Forum Replies Created
-
Posts
-
Hi guys?
Moved to Manhattan and was without phone or internet for 19 days?how does one live like that? Anyhoo, I am back with a?blazing new 15.5 Mbps fiberoptic communications system?connection. YAAAY!
?
Here's my take on ice: good and bad. It is good in that it reduces swelling temporarily; it is bad in that it?causes more precipitation of urate (urate solubility is extremely dependant on temperature…that's why we get it in our feet and hands.)
I think the bad outweighs the good.
Anyone who merely treats gout pain and ignores urate will soon find that he has made a bad mistake, because once tophi form and joint degradation occurs?there?is precious little that can be done to reverse the situation.? My God, how much trouble is it to take a 300 mg. allopurinol on a daily basis. It sure beats a?semi-annual or quarterly ?dose of prednisone for safety.
James,
?
Give it a month before making a judgement. Allopurinol is quickly broken down by xanthine oxidase (making XA unavailable for making uric acid,) The allopurinol is converted to OXYPURINOL which has a long half like and also blocks XA and is probably the chemixal which exhibits the most anti-urate properties.
It takes a week or so to get up to steady state oxypurinol levels (adding more and more each day.)
?
So after 2 weeks you should be getting readings that are better. But if you are still over 6.0 you will then probably need to up the ante to 400 mg. allopurinol after about a month. Before you do though, get a proper lab test.
?
Who knows though, maybe initial dosing frees up enough friable (loose)?deposits and sends them on their way, thereby keeping serum urate temporaily high.
?
I am going to disagree with Keith on the issue of allopurinol and body size. It seems logical to me that dosing?should depend on body mass, at least LEAN body mass.?
Allopurinol works on xanthines and nucleic acids?on a proportional level (One molecule allo attaches to one molecule XA nad saves one molexule xanthine from being converted to uric acid.)?
Thus the bigger man>> the?more food?he eats>> the more purines?he eats>> the more nucleic acids he breaks down>> the greater the need for allopurinol to control to safe levels.
Constipation isn't an expected? side-effect of allopurinol. Nobody here has reported it.
?
Maybe diet change between Egypt and home were a shock to the system.
?
But if you are going 4 times a day, it doesn't sound like constipation. Try to up your soluble fiber intake…maybe something like daily psyllium (Metamucil and cheaper store brands.)
Nothing to report,
?
My last use of marijuana FAR precedes my getting gout, and I have had gout almost 2 decades.
?
I would imagine each state where MMJ is legal would have it's own guidlines on qualifications for pain relief, but from your personal experience it doesn't seem particularly helpful.
?
Maybe others here have more experience.
hans,
?
I wish I could shed some light on the subject but my limited research has shown there are so many different ways to test for uric acid/urate that it is dizzy-making. I know it must be frustating to consistently get a point lower with your tester than at the lab. That's a reason why I never bought a tester…simple is not always best and it would bedevil me to have two different readings on which to base my decision making.
?
There are so many variables but I think I can reasonably be sure that one that the labs have considered is the effect of temperature. It should not matter whether urate has precipitated or not, it is probably all dissolved in some reagent before the actual test.
?
One thing I DID stumble upon, it seems that Vitamin C intake may interefere with the accuracy of some COLORIMETRIC methodology, and I am assuming that most home kits are reading color change of a reagent?that's the way they usually work.
?
I think the upping to 80 mg. Uloric is a terrific idea to get both tests always below 5.0.
?
How are the foot and the finger doing?
Yes, James,
?
To stop an attack in a day with a small amount of colchicine requires IMMEDIATE action. Once the pain has gone on for a day or more, a great deal more is required. I agree that most meds should be prescribed on the basis of body weight but it seems that calculation is only used for pediattric doses.
?
Your uric acid is not extreme and you MIGHT get away with 200 mg. allopurinol, but if I were you, I would start off with a standard 300 mg. dose. If I got spectacular results, like numbers in the 4's after 6 months, THEN I would consider dropping down to a 200 mg. dose. Why risk even ONE unnecessary?debilitating attack?
?
(I? went down to 200 mg for almost a year but got a lab reading of 6.7 and a couple suspicious foot twinges over the time, a couple stopped with low dose colchicine,?and returned to 300 mg. In the U.S. it is actually HALF the price to take 300 mg./day then to take 200.)
