23.172 (talk) 19:23, 2 June 2010 (UTC)

Check the research section. A couple new meds are listed there.--Doc James (talk · contribs · email) 10:00, 19 June 2010 (UTC)

Bicard

Krementz (talk) 18:09, 23 June 2010 (UTC) I added that gout has been treated with sodium bicarbonate, with a link to icuredmygout.org. This was reversed because lack of source. While I fully understand that this website is not as authoritative as, say, mayoclinic.com, it is a legitimate source. I am not affiliated with this site. Over 2,000 people have responded to his poll (since closed) whether the NaHCO3 helped them. I suffer from gout, and this cure worked for me. This link does _not_ point to a marketing site, the author is not looking for compensation (or even glory), and is supportive of traditional treatments for gout. My statement that NaHCO3 has sometimes been used as a remedy for gout is true, independent of whether traditional medical science has studied its efficacy. Wikipedia is not vouching that this treatment is recommended.

Yes there are lots of treatments whos usage is documented but unless it works this would be of questionable notability.Doc James (talk · contribs · email) 19:35, 23 June 2010 (UTC)

It looks an interesting site, and I don't doubt your experience; but you are making a medical claim and we have agreed that sources for those sort of claims need to be of the highest standard. The guideline WP:MEDRS documents consensus on what is required for sourcing a medical claim. With the best will in the world, the site you used is at best a primary source, and really doesn't qualify as a reliable source at all. While checking the claim, I found a forum post that refers to "Gout, Goutiness and their Treatment" by William Ewart, (published in 1896) which mentions sodium bicarbonate, so it seems to have been used in the past. I'd suggest you search Google Scholar for a recent review to support the claim - sodium bicarbonate appears to be mentioned in this 2001 review, but I can't see the full text to confirm what it says. At present, this article is a GA candidate, so editors will be strict on sourcing claims. I'd suggest doing some more research and bringing your findings to the talk page here. Even if it's only of historical importance, I'm sure that it would be a good addition if the sources exist. --RexxS (talk) 20:02, 23 June 2010 (UTC)

Even if it wasn't a medical claim, user polls aren't reliable sources. Anything user created isn't a reliable source. Unless they're a published expert in the field and their opinion is being sourced as such.--Crossmr (talk) 12:06, 24 June 2010 (UTC)

More to the point: Reliable Sources. Self-publishing claims, that isn't. 70.102.117.22 (talk) 22:49, 29 July 2010 (UTC)

Fructose & gout?

Recent research appears to show that in addition to Purines and beer, fructose (as a dietary "added sugar" from sucrose, honey, HFCS, agave and crystalline fructose, primarily) is a major player in triggering uric acid production. While it has been applied largely to Type 2 Diabetes, Obesity and Heart Disease, some have also considered that it may play a large role in worsening gout as well.

• "The Sugar Fix" [book] by Richard Johnson make copious mention of uric acid: [14]
• It is also mentioned briefly in Robert Lustig's lecture "Sugar: The Bitter Truth": [15] as well as an article he authored (not sure if/where it was published): [16]

Seems worth mentioning current research in the article (I'm sure there's stuff coming out in the relevant medical literature; probably with either Richard Johnson or Robert Lustig attached, among others)... Offered for what it's worth. 70.102.117.22 (talk) 22:22, 29 July 2010 (UTC)

Yes it is mentioned in the prevention section already "Dietary and lifestyle choices that are effective include reducing intake of food high in purines such as meat and seafood, consuming adequate vitamin C, limiting alcohol and fructose consumption" Doc James (talk · contribs · email) 22:36, 29 July 2010 (UTC)

Hmm, must have missed that. Sorry. Would think it would have been mentioned under Causes or Lifestyle-- Hmm, guess that the generic term "sugar" is mentioned in Lifestyle. Though, if I recall correctly, it was fructose and not glucose that was found to significantly raise uric acid levels during its processing in the liver. So, saying "sugar" seems a bit inspecific (if fructose containing sugars are the culprit and not glucose / galactose [non-fructose] based sugars like Dextrose [glucose], Maltose & Lactose). Just a thought... Though, one would prefer to cite reliable source(s) from the literature, if making such claims, obviously... 70.102.117.22 (talk) 23:00, 29 July 2010 (UTC)

You are completely correct and I have changed the text to reflect the source. Thanks. Doc James (talk · contribs · email) 23:21, 29 July 2010 (UTC)

Lead image

The cartoon is better than other images IMO.Doc James (talk · contribs · email) 21:08, 14 April 2010 (UTC)

