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A question that affects me in deciding to start this drug is:
Why ,once started, can't it be stopped?
If reactions occur to the drug it's recommended to stop it- so why can't it be used for a few months and then the patient SUA checked to see if lifestyle changes can hold the position steady?
Alternatively, if long term side effects are not wanted- a break taken to assess how the body restabilises around any worrying trend.
Oops!- this should have been in a 'Cure' thread
trev,
No not in the “cure” thread because gout in incurable!
Why for life? It is ideallly taken by people whose gout is caused by making too much uric acid. Much, if not MOST, of this uric acid is from normal (or abnormal) breakdown of lean tissue. The other more limited source is dietary intake and we all know how well we make healthy dietary changes for life.
Now let me add a third that is my own theory not likely to get published in JAMA: the body has feedback mechanisms and many of them work in a similar fashion. For us BP sufferers, block renin and the body makes more renin, block angiotensin attachement and the body makes more or increases the production of other chemicals that are equally agonistic, inhibit ACE and the body makes Ang-2 from CHYMASE instead, . Block ATTACHMENT of any of these chemicals and the body makes more attaching sites AND more chemicals.
I think it is likely that with allopurinol's blockage of of xanthine oxidase (which converts purines like xanthine and guanine to uric acid) causes the body to make MORE xanthine oxidase. IF that's true you can see the likely effect of cessation of allopurinol and a weeks drawdown of oxypurinol…it's long lasting and very helpful first breakdown product.) Thus I think a week OFF allopurinol for a regular user is more likely to cause an attack then all the beer in Munich!
I wince when I read a post that says, I took it for a month then stopped for a month and then took it again.
I'm tempted myself because I'd like to assess the efficacy of the losartan-furosemide dosing. I have long suspected that it was HCTZ alone that gave me gout, secondary gout if you will. But I'm a big pussy and don't want an attack. So for 2 months now, I have reduced my allopurinol from 300 mg (15 years at this dose) to 200 mg and next month. I'll MAYBE try 100 mg. This would be a LOT easier if I got some firm numbers from the doctor but I HATE doctoring…my bad!
I'd say IF you think you can control your uric acid without allo then GO FOR IT and try, kudos if successful, but to stop and start to “give your body a rest” sounds absolutely wrong to me. You'll set back your treatment big time. Remember, once you drop a load of crystals in a joint it can years or decades to resolve. (Wish me luck on my next foray to 100 mg. allopuinol.)
I agree about the body making more of what you try to stop. I recently had 4 BP drugs stopped in one day prior to starting another whack.
I was amazed the next day not to find a thumping heart and flushed face- but a normal BP reading. The reset in this case was the wrong way (fortunately) and somehow the body adjusted rather well. At this point my faith in medicine took a knock!
Certainly it flags up the bodies tendency to 'buck the meds' and cast doubts on a chemical view of the body being as progressive as Pharma would, seems/likes to claim.
Coming off could be titrated -as for dose effecteness equally.
OK , not for everyone , but a trial would lay down some ground rules, surely?
Another lack of options on the gout trail!
Your BP is controlled, so the major non-diet factor in your case seems to be weight [and maybe the stress of a Dr Visit? 🙂 ]
I have high hopes for your reducing your AlloP dose,I 'm sure with your insight you will get some ground rules for others on the path!
Hopefully, if you look into Leptin it will spark your fertile imagination as to possibilities on the weight front too.
The best time to try this though , is not as you reduce your AlloP doseage!
But… Self testing would cover for all but the worst glitches, I would hope.
My faith in gout self-testing took a hit when I saw the all-over-the-lot readings that so many here were getting and even some whacked out readings from my labs.
I thought why bother with the time and expense if I couldn't be sure of the results. I guess that's why GOOD studies involve hundreds of people and thousands of readings…the averages will win out.
And then you have to deal wqith post-prandial readings, preprandial readings, excercise induced readings, sleeping readings, stressed readings, and on and on. Uric acid might swing WILDLY over the course of a day.
