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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)
The connection between high purine and high protein diets needs explanation, because purines are not proteins. Una Smith 20:50, 4 June 2007 (UTC)
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.
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)
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).
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)
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
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)
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.
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.
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.
rstWhat about extra-articular effects of the deposition of uric acid crystals ?
Soft tissue, kidneys etc
Kpjas 07:43, 8 Oct 2003 (UTC)
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
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."
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)
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 •
contribs) 01:43, 6 July 2006.
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.
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)
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)
It wasn't clear - is only green tea and caffinated tea contraindicated in cases of gout? Or herbal teas as well?
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.
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)
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.
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)
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)
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 • contribs) 22:12, August 27, 2006
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)
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)
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)
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'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)
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)
'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)
2006 (UTC)
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}
I have removed this text below because it needs a citation.
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)
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:
I moved it here. Perhaps someone has an answer? - Smerdis of Tlön 18:39, 2 August 2007 (UTC)
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)
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)
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)
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)
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)
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)
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)
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)
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)
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)
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.
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)
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)
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)
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)
Excellent photo! Damn these little pointed crystals!-- Amadscientist ( talk) 02:07, 23 July 2009 (UTC)
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)
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]
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)
James A. Duke PHD, in The Green Pharmacy makes several comments:
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.
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)
Review doi: 10.1016/S0140-6736(09)60883-7 JFW | T@lk 23:07, 23 January 2010 (UTC)
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)
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)
Thanks I'll adopt that.-- Nnoddy ( talk) 08:48, 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.
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).
[3].
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)
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.
Damaged cells release sodium urate resulting in a supersaturated microenvironment and crystalisation of sodium urate triggering the innate immune response. [11]
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 • contribs) 03:08, 3 March 2010 (UTC)
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 • contribs) 12:38, 8 March 2010 (UTC)
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.
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.
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.
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.
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".
Missing yeast extracts from the list.
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?
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)
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Doc James ( talk · contribs · email) 01:33, 9 June 2010 (UTC)
Sorry, this article's prevention/management is a "choppy" mess to quote from the GA review. The problems:
I've done some reordering (keeping all the original material). [13] David Ruben Talk 01:52, 10 June 2010 (UTC)
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)
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.
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.
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)
The cartoon is better than other images IMO. Doc James ( talk · contribs · email) 21:08, 14 April 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. -- Versa geek 11:30, 6 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)
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!
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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)
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 Hańska 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 • 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/?title=Gout&oldid=296829182 3/27/2011 —Preceding unsigned comment added by 69.11.239.66 ( talk) 02:16, 28 March 2011 (UTC)
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)
Neogi, T (2011 Feb 3). "Clinical practice. Gout". The New England journal of medicine. 364 (5): 443–52.
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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)
"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
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.
Cariaso ( talk) 04:56, 21 October 2011 (UTC)
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)
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)
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12:35, 12 June 2012 (UTC)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)
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Doc James (
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02:23, 2 October 2012 (UTC)Proposed addtion.
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).
[2].
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]
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)
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)
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)
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)
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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)
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)
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)
The following discussion is closed. Please do not modify it. Subsequent comments should be made on the appropriate discussion page. No further edits should be made to this discussion.
Result: Keep the current infobox image. Both images, as well as others presented during the discussion, appear policy-compliant, so this is just a matter of opinion and counting votes. I counted 6 in favour of the current image out of 10 votes in total. Whether that is a consensus for the current image or a lack of consensus either way, the result is the same.
Is the current infobox image for Gout the preferable image? Or the proposed replacement? Or some other image? – JBarta ( talk) 00:32, 15 May 2014 (UTC)
"the word "caricature" essentially means a "loaded portrait") - so let's drop the word 'caricature'.
