Anyone (Other Than Glockman 99) Suffer With The GOUT?!?

Indomethacin works better than Ibuprofen. You can feel the pain easing within an hour.

Take Allopurinol if you are getting gout on a regular basis to prevent it occurring. Don't take it when you are having an attack though.

Drink more water to flush purines out of your system.
 
Indomethacin works better than Ibuprofen. You can feel the pain easing within an hour.

Take Allopurinol if you are getting gout on a regular basis to prevent it occurring. Don't take it when you are having an attack though.

Drink more water to flush purines out of your system.
Thanks, Andrew--I'll ask my doctor about Allopurinol when I see him on Tuesday. I've been drinking as much water as I can, too. Ibuprofen hasn't really been helping so I'll ask about Indomethacin as well. Then again, most pain medication does not work all that great on me. Even the shot they gave me in the ER didn't help much at all.
 
Indomethacin works better than Ibuprofen. You can feel the pain easing within an hour.

Take Allopurinol if you are getting gout on a regular basis to prevent it occurring. Don't take it when you are having an attack though.

Drink more water to flush purines out of your system.

That is absolutely not exactly true! :D

Indomethacin and Ibuprofen (along with a handful of other medications) are all non-streoidal anti-inflammatory pain relievers (NSAIDS). The reason there is a handful of medications that do exactly the same thing is that individuals respond best to different chemicals. Aunt Polly will swear by Ibuprofen, but neighbor Bill will swear up and down the Ibuprofen is worthless and that only Mobic works. Sometimes it takes trial and error, but there is no best NSAID (anti-inflammatory) that works best for all individuals.

Allopurinol is used to prevent gout attacks. But doesn't help clear an "outbreak" very well.

Colchicine is used to treat gout attacks. Great for clearing outbreak but is too nasty (side effects usually diarhhea) for daily preventative use in most folks.

NSAIDS are used to ease the pain and swelling that occur during an attack but won't help treat the cause of the attack.

Like was mentioned in previous posts, a gout attack is caused when certain waste products reach too high a concentration in the blood and begin to crystalize into solids. A variety of factors can compound this but the classic is lower temperature and lack of blood flow which causes a cold toe at night to begin the throbbing as tiny glass-like crystals begin to form in the joint.

If you can control it buy good diet kudos; but if not seek the dr. and get on the preventative allopurinol; and have either a bottle of colchicine on hand for outbreaks or have a script at your local pharmacy on file. A rx is good for a year from the date it was written; and having it on file is very useful if you go to Vegas, eat too much lobster, steak, and beer and need some colchicine. A pharmacy can transfer an rx from anywhere in the country (provided both pharmacies are open and you know your pharmacies phone number).

Then figure out which NSAID works best...hopefully ibuprofen as it is cheap and plentiful and OTC. :)
 
I suffered from gout several times between '99 and '01. It seemed to stop when I was in between careers and had to work a hard physical job in a lumberyard for a few months. The extra physical activity and corresponding weight loss seemed to keep it in check.

I got a couple of mild attacks later when I took a less physically demanding job. Then as I continued descending into middle age, I developed Type II diabetes and got on glucophage medication which seems to have a benefit of preventing gout attacks since I haven't had one since then. There are few things more painful than gout, and I am glad to be rid of it so far. You have my sympathy!
 
I've been taking Allopurinol (100 mgs once a day) for quite awhile now, and I haven't had another Gout attack in 3 or 4 YEARS. Every once in awhile I have a slight ache in the joint of my left big toe, but nothing too serious...No massive burning pain like I used to have. I have even tempted fate a few times by eating crab and shrimp, with no problems. I don't believe that I've kicked Gout's ass, but at-least it's in-check.
 
Gout isn't only caused by diet.
Gout attacks occur when uric acid crystals precipitate in an area (usually an extremity). Some people make too much and some people can't get rid of it. You need to get a full check-up from your primary care doctor if you have not done so lately. The weight issue can cause much more than gout down the road.

