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Sounds interesting and worth investigating; I wouldn't swop my Allopurinol for it though
But maybe a good supplement to consider to combat the effects on the liver of any long term medication. Fortunately, here in the UK, we will still be able to buy it, as the government has just decided to give the finger to proposed EU legistion banning supplements and herbal remedies. No doubt, the fact it's a multi million pound industry had something to do with it, rather than their faith in complementary medicine.
Sounds eminently plausible Trev. Seems like the body does its best to lay down deposits of crud wherever it can
trev said:
Makes me ask- is urate deposition involved in Alzheimers?- it's gettting so common, just like gout is increasing…
No, it's protein deposits rather than urate.
Have you tried 'finger cots' – like tiny condoms for your digits, so at least you should get a laugh down the pub
. Don't know if you can get ones especially for toes, but I've used them in the past and they're quite effective at keeping wounds clean. Can get a bit sweaty, so it's a toss up between keeping dirt out and letting air get in to help heal.1. The use of ice is effectively simple anaethesia; you'd undoubtedly have better and longer lasting results with novocaine
2. Gout is not a soft tissue (impact trauma) injury, so your reasoning is flawed. Gout is a systemic inflammatory response, which depends on blood flow to the area to complete its natural cycle. Icing hinders this process.
There's plenty of info online if you google Kidney stones. It would be handy to know what type of stones they are – most stones are calcium based, so not necessarily directly due to gout. Put a sieve in the pan when you pee and try to catch some to show your Dr – I think you'll certainly know when you're passing them if they're 4mm. The pain tends to move down to the groin as they pass into the bladder and beyond
Good luck.
trev said:
High iron is?on the bad to have list for gout- one reason why younger women?stay clear of gout, too.
A good argument for blood letting therapy?
Very interesting experiment Hans and yet another example of how gouties are often ahead of the game in understanding the discrepancies which exist in current medical practice. Unfortunately, it's probably only interesting to us.
My guess is that Drs are not terribly concerned about results that vary between less than 2mg/dl. Also, when you consider the normal fluctuation of SUA in the course of a day due to various factors: diet, exercise, hydration etc., they no doubt realise that a lab test is only a ballpark or snapshot figure. They probably conclude that as long as it's not off the scale and the process of urate lowering therapy is underway, everything will settle down in the end.
Only the best
http://www.goutpal.com/allopurinol.html
PS. Your query prompted me to have another search: found this (but no date):
“A continued high alcohol intake may also impair the response to allopurinol therapy by inhibiting the conversion of the drug to its active metabolite, oxipurinol. This results in reduced oxipurinol plasma levels, increased urinary excretion of unmetabolized allopurinol, and hence reduced urate-lowering effects. It follows that urate-lowering drugs are often less effective in patients with gout who continue to drink.”
apas.org.uk/liver-function-tests.asp [link now invalid]
Alcohol can also make Allopurinol less effective due to it being expelled quicker.
hansinnm said:
Post edited 3:19 pm – October 28, 2010 by hansinnm
Naproxen is a pain killer
Nope, sorry to be picky, but Naproxen is a NSAID. Its action as an anti-inflammatory may well reduce pain, but that is not its primary function. Morphine, codeine etc. are pain killers.
Chilli is a known trigger for gout flares because Capsaicin, the substance that give chillies their heat is well known to contain a neuropeptide associated with the inflammatory process. But it also probably depends on what you cook it with and where you are in your urate lowering therapy. If your medication regime is well established, as many on here testify, you can probably get away with almost anything.
Go very easy on the chilli. If you must, use fresh, milder chillies rather than powdered – more for flavour than heat. Use plenty of turmeric, ginger & garlic, all very anti-inflammatory.
toofast said:
Quick follow up…does anyone have the “whole” article in the Lancet ?
I'd love to read it, but not sure I want to spend the money to suscribe for a one time article?
Got my dates mixed up;first article (the one I referred to in the above post) was in Jan 2010
http://dl.dropbox.com/u/128596…..202010.pdf
Second one in the the Aug edition of the Lancet was an article on new gout drugs/research
A lot of UK Drs seem to be rather cautious with initial dosage, which is quite unnecessary; if you're allergic to it you generally find out pretty quick. My Dr put me on 100mg for 3 months, but because I have my own SUA tester (highly recommended), I could see it wasn't doing the job and so I doubled the dose after 1 month and made another appointment a week before they ran out. He agreed that what I'd done was entirely reasonable and even offered to make the next scrip for 300mg if I wanted.