?
I weigh about 210# at 6'2″.
It's our Southern States' CREPE MYRTLE:
?
- Although native only to India, the Philippines, Australia and East Asia, the Banaba bush has been introduced and subsequently become well established in warm climates worldwide. Common in Italy, southern France and the Iberian peninsula, the plant is also prevalent anywhere south of Zone 6 in the United States. Banaba thrives particularly well in milder climates that are not high in humidity, such as in Texas and southeastern California. In the United States, the Banaba bush is also known as the Giant Crape Myrtle, Cuddle Tree and Queen Crape Myrtle.
It's major claim to fame seems to be its hypoglycemic effect (mimicking insulin.) Of coures, IF this is true, then it is good or bad depending on your blood sugar. Obviously diabetics would need to take this stuff very carefully. Likewise? people who suffer bouts of hypogylcemia would want to avoid it.
?
Is there ANY plant on Earth for which someone hasn't made a medical claim?
Have him use an over the counter triple antibiotic (usually bacitracin, neomycin, and another) and apply it daily as long as the wound is open. Then dress it with sterile gauze. But don’t worry about the oozing. As long as there is white material coming out, the tophus is discarding urate.
I am not sure of the recommended medical treatment, but what I would do is hot water soaks (of course not scalding) with some basic material added, like several Tbsp baking soda. Maybe there is some question about whether your husband should have pierced the tophus, but now that it is a done deal, might as well make the best of it.
There SHOULDN’T be too much blood, I hope. If the exudate is almost all white, I would encourage drainage with some gentle massage while the foot is nice and warm. When he’s gotten out all that’s coming, use a little antibiotic and gauze it.
Repeat the next day.
With urate, my mottos is “better out than in.” Remember, once it heals over the urate purge ends.
(I punctured one on my thumb and squished and squeezed for a week, but I’m rid of that tophus.)
Have you moved yet? I'm in hell right now, but it won't last much longer. Just DO IT. Lynda
No, I'm in the middlse of that particular Hell too.
I have been on Probenicid with no luck and for the last year or so I have been taking Allopurinol and Cholchicine daily
Mike,
So then during your treatment with allopurinol, you were running uric acid levels of 9.0??? Did your doctor tell you that was absolutely NOT proper gout treatment? What amounts of allopurinol were you taking every day?
Are you taking 40 or 80 mg. Uloric?
Mike,
I am so sorry it came to amputation…which toe?
What kind of uric acidd numbers where you getting with allopurinol and probenecid? Wht are you getting now?
Yes, in the United Ststes colchicine is pretty much gone since the FDA gave exclusive patent rights to the 2,000 year old drug to AR Holding Company which appparently owns URL Pharma. The drug is now called COLCRYS and costs a fortune.
Thanks odo,
I'll add that to my gout lexicon.
A natural follow-up thought/question/musing. If alcohol “inhibits the conversion of allopurinol to oxypurinol” can we assume it interferes with the action of xanthine oxidase? That would seem logical. Interfering with the action of the enzyme might also decrease the more ”normal ” action of XA, the conversion xanthine and guanine to uric acid. If so the net result of alcohol might be positive or negative.
I have a vaguely similar situation with losartan…the drug eliminates uric acid and all it's homologues, thus it dumps uric acid, allopurinol, zanthine, oxypurinol. But the net effect is a slight lowering of SUA. so it is considered uricosuric.
I guess the question would be answered with a good study of gouties on 300 mg. allopurinol. Measure SUA before the study and have half the group party hearty with copious cocktails for a month…and the other have teetoal while they watch TV.
After 30 days measure everyone's SUA again. With a big enough group you could have 1/3 of the drinkers on wine, 1/3 on beer, and 1/3 on hard stuff.(If the booze is good I would be HAPPY to volunteer, unless they put me in the control group…that would cost them money.)
An interesting thought: both alcohol and allpurinol are found to benefit patients in long term heart failure. A reasonable premise is that perhaps each of these agents interferes with xanthine oxidase, thus sparing blood vessels from damage…both agents may this be protective fpor the same reason.
