This Is MS Multiple Sclerosis Community: Knowledge & Support

Has anyone seen/found the results to this study?


http://clinicaltrials.gov/ct2/show/NCT00067327

Estimated Enrollment: 30
Study Start Date: February 2002
Estimated Study Completion Date: September 2005

Detailed Description:
Uric acid is a natural inhibitor of certain chemistries associated with peroxynitrite, a product of inflammation. In animal models of multiple sclerosis (MS), these chemical reactions have been associated with breakdown of the blood-brain barrier and CNS tissue damage. In addition, MS patients have serum uric acid levels that are lower than age- and sex- matched healthy individuals. The primary purpose of this study to determine whether raising low serum uric acid levels by daily oral administration of its precursor inosine has an effect on the cumulative number of newly active lesions on magnetic resonance imaging (MRI) and to evaluate the safety and tolerability of inosine in patients diagnosed with relapsing remitting and secondary progressive MS.

Rainer, I haven't seen anything, but the US MS Society's roundup of agents in clinical trials for MS mentioned the inosine trial in 2006, and said results were not available. Now, the 2007 list has no mention of inosine. Since clinicaltrials.gov says it's completed, I'm going out on a limb and guessing that the results weren't impressive. Hopefully they'll release some results soon though.

fyi, i have been eating much liverwurst hoping to elevate my serum UA but at last test it was still bang on the MS patient average of 194. if i want to reach that optimal 290 i think i'm going to have to investigate the inosine avenue too.

I got a little more info on this study from the source.

"... we are still waiting for some of the data to be analyzed before we can publish anything. The results of our first trial a few years ago have been published and three other larger trials have been completed in Europe, with data from one already published. Their experience appears to be like ours, with a good enough effect to pursue larger studies if funding can be obtained.

Off the record, we have had remarkable success with several individuals who had high numbers of active lesions and lower than normal serum uric acid levels to begin with. The latter gives us some idea of whether or not there may be some success.

You may be interested to know that the idea that urate (raised by inosine) protects the brain in MS and other neurodegenerative diseases has a high likelihood of being followed up in a Parkinson’s trial."

Why spend all that money on inosine -- just consume lots of fructose!



Gout surge blamed on sweet drinks

BBC - Sugary drinks have been blamed for a surge in cases of the painful joint disease gout.

Men who consume two or more sugary soft drinks a day have an 85% higher risk of gout compared with those who drink less than one a month, a study suggests.

Cases in the US have doubled in recent decades and it seems fructose, a type of sugar, may be to blame, the British Medical Journal study reports.

UK experts said those with gout would be advised to cut out sugary drinks.

About 1.5% of the UK population currently suffers from gout and there has been an increase in numbers over the last 30 years - although the condition is more associated with Victorian times.

The symptoms of painful, swollen joints, mainly in the lower limbs, are caused when uric acid crystallises out of the blood into the joints.

US and Canadian researchers said the increase in cases had coincided with a substantial rise in the consumption of soft drinks.

Previous research had also shown that fructose increases levels of uric acid in the bloodstream.

To look in more detail, the team carried out a 12-year study of 46,000 men aged 40 years and over with no history of gout, asking them regular questionnaires about their diet.

Over the period, 755 newly diagnosed cases of gout were reported.

The risk of developing the condition was significantly increased with an intake level of five to six servings of sugary soft drink per week.

This link was independent of other risk factors for gout such as body mass index, age, high blood pressure and alcohol intake.

Diet soft drinks did not increase the risk of gout but fruit juice and fructose rich fruits (apples and oranges) were associated with a higher risk, the researchers said.

But this finding needs to be balanced against the benefit of fruit and vegetables in preventing other chronic disorders like heart disease and stroke.

Dr Hyon Choi, from the University of British Columbia, in Vancouver said dietary advice for gout had focused on restricting purine-rich foods, such as red meat and beer.

He said practitioners should advise patients with gout to reduce their fructose intake.

"I can think of some situations, for example in severe treatment failure gout, where reducing sweet fruits, such as oranges and apples could help," he added.

Dr Andrew Bamji, president of the British Society for Rheumatology, said anecdotally cases of gout appeared to be rising.

"When you think about it, it makes a lot of sense in that fructose inhibits the excretion of uric acid.

"I will certainly change my advice to patients and I suspect the number drinking fructose is quite large."

http://news.bbc.co.uk/2/hi/health/7219473.stm

Very interesting stuff...maybe part of how the CRABs work is related to uric acid.



Variation of serum uric acid levels in multiple sclerosis during relapses and immunomodulatory treatment.

Eur J Neurol. 2008 Feb 26 [Epub ahead of print]
Guerrero AL, Martín-Polo J, Laherrán E, Gutiérrez F, Iglesias F, Tejero MA, Rodríguez-Gallego M, Alcázar C.
Neurology Unit, Hospital Río Carrión, Palencia, Spain.

Uric acid (UA), a product of purine metabolism, may be an antioxidant, perhaps acting as a scavenger of peroxynitrite. Patients with gout have a reduced incidence of multiple sclerosis (MS). A number of studies found that patients with MS have low serum levels of UA, although it has not been established whether this represents a primary deficit or a secondary effect. UA has also been proposed as a marker of disease activity and response to immunosuppressive or immunomodulatory treatment.