If you are doing your own testing and show yourself to be knowledgeable about the condition (which you soon will be when you've been on here a while) Drs are much more likely to play ball. With a SUA in double figures, you almost certainly need to be on 300mg. – the sooner the better.
Ask him if he's read the latest gout review in the Lancet (Aug 2010) and you will undoubtedly get his attention.
I've posted a link on here somewhere.
UnfunnyPain said:
Is it safe to say that aside from a genetic disposition, this gout thing is most often triggered by long term alcohol use?
If you're not genetically disposed, long term alcohol will not trigger gout (may well trigger a host of other things however) Gotta have the gene Genie, then gout flares can appear for almost no reason, as if by magic
Gilles said:
He put him on anti-inflammatory but I don't know what it is.
Probably a corticosteroid like prednisone.
I think there are so many variables which affect meter readings that probably the most significant thing is whether you are on average above or below 6.00. I had a hospital blood test recently, which later came back at 5.00, but my reading as soon as I got home was 6.9. I notice my readings are higher when I haven't drunk as much water as I should; diet & exercise probably influences it too. They are just a snap shot of a continually fluctuating scale throughout the day, so while testing at a particular time of day provides some regularity of data, maybe testing at random times would show a broader spectrum of levels?
GoutPal said:
In the meantime, the best way is to use a free online storage facility, upload to your public area, and link here.
@everyone: This is also great for automatic backups. I link my data storage folders to DropBox, so files are automatically backed up remotely whenever I save them. It also means I can access them from any where I can get an Internet connection.
Sorry, I sat on the pointy hat
Okey dokey – abracadabra!
zip2play said:
Lancet got the first sentence precisely correct and hedged on the second.
To be fair, it does say elsewhere:
Allopurinol doses used in these trials were fixed and
too low; this fact cannot be emphasised enough. One
could reasonably argue that if allopurinol doses were
titrated to serum urate concentrations, the febuxostat
advantage might vanish, although the side-eff ect profi le
of allopurinol might also change. Accordingly,
febuxostat should be considered mainly for patients
intolerant to allopurinol, for those whose gout is not
controlled with other urate-lowering treatments, and
for those with renal insuffi ciency (but whose creatinine
clearance is higher than 30 mL/min).and in their final observations:
Time will tell how febuxostat or the pipeline drugs fit
into gout treatment algorithms. At the risk of sounding
critical, we remind readers that confusion about how to
use long-available drugs is a persisting issue with our
management of gout. Addition of new drugs alone will
not correct these pre-existing misconceptions. The
diagnosis should be substantiated by identification of
intra-articular monosodium urate crystals, guidelines
about the start of urate-lowering treatment should be
followed, prophylaxis against flares early in such
treatment should be given, low enough concentrations
of serum urate should be targeted, and long-term
adherence by patients should be sought. Most
patients with gout are handled by primary care providers
and fewer than 3% by rheumatologists.
Rheumatologists seem to be somewhat, but not
impressively, better at achieving target concentrations
of serum urate than primary care physicians (mean
serum urate concentrations 353 versus 413 μmol/L,
respectively, p=0·0004).81
A major concern is the continued use of allopurinol at
300 mg daily, or less in renal insuffi ciency, since these
doses are clearly inadequate in most patients.
Clinicians often use suboptimum doses of allopurinol in
patients with renal insufficiency for fear of precipitating
worsening renal failure or the sometimes fatal
allopurinol hypersensitivity syndrome. Nevertheless,
the approach should be to start low and go slow, with
careful monitoring while titrating upward to achieve
target serum urate values. Evidence that treatment of
hyperuricaemia in these patients might improve renal
function is encouraging. Higher doses of allopurinol
in patients with gout and renal insufficiency are not
associated with increased risk of hypersensitivity, but are
associated with better achievement of target serum urate
values (86%). Undertreatment for fear of side-effects
does disservice to patients since they are on a dose of
medicine that will not achieve the therapeutic goal,
which is to stop attacks and resolve tophi, but merely
slow the rate of progression.