A good study:
Effects of Xanthine Oxidase Inhibition With Allopurinol on Endothelial Function and Peripheral Blood Flow in Hyperuricemic Patients With Chronic Heart Failure Results From 2 Placebo-Controlled Studies
Wolfram Doehner, MD*; Nina Schoene, MD*; Mathias Rauchhaus, MD; Francisco Leyva-Leon, MD; Darrell V. Pavitt, MSc; David A. Reaveley, PhD; Gerhard Schuler, MD; Andrew J.S. Coats, DM; Stefan D. Anker, MD, PhD; Rainer Hambrecht, MD
From Clinical Cardiology, National Heart and Lung Institute, Imperial College School of Medicine (W.D., M.R., F.L.-L., A.J.S.C., S.D.A.), and the Department of Clinical Chemistry, Charing Cross Campus, Imperial College School of Medicine (D.V.P., D.A.R.), London, UK; and the Franz-Volhard-Klinik (Charité, Campus Berlin Buch) at Max Delbrück Centrum for Molecular Medicine, Berlin (W.D., S.D.A.), and the University of Leipzig, Division of Cardiology, Heart Center, Leipzig (N.S., G.S., R.H.), Germany.
Correspondence to Stefan D. Anker, MD, PhD, Clinical Cardiology, NHLI London, Dovehouse Street, London, SW3 6LY, UK. E-mail [email protected]
Background— In patients with chronic heart failure (CHF), hyperuricemia is a common finding and is associated with reduced vasodilator capacity and impaired peripheral blood flow. It has been suggested that the causal link of this association is increased xanthine oxidase (XO)–derived oxygen free radical production and endothelial dysfunction. We therefore studied the effects of XO inhibition with allopurinol on endothelial function and peripheral blood flow in CHF patients after intra-arterial infusion and after oral administration in 2 independent placebo-controlled studies.
Methods and Results— In 10 CHF patients with normal serum uric acid (UA) levels (315±42 µmol/L) and 9 patients with elevated UA (535±54 µmol/L), endothelium-dependent (acetylcholine infusion) and endothelium-independent (nitroglycerin infusion) vasodilation of the radial artery was determined. Coinfusion of allopurinol (600 µg/min) improved endothelium-dependent but not endothelium-independent vasodilation in hyperuricemic patients (P<0.05). In a double-blind, crossover design, hyperuricemic CHF patients were randomly allocated to allopurinol 300 mg/d or placebo for 1 week. In 14 patients (UA 558±21 µmol/L, range 455 to 743 µmol/L), treatment reduced UA by >120 µmol/L in all patients (mean reduction 217±15 µmol/L, P<0.0001). Compared with placebo, allopurinol improved peak blood flow (venous occlusion plethysmography) in arms (+24%, P=0.027) and legs (+23%, P=0.029). Flow-dependent flow improved by 58% in arms (P=0.011). Allantoin, a marker of oxygen free radical generation, decreased by 20% after allopurinol treatment (P<0.001). There was a direct relation between change of UA and improvement of flow-dependent flow after allopurinol treatment (r=0.63, P<0.05).
Conclusions— In hyperuricemic CHF patients, XO inhibition with allopurinol improves peripheral vasodilator capacity and blood flow both locally and systemically.
If XO inhibition occurs with alcohol, then the same concusion is likely. It may very well be the route of cardiac protection seen for drinkers.
Odo,
Do you have a source for that alcohol – allopurinol excretion increase connection?
Allopurinol is usually eliminated by rapidly being oxidized to oxypurinol by xanthine oxidase, and permanently tying up the enzyme. rather than by urinary excretion…although it DOES occur.
Then the oxypurinol is slowly excreted by the kidneys.
You just ask for a “Liver Panel.”
It's done with a small blood draw and usually includes around 5 items, always including ALT, AST, and bilirubin.
If you want to familiarize yourself with some of the specifics, here's a good overview:
http://www.labtestsonline.org/understanding/analytes/liver_panel/test.html
Interesting study report from the Journall of Nephrology, June. 2010:
ALLOPURINOL FOR CHRONIC KIDNEY DISEASE
Allopurinol is a drug used primarily to treat individuals with excess uric acid in their blood (hyperuricemia) – the agent inhibits an enzyme involved in the production of uric acid. Hyperuricemia can lead to gout and, in extreme cases, kidney failure. Elevated uric acid levels in the blood may also increase one’s risk of developing hypertension and heart disease. Patients with chronic kidney disease – who most often die from heart disease – often experience hyperuricemia because of decreased uric acid excretion in the urine; however, studies have not looked at the benefits of allopurinol in these individuals.