How is a cartoon better than an image of the actual disease?--Crossmr (talk) 04:42, 5 June 2010 (UTC)

Diagrams are often better than pictures. Think of Frank Netter.Doc James (talk · contribs · email) 05:47, 5 June 2010 (UTC)

This isn't a diagram.--Crossmr (talk) 08:52, 5 June 2010 (UTC)

Nearly are many of the images by Netter. I think they have done and interested job of representing pain in a picture as pain is the primary component of gout.--Doc James (talk · contribs · email) 13:26, 5 June 2010 (UTC)

I just checked several random major diseases and not one of them is illustrated with a cartoon. they're either illustrated by an image of the actual disease or a medical image of some sort.--Crossmr (talk) 00:20, 6 June 2010 (UTC)

I found the cartoon quite a surprise when I first visited this article. I don't think it's an appropriate illustration for an {{Infobox disease}} template. It would fit in fine in the History section, though. --CliffC (talk) 00:51, 6 June 2010 (UTC)

How about here Cluster_headache Doc James (talk · contribs · email) 02:43, 6 June 2010 (UTC)

I'd go with inappropriate there too. This isn't even some historical painting on the subject, it's something recent someone whipped up. Not remotely appropriate for identifying a disease.--Crossmr (talk) 11:21, 6 June 2010 (UTC)

<-Both cartoons do represent the most commonly identified symptom of the condition(s).. I'm not sure there is a good way to visually identify either condition otherwise. --Versageek 11:30, 6 June 2010 (UTC)

By identifying the disease. Perhaps Doc James could provide us with some kind of medical image of the disease in question. Excessive uric acid in the blood, or any image along these lines that could be appropriately licensed: [17], [18], [19], [20], etc.--Crossmr (talk) 11:33, 6 June 2010 (UTC)

As for cluster headache it could be appropriately illustrated with an image along these lines: [21], [22], [23] (2nd image), [24], these cartoony images don't adequately represent either of these.--Crossmr (talk) 11:36, 6 June 2010 (UTC)

I have to admit, those high-quality medical graphics that Crossmr linked are sweet.. what are the chances we could get something like them under the proper license? --Versageek 14:10, 6 June 2010 (UTC)

The lead should contain one of the best images in the article. The image of gout that I uploaded ( the one of the foot ) is a mild case and I do not think is good enough for the lead. Pain the main feature of this condition is not demonstrated as it is in the cartoon. I looked at the graphics mentioned and still think the classic cartoon is best. This cartoon is famous. I saw it before I got involved with Wikipedia. The cartoon says gout.Doc James (talk · contribs · email) 14:26, 6 June 2010 (UTC)

Actually the infobox should contain an image that adequately identifies the disease. One of the ones I provided, or something like them would do that job. Since you're a medical professional do you have access to public domain images like those? Perhaps an x-Ray of a gouty toe?--Crossmr (talk) 22:25, 6 June 2010 (UTC)

I took an x ray of gout today but it did not show much. I will get a better image when I see one but it could be months. Doc James (talk · contribs · email) 05:58, 7 June 2010 (UTC)

• FYI the cartoon struck me as odd in the lead. After reading the rationale presented here, I've expanded the caption [25]. Tweak as desired. -xeno^talk 16:44, 30 June 2010 (UTC)

Thanks Xeno an improvement. Doc James (talk · contribs · email) 16:49, 30 June 2010 (UTC)

For what it is worth: I have just suffered such an an attack and I think the cartoon creates a much better impression of the experience than the photo does. AlexFekken (talk) 07:23, 4 September 2010 (UTC)

Just uploaded a photo of one of my bouts with gout to the Commons (gout_advanced.jpg). Shows the whole foot swollen. I have others if wanted.Wrerick (talk) 20:11, 19 September 2010 (UTC)

The image does not seem to work... Doc James (talk · contribs · email) 20:36, 19 September 2010 (UTC)

71.84.106.178 (talk)GOUT03:22, 4 October 2010 (UTC)

Hello!

How related do you think Gout is to drinking beer (or alcohol)? Or do you think it would be more relevant if one had a high intake of sweets? What would be the most detrimental?

Thanks!

References are provided that deal with stuff in more detail. --Doc James (talk · contribs · email) 04:22, 4 October 2010 (UTC)

Reviews

• Doghramji PP, Edwards NL, McTigue J (2010). "Managing gout in the primary care setting: what you and your patients need to know". Am. J. Med. 123 (8): S2. doi:10.1016/j.amjmed.2010.06.005. PMID 20670699.  CS1 maint: Multiple names: authors list (link)

Doc James (talk · contribs · email) 13:33, 11 October 2010 (UTC)

Any relation to blood plasma?