Also, it may not be gout. The only way to get a definitive diagnosis is by the doctor aspirating joint fluid from the affected joint and then finding gout crystals in the aspirate.

Joint infections can look like gout, other types of arthritis can look like gout too.

Bottom line is see your doctor.

Good luck!
 
That is absolutely not exactly true! :D

Indomethacin and Ibuprofen (along with a handful of other medications) are all non-streoidal anti-inflammatory pain relievers (NSAIDS). The reason there is a handful of medications that do exactly the same thing is that individuals respond best to different chemicals. Aunt Polly will swear by Ibuprofen, but neighbor Bill will swear up and down the Ibuprofen is worthless and that only Mobic works. Sometimes it takes trial and error, but there is no best NSAID (anti-inflammatory) that works best for all individuals.

Allopurinol is used to prevent gout attacks. But doesn't help clear an "outbreak" very well.

Colchicine is used to treat gout attacks. Great for clearing outbreak but is too nasty (side effects usually diarhhea) for daily preventative use in most folks.

NSAIDS are used to ease the pain and swelling that occur during an attack but won't help treat the cause of the attack.

Like was mentioned in previous posts, a gout attack is caused when certain waste products reach too high a concentration in the blood and begin to crystalize into solids. A variety of factors can compound this but the classic is lower temperature and lack of blood flow which causes a cold toe at night to begin the throbbing as tiny glass-like crystals begin to form in the joint.

If you can control it buy good diet kudos; but if not seek the dr. and get on the preventative allopurinol; and have either a bottle of colchicine on hand for outbreaks or have a script at your local pharmacy on file. A rx is good for a year from the date it was written; and having it on file is very useful if you go to Vegas, eat too much lobster, steak, and beer and need some colchicine. A pharmacy can transfer an rx from anywhere in the country (provided both pharmacies are open and you know your pharmacies phone number).

Then figure out which NSAID works best...hopefully ibuprofen as it is cheap and plentiful and OTC. :)

<sigh>

Indomethacin is prescribed specifically for gout and joint pain. It is more effective than Ibuprofen. Don't we all know it is a Non Steroidal Anti-Inflamatory Drug, (as is Ibuprofen)? I wonder why you can buy Ibuprofen over the counter in a a pharmacy, but you need a prescription for Indomethacin? Perhaps it is more effective, stronger, more specialised?

http://www.medicinenet.com/indomethacin/article.htm

PRESCRIBED FOR: Indomethacin is used for the treatment of inflammation and pain caused by rheumatoid arthritis, ankylosing spondylitis, gouty arthritis, osteoarthritis, and soft tissue injuries such as tendinitis and bursitis.

http://www.gianteagle.com/healthnotes/Drug/Indomethacin.htm

Indomethacin is a member of the non-steroidal anti-inflammatory drug (NSAIDs) family of drugs. NSAIDs reduce inflammation (swelling), pain, and temperature. Indomethacin is used to reduce pain/swelling involved in osteoarthritis, rheumatoid arthritis, bursitis, tendinitis, gout, ankylosing spondylitis, and headaches.

I did point out you shouldn't take Allopurinol during an attack. The reason is you have to get rid of the inflamation first.

Lots of gout information here including the foods that can set off an attack. http://www.niams.nih.gov/hi/topics/gout/gout.htm

The most common treatments for an acute attack of gout are nonsteroidal anti-inflammatory drugs (NSAIDs) taken orally (by mouth), or corticosteroids, which are taken orally or injected into the affected joint. NSAIDs reduce the inflammation caused by deposits of uric acid crystals, but have no effect on the amount of uric acid in the body. The NSAIDs most commonly prescribed for gout are indomethacin (Indocin) and naproxen (Anaprox, Naprosyn), which are taken orally every day. Corticosteroids are strong anti-inflammatory hormones. The most commonly prescribed corticosteroid is prednisone. Patients often begin to improve within a few hours of treatment with a corticosteroid, and the attack usually goes away completely within a week or so.