To investigate, Marian Goicoechea, PhD, Jose Luño, MD (Hospital General Universitario Gregorio Marañón, in Madrid, Spain) and their colleagues conducted a prospective, randomized trial of 113 CKD patients who received either allopurinol (100 mg/day) or who continued taking their usual therapy. The researchers assessed kidney disease progression, cardiovascular events (such as heart attacks), and hospitalizations among patients in the study over two years.
The blood levels of uric acid and C-reactive protein (a marker of inflammation) significantly decreased in patients treated with allopurinol. In the control group, kidney function declined after two years, but in the allopurinol-treated group, kidney function improved. Allopurinol treatment slowed down kidney disease progression regardless of patients’ age, gender, and diabetes status; their blood levels of uric acid and C-reactive protein; the amount of protein patients lost in the urine; and the other types of medications patients used. In addition, compared with usual therapy, allopurinol treatment reduced the risk of cardiovascular events by 71 percent and the risk of hospitalizations by 62 percent.
While allopurinol has significant potential benefits for CKD patients, “these results have to be confirmed in larger prospective trials and are the basis for a hypothesis that still needs to be tested,” the authors wrote.
(and remember NOBODY makes money off allopurinol so when reports are positive, they are likely unbiased.)
Linda, Can you get less knee pain with a pillow under your knee when in bed? I would normall suspect a torn cartigege but that would hurt as much standing up…but then so would gout pain???
Mysterious.
Go to 300 mg. allopurinol and see what a year on it does. Don't hope for a lot. If you DO have success it will be slow.
Often surgery is the only way to get rid of a big old tophus.
brendan,
Your liver functions are only slightly elevated, of no immediate concern unless they go up a lot more..
If I had to make guesses, in order of preference for cause:
1. Heavy beer drinking…who do you think you are, ME?
2. Too long on colchicine. Colchicine is a strange animal: it readily raises liver enzymes and yet it is often used to TREAT liver ailments, it seems to slow the progression of sclerosis, seemingly by its anti-inflammatory properties.
What I would ABSOLUTELY NOT do is quit the allopurinol. Is is probably having little to do with your liver enzymes but a LOT to do with controlling your gout. You will regret stopping it for a couple months and restarting. That is a GUARANTEED way to provoke a serious gout attack.
So see if you can cut the beer drinking to 3 bottles, 3 nights a week (I know, not easy) for a month and retest, you might get an answer. Better yet, no alcohol for a month and retest. If still high, then go back on the sauce (maybe a little less) and stop the colchicine for a month and retest. You will have your answer.
If enzymes are still high only then CONSIDER a trial without allopurinol.
anirud,
Burroughs-Wellcome lost the patent for ZYLOPRIM (in USA,) ZYLORIC etc. around 1982. SInce then it is sold as the cheap generic drug, allopurinol.
It works very well…homeopathic medicines do not.
Some people can run a 9 uric acid without pain, but once you start getting attacks of FRANK gout (the FRANK meaning unmistakeable and extremely painful) in your big toe, intep or ankles, you'll know its time for the drug.
There are several drugs to choose from but allopurinol is the cheapest, with fewest side effects. Probably tens of millions of people pop their 300mg. pill every day.
If you need immediate relief from the attack, the best drug is colchine, probably very cheap in India, wheere most of it is made. *For ayurvedics, it's made from the Autumn Crocus.)
No, No….
Allopurinol is OXIDIZED to oxypurinol, thus allopurinol is a REDUCING agent and thus it is an “anti-oxidant.” Oxypurinol is FURTHER oxidized and thus also an “antioxidant.”
THe quotes are to illusrtate my feeling that antioxidant is merely a fashionable silly buzz word. ALL FOODS are anti-oxidants, reducing agents, that use up oxidizers for their metabolism and create energy.
So for your next ultra high dose of antioxidants have an 18 inch pizza.
“Free radical” is the buzzword for oxidants doiing their work…nascent oxygen oxidizing food and making the energy of LIFE. ALL bodily chemical reaction occur using temporary “free radicals.” To go further, O2 is inert…only when it breaks into individuall [O] can it oxidize…and release energy. ANd [O] is the ultimate and consummate free radical, called nascent oxygen…the only way it can do its work.