These same principles should apply to dosing of
febuxostat, or other urate-lowering treatments, apart
from drugs like pegloticase, for which the reason for
failure is generally the development of antibodies against
the drugs, not inadequate dosing. The excitement
generated by the appearance of new therapies offers an
ideal opportunity to re-educate our patients and ourselves
about gout so as to improve outcome in this highly
treatable disease.It's an interesting, although highly technical article, which survrys recent trials and the results of new approaches to gout treatment. I think it would be worth adding to the GoutPal data base.
IF ONLY SOMEBODY WOULD TELL ME HOW!
azasadny said:
A gentlemen on another forum sent me this info today and I wanted to share it…
I did a little reading on new gout drugs. Here is some info that might be interesting, or not.
1. Cheap Colchicine will leave the market this year. A company called URL Pharma has secured 3-year exclusivity for colchicine, now branded as Colcrys, and will jack the price to $5/pill.
2. Arcalyst (rilonacept) is a drug from Regeneron that will probably be approved by the FDA in early 2012. It is meant to be used with allopurinol to reduce the frequency of gout flares. Clinical trials showed 73% to 80% fewer flares in patients taking allopurinol + rilonacept, vs pts on allopurinol + placebo.
3. Krystexxa (pegloticase) from Savient has been recently been approved by FDA. It is a drug for patients with very severe gout – deforming/crippling gout. Clinical trials showed it was very effective for about 1/2 of those patients, the other 1/2 couldn't tolerate or didn't get beenfit from the drug. This is an expensive IV infusion drug.
4. RDEA594, a drug from Ardea, appears not particularly more effective than allopurinol in lowering serum uric acid, but the combination with allopurinol appears – though data is very preliminary – to be more effective that allopurinol alone. This drug is at least 2 years from the market.
5. Apparently 90% of gout cases are treated by primary care doctors, who under-treat the disease (e.g. don't prescribe high enough allopurinol dose) and aren't particularly up-to-date on the disease. This is claimed to be one obstacle to development of more effective gout drugs – drug companies aren't sure there's really a market here.
Great. Thanks posting this. It is clearly based on the recent Lancet article I mentioned in another thread, which I don't know how to post. I was going to do a similar summary, but you've saved me the trouble
Lyndak said:
How much fluid should we be drinking??
How long is a piece of string? I think it's such an individual thing, based on so many factors: are you a hot or a cold person? how well do your kidneys function, how high is your SUA etc. Rule of thumb, however, I would say 2-3 litres (and I struggle even with that) should be adequate under normal circumstances i.e not in acute gout attack phase. If I drank 6 litres a day I'd never get any work done
Lyndak said:
I will talk to my Nephrologist about increasing to 300mg, but I suspect that, since I have had improvement, he won't make the change.
Pretty sure he will and you should insist if he doesn't. 8.00 is not low enough and 100mg won't work any better in another 6 weeks than it does now.
Jon, while it is possible for gout to affect any joint, this is much more likely to be muscular tension related to the pain you are/have been experiencing. Especially so, as you describe the pain radiating to your jaw – maybe you've had a few headaches recently too?
Would advise a professional neck & shoulder massage, acupuncture, if you're up for it, and awareness concerning posture, jaw clenching etc. Try to keep your chin tucked in slightly, so that the back of the neck lengthens and make sure you aren't hunching your shoulders. Gentle daily stretching, though painful initially can help increase the range of motion (turning the head, up, down, side to side, letting the head hang to the side – try to touch your shoulder with your ear).
It is very tempting to think every pain is directly due to gout (which in a way it is) when in fact many of the postural adjustments we make when suffering an attack are to blame. These can also trigger a gout response as well, of course, but more commonly in the limbs.
azasadny said:
Watch your diet, too. I used to eat a lot of lentil soup from my local Lebanese restaurant (I'm a vegetarian) and the purine levels in the lentil soup cause myt gout to flare up.
I had the same problem with falafel
Effectively controlling symptoms is all well and good, as I discovered is possible with Chinese herbs, but without knowing SUA levels this will simply be slowing down or masking the steady build up of urate and other long term implications of high uric acid. I think once the science and progression of the disease is understood it is not easy to ignore this fact and convince oneself the situation is under control.
The good news is that if one is prepared to continue with a healthy gout diet (plus whatever supplements) when starting Allopurinol, it should be possible to reduce SUA to safe levels on a low dose.