I suffered from what I believed was gout a few years ago after donating blood plasma. Was it a coincidence? 184.96.206.16 (talk) 07:42, 19 October 2010 (UTC)

Cartoon and Hanska

First, I think the cartoon is fitting and provides both an historical perspective and an impressionistic depiction, which -- although unusual -- I find appropriate.

Whilst researching Balzac's wife Eveline Ha?ska today, I found this intriguing bit about her doctor's cure for gout:

Dr. Knothe's treatment for this was strange and barbarous: 'Every other day she has to thrust her feet into the body of a sucking-pig which has only just been slit open, because it is necessary that the entrails should be quivering. No need to describe the agonized squeals of the little pig, which does not realize the honour that is being done it.'

from Maurois, André. Prometheus: The Life of Balzac. New York: Carroll & Graf, 1965. ISBN 0-8818-4023-8.

I'm sure you don't want to list every harebrained ancient remedy for the disease, but if this is useful in any way, please have at it. Scartol o Tok 13:14, 26 December 2010 (UTC)

The current article sucks. I experience gout symptoms on and off, and had to revert to a 2009 version for the Prevention section. I agree that we don't need every wacko remedy, but the current version doesn't even mention cherries - an awesome prevention aid. The 2009 version also has a nice list of foods to avoid. For a sufferer, the current version reads like a commercial for the medical establishment. Useful article is here: http://en.wikipedia.org/w/index.php?title=Gout&oldid=296829182 3/27/2011 --Preceding unsigned comment added by 69.11.239.66 (talk) 02:16, 28 March 2011 (UTC)

Risk of Death

Don't have the articles on hand. Can someone elaborate as to the increased risk from cardiovascular disease? How solid is the information and can it be quantified better? MartinezMD (talk) 06:21, 22 January 2011 (UTC)

2011 review in NEJM

Neogi, T (2011 Feb 3). "Clinical practice. Gout". The New England journal of medicine. 364 (5): 443-52. PMID 21288096.  Doc James (talk · contribs · email) 07:28, 7 April 2011 (UTC)

Cheeries

Vitamine C reduced the risk of gout therefore one would expect cheeries to do the same. But we are not listing all Vit C containing foods. Also would need a review article. --Doc James (talk · contribs · email) 23:53, 14 May 2011 (UTC)

Rich man's Disease

"Gout was historically known as "the disease of kings" or "rich man's disease"." I do not question the validity of this claim but wish to see it given more explanation. For anyone not well read on the history of Gout this statement seems out of the blue and somewhat meaningless. Andreis 05/15/2011

Great if you wish to research and expand on this... If you need help access journal articles let me know. Doc James (talk · contribs · email) 02:41, 16 May 2011 (UTC)

Though it is out of the blue, I have heard this of goute. The reason that kings and wealthy men got goute is because they were sometimes fat and had a diet high in meat, which deprived them sevvs of the vegitables with vitimins to prevent gout. These people probably also lived a bit longer and older people suffer from goute in higher numbers. I am not offering any documention other than to verify that I have heard of this and it seems true. -- Preceding unsigned comment added by 141.116.212.32 (talk) 20:25, 5 March 2012 (UTC)

Genetics

While gout is directly caused by high uric acid levels, in "At least 10% of all gout cases in whites are attributable to" (source) rs2231142 a single-nucleotide polymorphism in the ABCG2 gene found in approximate 1% of caucasians and 10% of asians . This was removed for not being a review article. I'm not aware of any review which speaks about this as specifically as the paper above, however there are numerous sources which appear to validate the claim.