For some patients, the doctor may prescribe either NSAIDs or oral colchicine in small daily doses to prevent future attacks. The doctor also may consider prescribing medicine such as allopurinol (Zyloprim) or probenecid (Benemid) to treat hyperuricemia and reduce the frequency of sudden attacks and the development of tophi.

I prefer Allopurinol as that is what I was prescribed, it works and doesn't have the side effects of Colchicine.

Doctors have been using a drug called colchicine for centuries to treat gout attacks. Colchicine relieves pain while limiting the inflammation of the joint. Often the drug provides relief quickly but there are some side effects such as nausea, vomiting and abdominal pain.

Good info here http://en.wikipedia.org/wiki/Gout

including...

The mainstay of prevention is the drug allopurinol, a xanthine oxidase inhibitor, which directly reduces the production of uric acid. However, allopurinol treatment should not be initiated during an attack of gout, as it can then worsen the attack. If a patient is on allopurinol during an attack, it should be continued. However, if an attack occurs when the patient isn't on allopurinol yet, he has to wait until the end of the attack to start allopurinol.

The decision to use allopurinol is often a lifelong one. Patients have been known to relapse into acute arthritic gout when they stop taking their allopurinol, as the changing of their serum urate levels alone seems to cause crystal precipitation.

Allopurinol and uricosuric agents are contraindicated in patients with kidney stones and other renal conditions.

I hope the above proves what I said is accurate.
 
Sigh all you want; you are wrong.

Show me some studies that indicate indomethacin is more effective than ibuprofen in treating gout pain and you might have something.

To say that indomethacin is prescribed for gout simply means the drug reps did a good job to saturate the doctor's prescribing psyche for gout treatments..back in the 60's. Indomethacin is a dually poor NSAID. It has a greater risk of gastrointestinal problems and requires multiple daily dosing for effective treatment vs. other medications.

Indomethacin is approved to treat gout (which isn't something your links showed but I'll throw you a bone). So? Two things have to happen to get approval for an indication. 1) the drug has to actually treat the issue 2) the company has to be willing to submit for application for approval to the FDA (this costs millions). The reality is that many drugs are used for many many (gasp) unapproved indications, and they work.

The difference between ibuprofen and indomethacin is that you have a greater chance of stomach upset with indomethacin.

You can't use "which is still a prescription" as and indication of effectiveness. FYI Ibuprofen has prescription strengths as well. Several factors have to come together in order for something to become OTC. The patent has to expire, the drug has to be deemed safe enough to use that the average US citizen can use it without killing themselves (assuming they follow directions), the company has to apply to the FDA for OTC approval (again read big bucks). Thinking ibuprofen is inferior because it is OTC is a fallacy.

You did a fantastic layman's research job for your information. Indomethacin is not superior...what works for the patient is best. Ibuprofen is available over the counter...yet has prescription strengths. One need only increase the dosing of the OTC strength to get RX strength. Yet you can get 1000 tabs of ibuprofen for cheap and you don't need to go to a doctor or pharmacist. Don't forget what I initially said is that any given person responds differently. What works for one person doesn't necessarily work for another with NSAIDS.
 
What works for one person doesn't necessarily work for another with NSAIDS.

OK, fair enough, I'll agree with that.

I have used Indomethacin, which is better than Volsaid, which I have also been prescribed, which is better than 500 gr time release Ibuprofen taken twice daily also on prescription, but for something else.

http://www.humed.com/humc_ency/patient_education/000093_8.htm

Indomethacin (Indocin) is typically the first choice for patients who have no medical conditions that would preclude its use. Usually two to seven days of high-dose indomethacin will be sufficient to treat a gout attack. The first dose of indomethacin usually begins to act against the pain and inflammation within 24 hours and often much sooner.