Zad
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13:59, 20 May 2014 (UTC)Possible alternatives:
*Oppose current image, support photograph. We didn't have cartoons in the books at my medical school, we shouldn't have cartoons in an encyclopedia article on a serious medical topic. There should be a lede photograph as the reader is looking for that. A reader can't relate to a cartoon. It's misleading and unprofessional. SW3 5DL ( talk) 04:28, 22 May 2014 (UTC)
A bit of info on the Gillray image in this article... Was added to the body of the article in Nov 2005 by Pilatus. At some point later the caption is seen fleshed out [ nicely]. In Dec 2009 it was moved to the infobox by Doc James replacing the chemical symbol for Uric acid where it remains (at least for now). I haven't looked to see if this image has been problematic between the time Doc James moved it and now or why the caption was edited down. I would also mention that Doc James is by far the editor with the most edits to this article (441, with the second most active editor coming in at 89) so he has certainly contributed a lot here. – JBarta ( talk) 04:11, 23 May 2014 (UTC)
(Invited by RFC bot) *Mild oppose current image, support photograph assuming the drawing is not a realistic portrayal of the degree of swelling typically associated with gout (although IANADoctor). While readers will understand the demon is artistic license, they may be left with a wrong and unconscious first impression of what the swelling caused by the affliction looks like. That said, I don't know of any Wikipedia policies that mandate that the current image is disallowed, and there appears to be no consensus for change, so the current image will probably remain unless the active page editors change their mind. I acknowledge the current image does have encyclopedic merit, and I'd guess sufferers would be more likely to appreciate the depiction than take offense at it. Rolf H Nelson ( talk) 05:10, 30 May 2014 (UTC)
Comments
Balaenoptera musculus ( talk) 10:00, 23 May 2014 (UTC)
"Intangible concepts can be illustrated; for example, a cat with its claws out portrays aggression."( WP:PERTINENCE)
"For example, a photograph of a trompe-l'œil painting of a cupcake may be an acceptable image for Cupcake"( WP:PERTINENCE)
Comment On the question "Is it encyclopaedic?", it's interesting to note that the Encyclopædia Britannica uses the image "Origin of the Gout" to illustrate it's article on Gout. That's an 1815 print by Henry William Bunbury - same period and same style as the Gilray print. Balaenoptera musculus ( talk) 17:55, 23 May 2014 (UTC)
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 • contribs) 22:01, 28 July 2014 (UTC)
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)
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. [4] [5] 207.118.16.184 ( talk) 02:13, 15 November 2013 (UTC) Michael Hurwicz
References
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Not great, JAMA synopsis doi:10.1001/jama.2015.1881 JFW | T@lk 22:03, 9 June 2015 (UTC)
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)
Doc James ( talk · contribs · email) 21:57, 13 November 2015 (UTC)
Circling back from Wikidata:
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)
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)
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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)
The connection between high purine and high protein diets needs explanation, because purines are not proteins. Una Smith 20:50, 4 June 2007 (UTC)
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.
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)
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).
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)
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
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)
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.
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.
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.
rstWhat about extra-articular effects of the deposition of uric acid crystals ?
Soft tissue, kidneys etc
Kpjas 07:43, 8 Oct 2003 (UTC)
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
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."
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)
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 •
contribs) 01:43, 6 July 2006.
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.
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)
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)
It wasn't clear - is only green tea and caffinated tea contraindicated in cases of gout? Or herbal teas as well?
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.
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)
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.
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)
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)
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 • contribs) 22:12, August 27, 2006
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)
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)
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)
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'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)
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)
'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)
2006 (UTC)
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}
I have removed this text below because it needs a citation.
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)
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:
I moved it here. Perhaps someone has an answer? - Smerdis of Tlön 18:39, 2 August 2007 (UTC)
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)
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)
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)
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)
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)
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)
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)
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)
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)
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)
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.
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)
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)
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)
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)
Excellent photo! Damn these little pointed crystals!-- Amadscientist ( talk) 02:07, 23 July 2009 (UTC)
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)
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]
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)
James A. Duke PHD, in The Green Pharmacy makes several comments:
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.
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)
Review doi: 10.1016/S0140-6736(09)60883-7 JFW | T@lk 23:07, 23 January 2010 (UTC)
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)
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)
Thanks I'll adopt that.-- Nnoddy ( talk) 08:48, 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.
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).
[3].
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)
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.
Damaged cells release sodium urate resulting in a supersaturated microenvironment and crystalisation of sodium urate triggering the innate immune response. [11]
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 • contribs) 03:08, 3 March 2010 (UTC)
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 • contribs) 12:38, 8 March 2010 (UTC)
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.
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.
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.
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.
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".
Missing yeast extracts from the list.
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?
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)
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Doc James ( talk · contribs · email) 01:33, 9 June 2010 (UTC)
Sorry, this article's prevention/management is a "choppy" mess to quote from the GA review. The problems:
I've done some reordering (keeping all the original material). [13] David Ruben Talk 01:52, 10 June 2010 (UTC)
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)
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.