• [[[PubMed Identifier|PMID]] 18834626] Association of three genetic loci with uric acid concentration and risk of gout: a genome-wide association study.
• [[[PubMed Identifier|PMID]] 19503597] Meta-Analysis of 28,141 Individuals Identifies Common Variants within Five New Loci That Influence Uric Acid Concentrations
• [[[PubMed Identifier|PMID]] 19506252] Identification of a urate transporter, ABCG2, with a common functional polymorphism causing gout. (cited above)
• [[[PubMed Identifier|PMID]] 19890391] Common polymorphisms influencing serum uric Acid levels contribute to susceptibility to gout, but not to coronary artery disease
• [[[PubMed Identifier|PMID]] 20421215](not a review) The rs2231142 variant of the ABCG2 gene is associated with uric acid levels and gout among Japanese people

Cariaso (talk) 04:56, 21 October 2011 (UTC)

Yes so some gout is genetic and associated with certain loci.Doc James (talk · contribs · email) 05:12, 21 October 2011 (UTC)

'some loci' is usually quite broadly defined, often megabases. This is the specific causative single base change for a substantial % of cases. But as long as it's here on the talk page, good enough for me. Cariaso (talk) 07:33, 21 October 2011 (UTC)

It appears to be more of an association rather than a direct cause at this point. Doc James (talk · contribs · email) 07:52, 21 October 2011 (UTC)

The vast majority of GWAS findings are merely associations, but this one appears to have gone beyond that, and is being reported as a causal variant by 2 independent groups. [[[PubMed Identifier|PMID]] 19506252] "at least 10% of all gout cases in whites are attributable to this causal variant" and [[[PubMed Identifier|PMID]] 20421215] "The association of the causal ABCG2 rs2231142 variant with uric acid levels and gout was confirmed in a sample of Japanese ancestry. Our study emphasizes the importance of this common causal variant". Cariaso (talk) 08:04, 21 October 2011 (UTC)

Gout "at night" or "during sleep"?

The article currently states: 'Joint pain usually begins over 2-4 hours and during the night.[3] The reason for onset at night is due to the lower body temperature then.[1] Other symptoms that may occur along with the joint pain include fatigue and a high fever.' Is it sleeping or sleeping at night when a gout attack is triggered? Why would my body temperature be lower at night when I'm wrapped up in a duvet?109.76.183.199 (talk) 13:40, 21 April 2012 (UTC)

It's time of day - a person's circadian rhythm driven by cortisol. Awake/sleep would alter the numbers somewhat, but it's hormonal. Some of it is covered in the article Human body temperature.MartinezMD (talk) 02:49, 22 April 2012 (UTC)

Thanks! 93.107.2.255 (talk) 22:00, 20 May 2012 (UTC)

Should coffee (caffeine?) be avoided?

The article states: 'The consumption of coffee, vitamin C and dairy products as well as physical fitness appear to decrease the risk [of gout]". Now, I'm very confused. I adore coffee, but have been told that caffeine is a diuretic and as such should be avoided as you need as much fluid (water) in your body to flush out the uric acid. Which is correct? 93.107.2.255 (talk) 22:00, 20 May 2012 (UTC)

As stated coffee decreases the risk. Never seen a ref recommending that it be avoided. --Doc James (talk · contribs · email) 09:37, 21 May 2012 (UTC)

Review

• Hamburger, M (2011 Nov). "2011 recommendations for the diagnosis and management of gout and hyperuricemia". The Physician and sportsmedicine. 39 (4): 98-123. PMID 22293773.  Doc James (talk · contribs · email) 12:35, 12 June 2012 (UTC)

Refractory chronic gout

This content was uploaded on behalf of Savient Pharmaceuticals to create awareness surrounding gout and refractory chronic gout.Gout2012 (talk) 14:48, 25 June 2012 (UTC)

This content was removed as we do not format like this and we already covered this content in the article. Doc James (talk · contribs · email) (please reply on my talk page) 23:39, 25 June 2012 (UTC)

Two new papers

• Khanna, Dinesh (1 October 2012). "2012 American College of Rheumatology guidelines for management of gout. Part 1: Systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia". Arthritis Care & Research. 64 (10): 1431-1446. doi:10.1002/acr.21772. 

• Khanna, Dinesh (1 October 2012). "2012 American College of Rheumatology guidelines for management of gout. Part 2: Therapy and antiinflammatory prophylaxis of acute gouty arthritis". Arthritis Care & Research. 64 (10): 1447-1461. doi:10.1002/acr.21773.  Doc James (talk · contribs · email) (if I write on your page reply on mine) 02:23, 2 October 2012 (UTC)

Pathophysiology

Proposed addtion.

Mechanisms

A Runaway Chemical Crystalisation

An acute attack occurs as a result of an inflammatory reaction to crystals of sodium urate that are deposited in the joint tissue. The inflammatory response involves the local infiltration of granulocytes which phagocytise the urate crystals. Lactate is high in synovial tissues and in the leucocytes that are associated with the inflammatory process which also favours the deposition of uric acid.