Ibuprofen, naproxen, sulindac, or others are good alternatives particularly for elderly patients who might experience confusion or bizarre sensations with indomethacin. (Aspirin is an NSAID, but is associated with a higher risk for gout and should be avoided.)

and http://www.lycos.com/info/indomethacin--effects.html

Indomethacin is the strongest of the available traditional NSAIDs, although it has significant adverse GI and CNS effects and a potential to increase blood pressure. It is best used for short-term (eg, acute) flares.
 
Man, you don't know what a gout attack is until you have one! I had one about 6 years ago and will never forget it.

Mine started with just a simple sore, right big toe when I woke up one morning and by the next day, I couldn't walk! After about 2 days, my whole foot and calf were terribly swollen. It lasted for about 2 weeks and if anyone even came near me, I screamed at them to stay away!

I didn't go to the doctor, (I NEVER do for ANYTHING), and treated it with Ibuprofen that a forum member on CPF recommended to me and just "crutched" it around everywhere.

Thank God I haven't had another attack since. Just thinking about it all these years later still takes my breath away! :eek:
 
Man, you don't know what a gout attack is until you have one! I had one about 6 years ago and will never forget it.
Yup, I think that the burning pain of a full-blown gout attack is worse than having a rabid weasel eat your eyeballs out of your head while your legs are being chewed-off by a pack of wolves.:eek:.
 
I used to get it to the point I couldn't stand to have even a sheet on my feet at night. Trying to lose weight and control my type 2 diabetes I cut way back on anything with flour, refined sugar, and other carbs and I haven't had any problem since. I also had a lot of pain in my lower legs. That is gone also.
 
I was just watching something about the Spanish-American War on the history channel. Apparently while the Buffalo Soldiers, Teddy Roosevelt, and the rest of the army was taking San Juan hill, the US general (a tubby 300 pounder), was way behind friendly lines held up with a massive gout attack.

Thank your stars, we have what we do for gout these days...I think the tubby general had to tough it out in bed.
 
For years they have been recommending to avoid coffee if you have gout. Now there's a study that shows that coffee can help to fend off gout:

Increased Coffee Consumption May Reduce Risk for Gout in Men CME/CE

News Author: Laurie Barclay, MD
CME Author: Laurie Barclay, MD
Disclosures
Release Date: May 25, 2007; Valid for credit through May 25, 2008
Credits Available

Physicians - maximum of 0.25 AMA PRA Category 1 Credit(s)&#8482; for physicians;
Family Physicians - up to 0.25 AAFP Prescribed credit(s) for physicians;
Nurses - 0.25 nursing contact hours (None of these credits is in the area of pharmacology)

May 25, 2007 &#8212; Long-term consumption of coffee is associated with reduced risk for gout in men older than 40 years, according to the results of a prospective study reported in the June issue of Arthritis & Rheumatism.

"Coffee is one of the most widely consumed beverages in the world and may affect the risk of gout via various mechanisms," write Hyon K. Choi, MD, DrPH, from the University of British Columbia in Vancouver, Canada, and colleagues. "A study of a nationally representative sample of US adults showed that coffee consumption was associated with a lower serum level of uric acid and a lower frequency of hyperuricemia."

The study cohort from the Health Professionals Follow-Up Study consisted of 45,869 men with no history of gout at baseline. Validated questionnaires were used to measure intake of coffee, decaffeinated coffee, tea, and total caffeine every 4 years for 12 years, and a supplementary questionnaire was used to determine whether participants met the American College of Rheumatology survey criteria for gout.

During the 12-year study, there were 757 confirmed incident cases of gout. Increasing coffee intake was inversely associated with the risk for gout, with multivariate relative risks (RRs) for incident gout of 1.00, 0.97, 0.92, 0.60 (95% confidence interval [CI], 0.41 - 0.87), and 0.41 (95% CI, 0.19 - 0.88) for coffee consumption categories of 0, less than 1, 1 to 3, 4 to 5, and 6 or more cups per day, respectively (P for trend = .009).