We retrospectively reviewed 83 relapsing-remitting or secondary progressive MS patients (64 females and 19 males) followed in our Neurology Unit. We collected data concerning demographic variables as age and sex, and clinical variables as age of onset, clinical type, disease duration, EDSS score and total number of relapses. We considered UA levels in three different situations: during a relapse, during remission period and during remission period under immunomodulatory treatment [Interferon Beta 1a im (Avonex; Biogen Idec Inc., Cambridge, MA, USA), Interferon Beta 1a sc (Rebif; Serono Europe Limited, London, UK), Interferon Beta 1b (Betaferon; Bayer Schering Pharma AG, Berlin, Germany) or Glatiramer Acetate (Copaxone; TEVA Neuroscience LLC, Kansas City, MO, USA)]. A Wilcoxon matched pairs test was carried out to determine differences between groups. A P-value less than 0.05 was considered statistically significant.

In 33 patients, we were able to compare at least one UA value obtained during a relapse with at least one when remission without treatment. Mean serum UA levels were significantly lower when measured during a relapse (r: 0.39, P: 0.024). In 27 cases, we compared at least one remission value without treatment with at least one obtained during remission and immunomodulatory treatment. Mean serum UA levels significantly increased when determined during Interferon Beta or Glatiramer Acetate therapy (r: 0.84, P < 0.001).

Although we do not know exactly whether and how UA is involved in MS pathogenesis, our data suggest that UA might reflect disease activity or treatment response in MS.

Pubmed URL

Very interesting!
Husband's been on inosine supplements for a year, as well as copax (GA).
His serum uric acid levels were low on diagnosis, and are now considered high normal. We keep our eye on it, since I didn't want to give the poor guy gout, along with MS.

best,
AC

_________________
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS

Hi Dignan,
That's an interesting find. It appears to confirm that uric acid levels are significant in MS although, as they say, whether causative or secondary remains to be seen. I take Inosine to raise my levels although I've never had them checked, which is a bit naughty.
The statements at the beginning of the article were a bit of a surprise to me though: I understood that it was absolutely established that UA IS a scavenger of peroxynitrite, IS an antioxidant, and that gout and MS are 100% mutually exclusive, so their hesitancy was unexpected,

_________________
Dom

I raised this possibility with my wife's neuro, and even mentioned the theory that gout and MS and mutually exclusive. He was pretty dismissive - he commented:

"look at who gets gout - older men; look at who gets MS - young women; it's not surprising that people with gout don't have MS".

Sigh.

Sorry, MJS...
not all neuros are open to "alternative" views.
Just got back from one year appointment with my husband's neuro. His 20 lesions are still there, but none enhancing (vs. 6 last year), and no new lesions after one year.

Uric acid has been part of his picture, with inosine supplements and copaxone treatment. He was low at dx, with several enhancing lesions and is now high normal, with no progression one year later.

His doc says to keep doing what we're doing, and she supported the inosine. We realize that nothing's guaranteed with MS, but we're hopeful today.

leave no stone unturned!
AC
ps Glad to see your smiling face, Dom! Missed you, but glad you've been composing.

_________________
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS

from memory it wasn't a 100% mutually exclusion between gout and MS.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=18479

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=18479&rendertype=table&id=T1
They would of expected 62 if gout made no difference, but they only found four. still not zero.

Hi Cure,
I've just had another look, and it seems you can find reports that take either position: some say categorically that gout and MS are mutually exclusive; some say, " almost", or, " virtually". I've been thinking about it and come up with a scenario which might explain how the two conditions could coexist but still have uric acid at their base, (this is pure speculation on my part): supposing some people have wildly varying levels of uric acid in their bloodstream, the high periods could account for the build up of crystals and so the appearance of gout, then if it plummets dramatically an MS exacerbation could occur even while the symptoms of gout are still present.

AC,
Thanks for that, and I'm glad your husband is doing well. His doc sounds very approachable – I wish they all were – and I think the evidence is mounting that uric acid is a key player in MS. It's probably worth bearing in mind that a small number of people who take Inosine actually respond with a lowering of uric acid levels… just another reminder that there is probably never going to be a " one size fits all" solution.
By the way, " composing" is going to take up a lot of my time for the foreseeable future, however, I'm not planning to start decomposing for a while yet.

MJS,
Please convey my delight to your wife's neurologist at discovering that I can't possibly have MS. Last time I checked I definitely wasn't a young woman!
As you said… " sigh",

_________________
Dom

I did read almost every post in this forum regarding the use of inosine for MS but I'd like to have personal depositions about what results good or bad every individual has to mention.
Preferably type or MS and duration, type of other medicines/regimes used, dosage and duration of inosine as a supplement etc.
I collected recently some publications about inosine and are all very promising!
Thanks in advance
Jim

I have taken inosine for several years. It has not prevented treatment induced relapses for me.

_________________
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,

Have you had a blood analysis for uric acid before start inosine?
As I understand it there are so many variations in this disease that every one should investigate by himself what his case is, if you have not had low uric acid before inosine is quite logical to not see any improvement.