B Kamikaze leucocytes

Self Perpetuating Fatal Phagocytosis

KT Rajan studied phagocytosis of urate crystals by polymorphonuclear leucocytes. From his investigations with specific reference to phagocytosis of urate crystals by polymorphonuclear leucocytes he proposed a sequence of events that may initiate the inflammatory reaction in acute gout. He concluded that :

(1) neutrophil leucocytes avidly ingest microcrystals of sodium monourate

(2) this causes the rapid degranulation and disintegration of the leucocytes

(3) fresh leucocytes ingest the debris and crystals liberated by the dead cells, and in their turn degranulate and die, thus possibly establishing a vicious circle in the system.

In support of his theory Rajan quoted research in the 1960's where McCarty demonstrated that:

The severity of the inflammatory reaction is dependent on the number of neutrophils that are available at the time of invasion by the bacteria or toxic agent. In agranulocytosis the reaction to bacterial invaders by the host is functionally deficient and acute gouty effusions provoked by injecting crystals of uric acid into joints can be abolished by pretreating the host with drugs like vinblastine which reduce the total number of leucocytes available. (McCarty, 1965).

.

C Matchstick Model

Theodore Fields Director, Rheumatology Faculty Practice Plan, Hospital for Special Surgery New York suggests that

Whatever the cause of elevated uric acid levels, the key event in gout is the movement of uric acid crystals into the joint fluid. Inflammatory chemicals are released when the body's defense mechanisms, engulf the uric acid crystals. All the signs of inflammation, including heat, redness, swelling and pain are caused by these chemicals. (cytokines) The inflammation attracts more white blood cells to the joint, which increases the inflammation.

Theodore stated

"When thinking of gout, a useful model has been proposed by Wortmann. Uric acid crystals can be thought of like matches, which can sit quietly or can be ignited. Crystals can be present for years in the cartilage, or even in the joint fluid, without causing inflammation. Then, at some point, due to increasing number of crystals or other inciting factor, the matches are "struck" and the inflammation begins. This analogy is important both for conceptualizing the uric acid crystals in the joint and for understanding the various types of gout treatment (see below) - some of which attack the inflammation (pour water on the flaming matches) and some of which remove the uric acid crystals (take away the matches)."

D MicroTophi Grenades Urate Crystals in microtophi are normally covered with proteins that block the crystals from binding to cell receptors. When the coating is lost or the tophi burst the crystals suddenly bind to cells suddenly causing the inflammation.

E Crystalisation from Supersaturated Fluid Damaged cells release sodium urate resulting in a supersaturated microenvironment and crystalisation of sodium urate triggering the innate immune response.[26]

What Could End the Attack?

Humans lack the uricase enzyme that converts urate to the more soluble and easily excreted compound allantoin in most mammals. The tangible presence of tophi is a fair indication that the human body does not have an effective means of eliminating monosodium urate monhydrate crystals once they have formed. The body's visible solution is to encapsulate the crystals and prevent interaction with the immune system.(hide the matches)

Anti-inflammatory drugs are effective in acute epsiodes and the body has a range of anti-inflammatory cytokines including, IL-1RA, IL-10, and transforming growth factor (TGF)-beta that are produced.[27](pour water on the flaming matches)

This proposed contribution has been subjected to lengthy scrutiny. Any comments?Nnoddy (talk) 02:43, 10 March 2013 (UTC)

Oppose Much of the text is not properly referenced. Google Knol is not a suitable source. Emedicine is sort of on the edge. References and headings are not formatted properly. Still needs a fair bit of work. Please see WP:MEDMOS for formatting and WP:MEDRS for reference requirements. Doc James (talk · contribs · email) (if I write on your page reply on mine) 15:48, 10 March 2013 (UTC)

Minor typo

Third word of second paragraph reads "maybe" as an adverb, when in fact it should read "may be" as a modal verb with verb. Uq (talk) 19:12, 20 March 2013 (UTC)

Thanks Doc James (talk · contribs · email) (if I write on your page reply on mine) 22:45, 20 March 2013 (UTC)

Spelling correction

In the section titled "Prophylaxis", there is a misspelled word toward the end of the first paragraph. The word "discontinuation" should not contain the letter "e". (See pasted text below.)