For decaffeinated coffee, the multivariate RRs for 0, less than 1, 1 to 3, and 4 or more cups per day were 1.00, 0.83, 0.67 (95% CI, 0.54 - 0.82), and 0.73 (95% CI, 0.46 - 1.17), respectively (P for trend = .002).

These associations were independent of dietary and other risk factors for gout such as body mass index, age, hypertension, diuretic use, alcohol consumption, and chronic renal failure. Total caffeine from all sources and tea intake were not associated with the risk for gout.

"These prospective data suggest that long-term coffee consumption is associated with a lower risk of incident gout," the authors write.

Study limitations include self-report of coffee consumption, restriction to male healthcare professionals in the cohort, observational design, and inability to rule out the possibility that unmeasured factors might contribute to the observed associations.

The National Institutes of Health and TAP Pharmaceuticals supported this study. Some of the authors have disclosed various financial relationships with TAP and/or Savient Pharmaceuticals.

Arthritis Rheum. 2007;56:2048-2054.
Clinical Context

Gout is the most common inflammatory arthritis in adult men, and its incidence may be increasing. Therefore, identifying modifiable risk factors for gout is an important first step in preventing and managing this condition. Coffee consumption may affect the risk for gout by reducing serum uric acid levels and affecting insulin resistance, as well as by other mechanisms.

Because coffee is one of the most widely consumed beverages in the United States and worldwide, information about the health effects of coffee are important for public health, as well as to allow informed decisions regarding coffee consumption. The present prospective study evaluated the relationship between intake of coffee, decaffeinated coffee, tea, and total caffeine and the incidence of gout in a cohort of 45,869 men with no history of gout.
Study Highlights

* The Health Professionals Follow-Up Study is an ongoing longitudinal study of 51,529 male dentists, optometrists, osteopaths, pharmacists, podiatrists, and veterinarians who were predominantly white (91%) and aged 40 to 75 years in 1986.
* Of the 48,642 men who provided complete information on coffee, 2773 (5.7%) reported a history of gout on the baseline questionnaire and were excluded from this analysis.
* The cohort for this study consisted of 45,869 men with no history of gout at baseline. Validated questionnaires were used to measure intake of coffee, decaffeinated coffee, tea, and total caffeine every 4 years for 12 years, and a supplementary questionnaire was used to determine whether participants met the American College of Rheumatology survey criteria for gout.
* At baseline and every 2 years thereafter, participants provided information on weight, regular use of medications (including diuretics), and medical conditions (including self-reported clinician-diagnosed chronic renal failure and hypertension).
* During the 12-year study, there were 757 confirmed incident cases of gout.
* With increasing coffee intake, frequency of history of hypertension and diuretic use tended to decrease, but intakes of alcohol, meat, and high-fat dairy foods tended to increase.
* Increasing coffee intake was inversely associated with the risk for gout. Multivariate RRs for incident gout were 1.00, 0.97, 0.92, 0.60 (95% CI, 0.41 - 0.87), and 0.41 (95% CI, 0.19 - 0.88) for coffee consumption categories of 0, less than 1, 1 to 3, 4 to 5, and 6 or more cups per day, respectively (P for trend = .009).
* There was a modest inverse association between decaffeinated coffee consumption and incidence of gout. For decaffeinated coffee, the multivariate RRs for 0, less than 1, 1 to 3, and 4 or more cups per day were 1.00, 0.83, 0.67 (95% CI, 0.54 - 0.82), and 0.73 (95% CI, 0.46 - 1.17), respectively (P for trend = .002).
* These RRs for caffeinated and decaffeinated coffee did not change materially after additional adjustment for smoking. These associations were independent of dietary and other risk factors for gout such as body mass index, age, hypertension, diuretic use, alcohol consumption, total meat intake, and chronic renal failure.
* Total caffeine from all sources and tea intake were not associated with the risk for gout.
* Study limitations include self-report of coffee consumption, restriction to male healthcare professionals in the cohort, observational design, and inability to rule out the possibility that unmeasured factors might contribute to the observed associations.