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.
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)
The cartoon is better than other images IMO. Doc James ( talk · contribs · email) 21:08, 14 April 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. -- Versa geek 11:30, 6 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)
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!
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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)
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 Hańska 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 • 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/?title=Gout&oldid=296829182 3/27/2011 —Preceding unsigned comment added by 69.11.239.66 ( talk) 02:16, 28 March 2011 (UTC)
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)
Neogi, T (2011 Feb 3). "Clinical practice. Gout". The New England journal of medicine. 364 (5): 443–52.
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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)
"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
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.
Cariaso ( talk) 04:56, 21 October 2011 (UTC)
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)
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)
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12:35, 12 June 2012 (UTC)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)
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Doc James (
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02:23, 2 October 2012 (UTC)Proposed addtion.
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).
[2].
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]
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)
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)
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)
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)
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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)
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)
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)
The following discussion is closed. Please do not modify it. Subsequent comments should be made on the appropriate discussion page. No further edits should be made to this discussion.
Result: Keep the current infobox image. Both images, as well as others presented during the discussion, appear policy-compliant, so this is just a matter of opinion and counting votes. I counted 6 in favour of the current image out of 10 votes in total. Whether that is a consensus for the current image or a lack of consensus either way, the result is the same.
Is the current infobox image for Gout the preferable image? Or the proposed replacement? Or some other image? – JBarta ( talk) 00:32, 15 May 2014 (UTC)
"the word "caricature" essentially means a "loaded portrait") - so let's drop the word 'caricature'.
Zad
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13:59, 20 May 2014 (UTC)Possible alternatives:
*Oppose current image, support photograph. We didn't have cartoons in the books at my medical school, we shouldn't have cartoons in an encyclopedia article on a serious medical topic. There should be a lede photograph as the reader is looking for that. A reader can't relate to a cartoon. It's misleading and unprofessional. SW3 5DL ( talk) 04:28, 22 May 2014 (UTC)
A bit of info on the Gillray image in this article... Was added to the body of the article in Nov 2005 by Pilatus. At some point later the caption is seen fleshed out [ nicely]. In Dec 2009 it was moved to the infobox by Doc James replacing the chemical symbol for Uric acid where it remains (at least for now). I haven't looked to see if this image has been problematic between the time Doc James moved it and now or why the caption was edited down. I would also mention that Doc James is by far the editor with the most edits to this article (441, with the second most active editor coming in at 89) so he has certainly contributed a lot here. – JBarta ( talk) 04:11, 23 May 2014 (UTC)
(Invited by RFC bot) *Mild oppose current image, support photograph assuming the drawing is not a realistic portrayal of the degree of swelling typically associated with gout (although IANADoctor). While readers will understand the demon is artistic license, they may be left with a wrong and unconscious first impression of what the swelling caused by the affliction looks like. That said, I don't know of any Wikipedia policies that mandate that the current image is disallowed, and there appears to be no consensus for change, so the current image will probably remain unless the active page editors change their mind. I acknowledge the current image does have encyclopedic merit, and I'd guess sufferers would be more likely to appreciate the depiction than take offense at it. Rolf H Nelson ( talk) 05:10, 30 May 2014 (UTC)
Comments
Balaenoptera musculus ( talk) 10:00, 23 May 2014 (UTC)
"Intangible concepts can be illustrated; for example, a cat with its claws out portrays aggression."( WP:PERTINENCE)
"For example, a photograph of a trompe-l'œil painting of a cupcake may be an acceptable image for Cupcake"( WP:PERTINENCE)
Comment On the question "Is it encyclopaedic?", it's interesting to note that the Encyclopædia Britannica uses the image "Origin of the Gout" to illustrate it's article on Gout. That's an 1815 print by Henry William Bunbury - same period and same style as the Gilray print. Balaenoptera musculus ( talk) 17:55, 23 May 2014 (UTC)
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 • contribs) 22:01, 28 July 2014 (UTC)
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)
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. [4] [5] 207.118.16.184 ( talk) 02:13, 15 November 2013 (UTC) Michael Hurwicz
References
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Not great, JAMA synopsis doi:10.1001/jama.2015.1881 JFW | T@lk 22:03, 9 June 2015 (UTC)
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)
Doc James ( talk · contribs · email) 21:57, 13 November 2015 (UTC)
Circling back from Wikidata:
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)
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)