Prophylaxis

A number of medications are useful for preventing further episodes of gout, including xanthine oxidase inhibitor (including allopurinol and febuxostat) and uricosurics (including probenecid and sulfinpyrazone). They are not usually commenced until one to two weeks after an acute attack has resolved, due to theoretical concerns of worsening the attack,[2] and are often used in combination with either an NSAID or colchicine for the first three to six months.[6] They are not recommended until a person has had two attacks of gout,[2] unless destructive joint changes, tophi, or urate nephropathy exist,[5] as medications have not been found cost effective until this point.[2] Urate-lowering measures should be increased until serum uric acid levels are below 300-360 µmol/l (5.0-6.0 mg/dl), and are continued indefinitely.[2][6] If these medications are being used chronically at the time of an attack, discontinueation is recommended.[3] If levels cannot be brought below 6.0 mg/dl and there are recurrent attacks, this is deemed treatment failure or refractory gout.[42] Overall, probenecid appears less effective than allopurinol.[2]

Pascazio (talk) 11:42, 14 September 2013 (UTC)

Thanks Doc James (talk · contribs · email) (if I write on your page reply on mine) 12:20, 14 September 2013 (UTC)

Infobox image

Shouldn't the infobox image be a photograph of a typical case of gout rather than a caricature? I have just been diagnosed with gout, and, if I was not so familiar with the way Wikipedia is written, I would have found that image very frightening as a possible way in which the disease might develop. We have WP:MEDRS to ensure that the textual content of medical articles is soundly based on generally accepted research, but that accuracy can be undone if the first thing that draws people's attention when they come to this page is such a shocking image. Phil Bridger (talk) 11:40, 26 September 2013 (UTC)

I see that the inclusion of images in medical articles for shock value is clearly prohibited by WP:MEDMOS#Images, so I have gone ahead and removed the caricature. Of course I have no objection to its replacement by a suitable image, maybe the image currently in the "signs and symptoms" section. Phil Bridger (talk) 12:06, 26 September 2013 (UTC)

I'm not sure that WP:MEDMOS#Images really covers this - it is genuine photographs that people find scary. I have re-added it lower down. Sorry to hear about your case, but I wouldn't worry too much. As someone diagnosed many years ago, I recommend watching dehydration very carefully - I successfully avoided attacks for several years just by doing this (by monitoring urine colour & drinking water as necessary - there was a lag about 48 hours between dehydration & the onset of an attack). Since I got lazy at that, ongoing allopurinol has completely solved the problem. Doctors underestimate the impact of dehydration imho, but I suppose people vary. Johnbod (talk) 13:00, 26 September 2013 (UTC)

Phil you are joking right? Doc James (talk · contribs · email) (if I write on your page reply on mine) 23:01, 26 September 2013 (UTC)

No. Phil Bridger (talk) 13:13, 30 September 2013 (UTC)

No, I didn't think you were. Johnbod (talk) 08:30, 1 October 2013 (UTC)

Semi-protected edit request on 22 January 2014

Please change "Gout has become more common in recent decades, affecting about 1-2% of the Western population at some point in their lives." to "Gout has become more common in recent decades, affecting over 3% of the Western population at some point in their lives". Additional update info may be found in the referenced article. Noted in Medpage Today 01/21/2014 Source: Annals of the Rheumatic Diseases Source reference: Kuo C-F, et al "Rising burden of gout in the UK but continuing suboptimal management: a nationwide population study" Ann Rheum Dis 2014; DOI: 10.1136/annrheumdis-2013-204463. 75.100.38.188 (talk) 05:03, 22 January 2014 (UTC)

We use secondary sources rather than primary sources per WP:MEDRS Doc James (talk · contribs · email) (if I write on your page reply on mine) 05:46, 22 January 2014 (UTC)

Urate and parkinson's

The Australian ABC radio's Health Report recently included a piece on good effects of raised urate levels identified by new research.

The transcript can be found here: ABC Radio National - Gout and Parkinsons

Is it reasonable to include something based on this to the article? --180.149.192.139 (talk) 07:36, 12 February 2014 (UTC)

No we need high quality sources per WP:MEDRS. We do not use popular press. 11:25, 12 February 2014 (UTC)

It's all from a JAMA Neurology press release - 23 December 2013, as here, if anyone has the actual paper. Johnbod (talk) 22:21, 12 February 2014 (UTC)

A primary source and not a very good one at that. Doc James (talk · contribs · email) (if I write on your page reply on mine) 11:32, 13 February 2014 (UTC)

Infobox image.... again

The cartoon image with the big spider and devil's tail is a REALLY bad choice for the infobox. It's unencyclopedic, misleading, and there are better images to lead with. I stumbled on this page looking up "gout". Gout is caused by spiders? Big spiders? What is that hooky thing and what the hell am I looking at? These were my thoughts until I looked further down the article. I notice this has been brought up before, yet the image was reinserted. Hopefully it will stick this time. - JBarta (talk) 21:11, 14 May 2014 (UTC)

It is a very historical image and is very encyclopedic. And is not a spider but a devil. The image of gout fits best in the signs and symptoms section. Doc James (talk · contribs · email) (if I write on your page reply on mine) 22:17, 14 May 2014 (UTC)

RfC: Is the is the current infobox image preferable?