Pearls for Practice

* In a large, long-term prospective study of male healthcare professionals aged 40 years and older, long-term caffeinated coffee consumption was associated with a lower risk for incident gout.
* In this study population, long-term consumption of decaffeinated coffee was associated with a modest reduction in risk for incident gout. Tea intake and caffeine intake from all sources were not associated with risk for gout.



Medscape Medical News 2007. ©2007 Medscape
 
Interesting stuff Jeff. Maybe that's why I haven't had a another attack because I've UPPED my coffee cosumption since the attack 6 years ago.
 
That's an interesting article. My research skills aren't too high these days but I went through it a couple of times and I think there's way too many holes in the research to put too much stock into the results. The fact that it (admittedly) doesn't account for any of the other factors really doesn't give it too much credit (e.g. alcohol consumptuion, diet, family gout history, etc.). That combined with self reporting also makes it less credible and there's nothing about what kind of coffee (and also what they put in their coffee--cream, sugar, etc.). There's also no mention of how many people dropped out of the study during the 12 years (there had to be at least some dropouts out of 50,000 participants over 12 years). The first study also doesn't mention anything about ethnicity (although I don't think there's any evidence to support a relationship between race and gout) and I think a baseline uric acid level prior to the study would've been good too (some people naturally have higher levels of uric acid). It was an interesting read, though, and I admit that the numbers look like a bunch of gibberish since I never really was good at reading stats.

Well, I am finally walking without a limp after 2+ weeks though there are still some slight issues with the ankle. It's pretty weak so if I walk across uneven ground I have a tendency to twist it, and there's still a little bit of swelling although it fits in my shoe a lot easier now. My doctor didn't have much to say (didn't even look at my ankle) so that didn't help too much. I've been trying to drink as much water as I can and I cut out a lot of foods the past couple of weeks. It really started to get better this weekend when I went all vegetarian--had a lot of Subway veggie sandwiches and boca burgers and things like that. I don't intend to become a pure vegetarian, but to just get it out of my system for now is worth it. I hope I never have to feel this again. My biggest problem is I don't know what caused it this time so I don't know what to avoid. I also need to cut down on my weight (I did manage to lose 5 pounds last week). I'm also getting real irritated with my research since I can find things that say to eat things like white rice and white breads and then I'll find somewhere else that says to eat brown rice and brown bread. I've also seen somewhere that salmon can be beneficial to gout when another site said that it was bad for it--real annoying. I guess it's just going to be a matter of moderation in all things and hope it never matters to me again.
 
One of my best friends has been on the Adkins diet, fervently, for several years. He does keep his weight down with the lack of carbs. But he has had a couple of "Gout Attacks".
My Better Half had a round of gout after splurging on shellfish and Chardonnay , and much more rich breakfasts and lunches than normal on a business trip a couple of years ago. Alot of less rich food and beverage backed her off the gout....lots more vegetables, and God Forbid, less wine and less higher sugar/higher fat food....
They used to call gout an illness of the "very well to do"...like royalty because they could afford and get rich food and drink.....
Get well"er".
 
I think that the coffee study included mostly people of European extraction. It is just a prospective study, but it is a rather large one. It at least calls into question the practice of discouraging coffee consumption.

As I read the summary: "These associations were independent of dietary and other risk factors for gout such as body mass index, age, hypertension, diuretic use, alcohol consumption, and chronic renal failure." It indicates that these factors were evaluated statistically for their normal population distributions and the test results did not come from a skewed collection of subjects (not skinny people who didn't drink for example). The study looks promising.
 
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