Reminds me of my old Atkins foray…yes, hit me with a hammer. All the proponents were pointing to LOW triglyceride levels (a main praise point) but all tests were done after a 14 hour fast, NOBODY got tested after they went home and had 6 slices of bacon, 3 eggs and a wasa cracker with an ouncee of butter on it. Obviously all that grease quickly hit the bloodtream but never showed up on any testing.
I mean what is the point of basing almost ALL blood testing on fasting samples when the ONLY time people fast is before a blood test…or they live in Sudan!
zip2play said:
Post edited 5:38 pm – July 28, 2009 by zip2play
I mean what is the point of basing almost ALL blood testing on fasting samples when the ONLY time people fast is before a blood test…or they live in Sudan!
I find that silly as well. If crystals form at high blood uric levels then why would the crystals care about empty stomach readings? They will form when ever the readings are high…after sports or first thing in the morning.
That said empty stomach first thing in the morning readings is the only qualitative way of comparing your readings from one month to the next. Other wise factors like food you ate etc will come into play and complicate matters more that they already are.
zip2play said:
Post edited 5:38 pm – July 28, 2009 by zip2play
My faith in gout self-testing took a hit when I saw the all-over-the-lot readings that so many here were getting and even some whacked out readings from my labs.
Yeah me too but it was semi restored when my home test reading perfectly matched the one taken at the docs place. Both taken first thing in the morning on empty stomach on the same day. That said it all feels like hocus pocus science.
I must stress at my quote above :
“Next day not to find a thumping heart and flushed face- but a normal BP reading” ….
that prior to this, and numerous combinations of potent lowering drugs, my BP had been nowhere near normal – ever!
I've lost over 6 months work [though needed a break, true!] through this factor.
trev said:
Post edited 11:19 am – July 28, 2009 by trev
A question that affects me in deciding to start this drug is:
Why ,once started, can't it be stopped?
If reactions occur to the drug it's recommended to stop it- so why can't it be used for a few months and then the patient SUA checked to see if lifestyle changes can hold the position steady?
Alternatively, if long term side effects are not wanted- a break taken to assess how the body restabilises around any worrying trend.
Oops!- this should have been in a 'Cure' thread
It is not true to say that allopurinol cannot be stopped, it is more true to say that uric acid monitoring cannot be stopped. I.e. once you have successfully reduced uric acid below 5 or 6mg/dL, and kept this down without a gout flare for 6 months, then you have a sound basis to experiment with reduced dosage.
In “Long-term use of allopurinol in the treatment of gout”, Kersley cites 2 out of 54 cases where allopurinol was discontinued. He suggests that:
[where uric acid] is only a little raised, a watching brief may be preferable to persuading the patient to undertake indefinite medication.
However, and Zip2play is gonna love this, he continues:
We still come back to the old saying that the success of anti-gout treatment depends on the doctor-patient relationship engendered by proper explanation of his disease to the patient.
I'd say it is a question of managing your uric acid until you have been free of gout pain for 6 months, with a stable uric acid level. Reduce the dosage, possibly to zero, but keep checking to make sure it stays down at the very low 6 level.
We still come back to the old saying that the success of anti-gout treatment depends on the doctor-patient relationship engendered by proper explanation of his disease to the patient.
You got a typo there; it should read “by proper explanation of the patient's disease TO THE DOCTOR.” And for this you need to be a very PATIENT patient because doctors get very crabby when you point out their inadequacies.
THeir favorite trite comment is “Where did YOU go to medical school?” I;ve got a response I;m DYING to use, but haven't: :”My medical training is MUCH better than yours because I have an MBA!” Think about it.
I would say that SOME patients might come off allopurinol, but I think Kersley's study showing that 2 out of 54 were successful might be spot-on. And 3.7% coming off the drug is near enough to zero for me. Personally I have never heard of a patient coming off allopurinol without a drug replacement. THis of course ASSUMES an initial correct diagnosis of gout after several attacks. ANd even Kersley's study might have 2 people who were misdiagnosed.