Hyperuricemia cause contradiction

The "Cause" section states that hyperuricemia is the cause of gout. The blood test section states that half of people with gout do not have hyperuricemia and that most people that do have hyperuricemia do not have gout. These two sections are contradictory.

I believe it should be reworded to list some "possible contributing factors" as it appears no single direct cause is known. If it is directly listed as a cause, then that source could be cited; although it still appears that different sources do not agree on a single underlying cause.

Hyperuricemia has some correlation and genetics also can play a role. Diet is not directly related to gout, but a method of controlling hyperuricemia. -- Preceding unsigned comment added by Jmbise (talk o contribs) 22:01, 28 July 2014 (UTC)

Yes the cause is high uric acid but by the time you measure it, it may be in the normal range. That gout is cause by uric acid precipitating is agreed upon. Doc James (talk · contribs · email) (if I write on your page reply on mine) 22:12, 28 July 2014 (UTC)

Yes, perhaps it should be worded to state that? "Gout is caused by uric acid precipitating" or "developing into uric acid crystals in the joint" as opposed to "high uric acid levels in the blood", which is not the direct cause. As this article states, 10% of people with hyperuricemia may develop gout. If it caused gout, that would be much higher. Higher uric acid levels can make it more likely to develop uric acid crystals, but people with low uric acid levels and other factors (poor circulation) can develop crystals as well. Jmbise (talk) 22:28, 28 July 2014 (UTC)

Excellent point. Thanks. Doc James (talk · contribs · email) (if I write on your page reply on mine) 22:52, 28 July 2014 (UTC)

Natural gout treatments

Why no mention of natural treatments for gout?

I've started using a widely-available, liquid extract of celery seed, added to water, to treat a classic case of chronic (over 1 year) gout in the big toe.

I obtained relief within hours, at half the label dose, and have had no recurrence after one week of use.

75.253.149.201 (talk) 17:45, 20 August 2012 (UTC)

On Wikipedia, information added to articles are required to have reliable sourcing; for medical sources, this guideline is at WP:MEDRS. Your own personal testimonial does not qualify. We would be happy to include information on alternative treatments should they be appropriately sourced. Yobol (talk) 17:58, 20 August 2012 (UTC)

A study published in Arthritis & Rheumatism, a journal of the American College of Rheumatology (ACR), reports that patients with gout who consumed cherries over a two-day period showed a 35% lower risk of gout attacks compared to those who did not eat the fruit. The study also suggests that risk of gout flareups was 75% lower when cherry intake was combined with the uric-acid reducing drug, allopurinol, than in periods without exposure to cherries or treatment. 207.118.16.184 (talk) 02:13, 15 November 2013 (UTC) Michael Hurwicz

We use secondary sources per WP:MEDRS. This is a primary source. Doc James (talk · contribs · email) (if I write on your page reply on mine) 02:19, 15 November 2013 (UTC)

I first heard about it from a coworker, although I've never had gout. Something both considered common knowledge and receiving media attention articles.mercola.com/sites/articles/archive/2012/10/15/cherries-reduce-gout-attack-risks.aspx 1] 2 3 4 for the research in the area should be at least mentioned in a encyclopedic article. 108.180.175.98 (talk) 00:52, 4 December 2014 (UTC)

NSAIDS

Not great, JAMA synopsis doi:10.1001/jama.2015.1881 JFW | T@lk 22:03, 9 June 2015 (UTC)

Surgical treatment is effective

I've had Gout two times the last 2 years, both in the big toe. Both times, The doctor in Vietnam simply applied some local anesthetic, and simply cut out the bad stuff. And in less than 24 hours, I was relatively pain free, I had no problems putting on socks or shoes.. I don't know how common this treatment is outside of Vietnam, but.. Would appreciate it being part of the treatment section ^^ Divinity76 (talk) 10:25, 5 October 2015 (UTC)

That doesn't sound like gout, which doesn't (in typical early episodes) have "bad stuff" to cut out. Johnbod (talk) 15:01, 5 October 2015 (UTC)