Let me go simple (but not disparaging.) Wood, coal and petroleum are the ultimate antioxidants…they all use up oxidizers, primarily oxygen to burn them.
Can you see how in a universe of REDOX reactions (that's what they're called) there is nothing unuoque about antioxidants except for people PEDDLING the concept. They are in reality anything that can be burned.
I'm not being glib…just real.
dp,
You're doing well and I'm happy you are getting good results with the 40 mg. dosage. Is your insurance covering your costs pretty well?
Eight episodes in 3 years is nothing to sneeze at…that's a lot of pain. It's probably even more attacks than I had before I started treatment. (Since it's been 15 years acute attack free I wonder if I can throw away the crutches. But we all know Murphy's law.)
Here's allopurinol:
and here's the xanthine (the major dietary purine) that it mimics:
See how devilishly clever the drug is? Notice only that single misplaced nitrogen. You can ignore the attached hydrogens and that double bonded oxygen…it readily picks up an H to form an OH. So along comes a xanthine oxidase enzyme and it gets confused and thus ignores a lot of the xanthine…whiich you pee out.
Ouch,
A 5 hour drive each way is a killer.
But yes, in past times before MRI's and doctors who study NOTHING about gout anymore, colchine response was considered diagnostic for gout. But that was when colchicine was used in 12-16 pill regimens for a day's treatment.
If pain is not resolved with 16 colchicine it is not likely to be gout.
But doctors think they are smarter now and have dismissed 2,000 years of gout history. Now they have the big Monte Python “machine that goes BEEP” that costs a fortune but nobody is sure what it does…except go beep. And the U.S. has an FDA that gives away patents on 3,000 year old drugs to drug companies that are generous with campaign contributions.
Make sure your dad starts on 300 mg. allopurinol if he hasn't already. THis dosage is important.
I haven't ever taken ketoprofen and my stomach will not tolerate ibuprofen so I doubt I ever will.
But I can attest to the fact that I have often taken 300 mg. allopurinol along with a half pound of cherries in one sitting followed by the other half pound the next day. I am crazy for cherries when they do their two week cheapie period in May or June ($.99 per pound when lucky.) There have probably been weeks where I have downed 3 pounds of cherries.
I can guarantee no interaction…maybe a little loose bowels the next day from so much fruit but that would be with or without the allopurinol.
I've done a couple periods of an ounce of cider vinegar per day (I love the taste) when someone or other talks it up as a great tonic. I haven't found that it does anything, good or bad. Certainly no reaction with allopurinol.
In truth though, I think any connections between gout and cherries or ACV is strictly a gimmick to sell cherries and apples. Just old wives tales.
And a lowered salt intake might help.
(Forget that I mentioned thiazide…never a good idea with gouties.)
I will say NO for myself….althougn I do tend to retain a LOT of fluid with high salt intake,
Is it possible your gout and your knee problem are unrelated?
Have you ever tried a diruretic like thiazide or fiirosemide (Lasix?) Unless you have low blood pressure why not give a try for a week and see if it helps with knee swelling? Anyone you know with hypertension can probably give you a handdful.
Are you taking any calcium channel blocker…they are notorious for causing edema.
I find grated allopurinol makes a nice condiment to top off a curry. And toss in some Autumn crocuses.
Yummy.
My curries must taste like fire and cause the back of my head to drip sweat, otherwise I consider them failures.
When I ask for a Vindaloo extra spicy, the chef usually comes out and try to dissuade me, since he clearly sees I'm a Caucasian.
Only one meal had me screaming for help but that was a Korean Beef dish floating in a carmine red chili oil. Even Satan has to say no to that one. It should have been called Beef Auto De Fe. I think actually that's how they killed Joan of Arc, or Joan of Seoul.
Thank you hans.
I stole this and pasted it on my senior board.
Cialis will outsell the Viagra drink becasue one glass lasts 3 days and it will be called “MOUNT & DO & DO & DO & DO.” Gotta be careful turning around in crowds so that you don't put somebody's eye out.
Baz,
Second if I missed just one tablet I would suffer a severe attack. Now I've only ever had mild attacks and they are bad enough, I dread to think how agonising a severe attack must be.