As for the watching the patient with uric acid only a little raised and keeping him drugless because he's be afraid of a life of treatment …there is an underlying ugly ”wink-wink-nudge-nudge” that ends with “until he comes in screaming with pain BEGGING me for allopurinol.” Hearty guffaws all 'round the doctor's symposium.
Now, all that said, I MIGHT be a candidate for eventual stoppage of allopurinol because I am relatively certain that I have SECONDARY gout caused by Hydrochlorothiazide. Since I have stopped the thiazide several years ago, its consequential gout may have gone bye-bye. But as a minimum dietary intervention, absent the allopurinol I would have to avoid beer.Hydrochlorothiazide
Trouble is that awful effect that once you have gout, a uric acid level that is completely tolerable for a normal person becomes crystallizable. Perhaps it is because urates, once formed in a joint will NEVER leave completely…and thus always present a site for easy crystallization of a saturated uric acid solution. Another possibility is that the immune system LEARNS its enemies…and thus once an attack is made on uric acid, subsequent attacks become quicker, easier, and more vicious.
This is hard to phrase: But what I am saying is that GOUT makes gout incurable and once gout strikes and is treated you can never get back to a goutless state…and a goutless state is one that can do without allopurinol.
Did that make sense?
If one was able to eliminate most crystals from years of Alliporuniol use, and then they stopped taking the drug, couldn't they potentially go for years again without another flare up?…since the crystals would have to start from nearly scratch again
Once you know your particular pattern with gout, it can be managed.
With regular yearly blood checks ,at the minimum , no doubt many could manage without year on year UA lowering drugs from what's said here, but not everyone.
Hopefully more research will lead to a better understanding of this quite common ,but unduly painful illness, as well as more choice in drug therapy -as seems to be occurring slowly.
With serious outcomes for health possible- Gout definitely can't be ignored.
Knew I'd get a good doctor-patient response
zip2play [also] said:
Trouble is that awful effect that once you have gout, a uric acid level that is completely tolerable for a normal person becomes crystallizable. Perhaps it is because urates, once formed in a joint will NEVER leave completely…and thus always present a site for easy crystallization of a saturated uric acid solution. Another possibility iis that the immune system LEARNS its enemies…and thus once an attack is made on uric acid, subsequent attacks become quicker, easier, and more viscious.
This is hard to phrase: But what I am saying is that GOUT makes gout incurable and once gout strikes and is treated you can never get back to a goutless state…and a goutless state is one that can do without allopurinol.
Did that make sense?
This makes perfect sense to me. There are a few recent articles that seem to suggest that gout immune system reactions are extremely complicated, i.e. more than just white blood cells trying to kill the undead uric acid crystal. The possibility of the immune system learning swifter responses makes the situation quite perilous – gout makes gout incurable, indeed.
Your explanation is the best I've seen to date, especially the point about permanent urate deposits.
There are hints of a fuller explanation in some recent research. However I have extreme difficulty getting my head round statements like:
Monosodium urate (MSU) crystals are potent inducers of inflammation. Within the joint, they trigger a local inflammatory reaction, neutrophil recruitment, and the production of pro-inflammatory cytokines as well as other inflammatory mediators. Experimentally, the uptake of MSU crystals by monocytes involves interactions with components of the innate immune system, namely Toll-like receptor (TLR)-2, TLR-4, and CD14. Intracellularly, MSU crystals activate multiple processes that lead to the formation of the NALP-3 (NACHT, LRR, and pyrin domain-containing-3) inflammasome complex that in turn processes pro-interleukin (IL)-1 to yield mature IL-1β, which is then secreted. The inflammatory effects of MSU are IL-1-dependent and can be blocked by IL-1 inhibitors. These advances in the understanding of hyperuricemia and gout provide new therapeutic targets for the future.
Does it say “We can relieve some pain and inflammation by blocking IL-1, but gout makes gout incurable?”
2011 Update
For more information, see Is Allopurinol A Lifetime Drug?.
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