Yes, he's mistaking gout with something else. There's nothing to cut in gout. It's joint inflammation.MartinezMD (talk) 18:00, 5 October 2015 (UTC)

Testing new infobox

• User:Doc James/Infobox medical condition
• Lots of work yet to do

Doc James (talk · contribs · email) 21:57, 13 November 2015 (UTC)

What is the source of the last line (about prevalence)? Is it Wikidata? The syntax doesn't really make sense (should be "per cent", literally "per hundred", rather than "percentage" that is generally not used with a specific value); the value presented imperfectly captures the complex prevalence described in the article and references. -- soupvector (talk) 01:30, 22 December 2015 (UTC)

Comes from here [30]. Agree Wikidata has limitations and is very slow to edit. Doc James (talk · contribs · email) 03:49, 22 December 2015 (UTC)

I changed it in wikidata from "percentage" to "percent sign", but now it looks silly - shouldn't the code convert "percent sign" to a symbol? Also, the reference says "1-2", not "1.0+/-0.5", but I guess this supports various representations that "1-2" might be misinterpreted to mean a difference rather than a range? I think we have a ways to go before having a robust wikidata interface. Maybe too early to put into production. -- soupvector (talk) 13:25, 22 December 2015 (UTC)

Yes we cannot do 1-2 from Wikidata. The best we could get was 1.5 +/- 0.5. Yes agree this is beta and too early for main stream production. Doc James (talk · contribs · email) 18:23, 22 December 2015 (UTC)

I'll go ask at Wikidata's Project Chat.[31] Maybe someone will know how to solve this. WhatamIdoing (talk) 18:04, 24 December 2015 (UTC)

• For more freedom in testing & trying I have created Draft:Gout. Please keep in mind that the actual discussed proposal is defined in Template talk:Infobox medical condition#Proposal 1 December 2015, not the draft page as it happens to be. -DePiep (talk) 08:43, 23 December 2015 (UTC)
  • I do not think their is anything wrong with having a single article presented in a different way, live. Having two infoxes is not needed [32] Doc James (talk · contribs · email) 20:43, 23 December 2015 (UTC)
    • This is not testing. This is an okayish alternative. With significant support for the idea here Additionally it has been in place for a month. Doc James (talk · contribs · email) 20:48, 23 December 2015 (UTC)
    • Who cares if it's "testing"? The alleged "no testing in mainspace" rule simply doesn't exist. The actual rule is, if it improves the article, then keep the change. I believe that the new version improves the article for the likely audience (i.e., regular people like students writing papers for health class, not professional medical coders [who will prefer having the ICD codes at the top]) and therefore should be kept. WhatamIdoing (talk) 17:58, 24 December 2015 (UTC)
      • • "Testing" matters because the issue is under discussion (ie no consensus) and the version is not stable. Other arguments should be at the talkpage as you know, not in the article. Instable templates and setup is not fit for FA articles (so the page must be reviewed). As you know that the discussion has not resulted in a consensus yet, and now Doc James does not bother to contribute to the discussion any more. This version is just "I can't explain or convince what I want, so I push my version anyway this way". -DePiep (talk) 06:55, 29 December 2015 (UTC)

Circling back from Wikidata:

• Right now, "prevalence" can't support a range.
• Numbers in that field are supposed to be 0 to 1 (aka 0% to 100%). So it shouldn't be "1 to 2"; it should be "0.01 to 0.02" (assuming that it could support a range).
• It also can't support different prevalences for different ages/sexes/locations/ethnicities/whatever else might matter.

Eventually, it will probably support all of these things. In the meantime, something we can do is to make sure that "1%" is recorded as "0.01", and that any templates pulling this information do a quick calculation (0.01 = 1%) for readability. WhatamIdoing (talk) 05:30, 29 December 2015 (UTC)

Advice for sufferers

i have gout and this article in it's current state doesn't help at all. too much western medicine information. it should have more of what the individual can do for their gout. right now it is not a good place to go for a person with gout.Somebodyleveled (talk) 15:15, 23 December 2015 (UTC)

It is called evidenced based medicine and yes we concentrate on that. Doc James (talk · contribs · email) 15:49, 23 December 2015 (UTC)

Somebodyleveled, I suggest you read WP:MEDRS and WP:NOTADVICE. The article isn't about what a person can do for themselves; it is about the disease as a whole. And any treatment information has be reliable.MartinezMD (talk) 17:13, 31 December 2015 (UTC)

Source of the article : Wikipedia