Allopurinol disappears quickly but oxidozes to an effective metabolite, oxypurinol. every bit as effective and oxypurinol has a very long half life. You can skip alopurinol for several days and still be pretty well protected.
And as odo said, get RIGHT onto 300 mg. THEN test in 3 months and see i it can be lowered. Taking 100 mg for a couple months is just bad medicine prescribed by someone who should NOT be treating gout. If you are allergic to allopurinol you will find out fast enough with either dosage.
Warning HAVE to cover all contingencies. Most often side effects are broken down by those with higher incidence and those apt to occur in less than 1% of patients. Liver damage seems in this less than 1% for both of these drugs. I would choose either indomethacin OR colchicine but not both. THe more drugs, the more likely the untoward side effects.
Neither is, or should be, intended for long term use.
Long term controol of gout involves xanthine oxidase inhibitors (allopurinol) or uricosurics. Pain killers are for short term use during acute flares…for this colchicine is the most effective.
Just a couple peripherals:
We HEAR anecdotal stories about “an SUA of 10″ without gout. It may be just that, anecdotal. I'll stick my neck out and say, show me a person who tests a 10 SUA and I'll show you a man who will be writhing in pain within a year.
You said “Don't bore me/us with pH's, temperatures, MSU's crystals, tophi, and whatever else is floating around the globe.” but it very well might just be the concurrence of unfortunates that at one tiime and place for one individual in ONE joint that these come together and crystals form. Once crystals form there is a locus of precipitation and the body can no longer keep a supersaturated serum/synovial fluid. More crystals grow atop the other crystals. Once a goutie, always a goutie.
The only difficulty is the WHY of the original precipitated crystals.
To that why is the compounded why of the immune system attack. It is the same question asked by a person who gets bitten by a yellowjacket and says DAMN! and another person drops dead from anphylactic shock. Some immune systems obviously ignore a uric acid crystal whiile others are driven WILD by it. Some people were immune to plague in the 13th century and an aside that is fascinating: descendents of these people have a highly disproportunate immunity to AIDS.
If we were all the same, the human race would have been wiped out by the 1918 influenza. Diversity is our friend but the price of diversityy is that some of us have gout, polio, tuberculosis, cancer, psoriasis, lupus, and warts.
As for the writing in pain with an SUA of 5.0 mg/dL, remember the concentration next to a pure urate tophus is 100% or with an assumed densityy of 1.87 that's an SUA of 187 grams/dL (or 100 grams of water) or 187,000mg./dL and that's a HELL of a lot of urate….twenty eight THOUSAND times the soluble limit. So to have it disperse around the edges and immediately reconstiitute itself would be the rule rather than the exception. That's why dissolving big tophi is so challenging. It's like trying to dissolve Mount Rushmore with a water pistol.
That's also why it is so important to lower uric acid before the first perceptible tophus forms. In an ideal world, brilliant doctors would be able to diagnose gout at the first sign of the first attack and begin treatment to guarantee a second attack never occurred.
There is an evolutionary benefit to uric acid, of that I am certain and I very much doubt it has ANYTHING to do with it being reducing agent (aka antioxidant, like wood) becasue there are thousands of reducing agents…like ALL FOOD. That benefit is, to date, alas, unknown. It may never be known. I am also convinced that it has something to do with man's overeating of meat and protein (hence, the rich man's disease and now Everyman's disease) and I also suspect it plays a role in man's intelligence…there have just been too many geniuses with gout.
It's probably hormonal: prepubescent boys don't have it, premenopausal women rarely get it. It is a man's disease. If good records were kept it would be curious to see if castrati ever got gout. It would be informative to compare testosterone levels with gout…Alzheimer's development with gout. But in the modern world if there's no money to be made, there's no funded research. PURE science is a thing of the past. If you can make billions or blow up a city then there's money.
All in all though, it is an IMMENSELY complicated and interesting disease.
I've thought long and hard about those pre-amps and if I keep the records, I will pick one up, I;ll have no choice if I want to upgrade my receiver. I am always fearful about putting any extra equipment in line for fear of sound degradation. But after all, what is a a phono inpur on a receiver except a built in preamp.
At least the one MYFOOTHURTS (thank you) recommended looks more professional than some of the preamps I've seen.
