Attn: Jimmylegs Re: Uric Acid

If it's on your mind and it has to do with multiple sclerosis in any way, post it here.

Attn: Jimmylegs Re: Uric Acid

Postby NHE » Tue Jan 09, 2007 5:59 pm

Hey,
I just ran across this on another newsgroup and I was wondering if you had any thoughts you might be able to share on the subject?
    Serum uric Acid and cognitive function in community-dwelling older adults. Neuropsychology. 2007 Jan;21(1):136-40.

    Among possible markers of age-related cognitive decline, uric acid (UA) is controversial because it has antioxidant properties but is increased in diseases that often lead to cognitive impairment. In this study of 96 elderly adults, participants with mildly elevated (but normal) serum UA were 2.7 to 5.9 times more likely to score in the lowest quartile of the sample on measures of processing speed, verbal memory, and working memory. Even after controlling for age, sex, race, education, diabetes, hypertension, smoking, and alcohol abuse, the multivariate-adjusted odds of poor verbal memory and working memory remained significant (ps < .05). Despite its antioxidant properties, these findings suggest that even mild elevations of UA might increase the risk of cognitive decline among older adults. ((c) 2007 APA, all rights reserved).
Here's a discussion of the research (sorry I don't have a url for this).
    Newswise - Researchers at the Johns Hopkins and Yale university medical schools have found that a simple blood test to measure uric acid, a measure of kidney function, might reveal a risk factor for cognitive problems in old age. Of 96 community-dwelling adults aged 60 to 92 years, those with uric-acid levels at the high end of the normal range had the lowest scores on tests of mental processing speed, verbal memory and working memory.

    The findings appear in the January issue of Neuropsychology, which is published by the American Psychological Association (APA).

    High-normal uric acid levels, defined in this study as 5.8 to 7.6 mg/dL for men and 4.8 to 7.1 mg/dL for women, were more likely to be associated with cognitive problems even when the researchers controlled for age, sex, weight, race, education, diabetes, hypertension, smoking and alcohol abuse. These findings suggest that older people with serum (blood) uric-acid levels in the high end of the normal range are more likely to process information slowly and experience failures of verbal and working memory, as measured by the Wechsler Adult Intelligence Scale and other well-established neuropsychological tests.

    "It might be useful for primary-care physicians to ask elderly adults with high normal serum uric acid about any problems they might be having with their thinking, and perhaps refer those who express concern, or whose family members express concern, for neuropsychological screening," says lead author David Schretlen, PhD.

    The link between high-normal uric acid and cognitive problems is also sufficiently intriguing for the authors to propose clinical studies of whether medicines that reduce uric acid, such as allopurinol, can help older people with high-normal uric acid avoid developing the mild cognitive deficits that often precede dementia.

    For reasons that are not entirely clear, uric acid levels increase with age, says Dr. Schretlen. Higher levels of uric acid are linked with known risk factors for dementia, including high blood pressure, atherosclerosis, Type 2 diabetes and the "metabolic syndrome" of abdominal obesity and insulin resistance. Dr. Schretlen also says there is mounting evidence that end-stage renal (kidney) disease increases the risk of cognitive dysfunction and dementia in elderly adults. Given this web of connections, uric acid could potentially become a valuable biological marker for very early cognitive problems in old age.

    The researchers say that it's unclear why mild cognitive problems appear with high-normal uric acid because, paradoxically, uric acid also has anti-oxidant properties that are thought to be protective in other situations. The authors are also researching links between uric acid and vascular damage in the brain and attempting to dissect which aspects of uric acid and its production help or hurt the nervous system.

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Postby CureOrBust » Tue Jan 09, 2007 7:12 pm

NHE wrote:Higher levels of uric acid are linked with known risk factors for dementia, including high blood pressure, atherosclerosis, Type 2 diabetes and the "metabolic syndrome" of abdominal obesity and insulin resistance.

NHE wrote:... The authors are also researching links between uric acid and vascular damage in the brain ...

I found these two points of interest, as I saw a tv special which interviewed a researcher and her theorey that Alzheimer is actually a vascular disease. She popped up brain autopsy slides where she showed that all plaques had a small capilliary passing through them, and believed it was because of a failure in the capilliary caused by hardening, and thereby raised blood pressure. Its also been found that people on blood pressure medication also had a lower incidence of it. You can read the shows transcript at:
http://www.abc.net.au/catalyst/stories/s1610402.htm

She lost me a little with her absolutes.
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uric acid/cognitive comments

Postby jimmylegs » Tue Jan 09, 2007 7:42 pm

hi there, absolumente!

first of all i went looking for the full text so i could get the numbers when they said "high-normal uric acid". unfortunately it looks like my school access won't let me at it until next month.

in the meantime, let's take a guess at what they meant by normal and slightly elevated. according to medline, the serum uric acid "normal range" is 3.0 and 7.0 mg/dL (Uric acid 1 mg/dL = 59.48 µmol/L) so that would be say, 240 to 420 in my language. if i understand the term "normal" correctly, this would indicate that you have the most people with uric acid levels at around 330.

you can get gout as low as say 360. that sounds like it qualifies as mildly elevated. so let's say that going over 360 might not be in people's best interests, but it's still well within the "normal" range. so, maybe you can start to have cognitive problems in that upper end of the normal range also.

to review, in previous studies it's been found that ms patients averaged 194 for serum uric acid, while those in attack were at 160 and those in remission were around 230. and the healthy controls averaged 290, well under that 330 that i've proposed as a possible central "normal" (which i believe includes some 'unhealthy controls") value.

at my last test i was 194. actually 193.87 or something like that, but that's just splitting hairs ;) i'm aiming for 290.

so, digging into uric acid and cognitive stuff a little deeper, i also have read that accumulation of copper can contribute to reduced uric acid in MS patients <shortened url>. so i thought, hmm i wonder if low copper could possibly be associated with the elevated uric acid in these cognition studies? so i did a search on copper cognitive and came up with this:

Cognitive decline correlates with low plasma concentrations of copper in patients with mild to moderate Alzheimer's disease.Pajonk FG, Kessler H, Supprian T, Hamzei P, Bach D, Schweickhardt J, Herrmann W, Obeid R, Simons A, Falkai P, Multhaup G, Bayer TA.
Department for Psychiatry, Saarland University, Building 90, 66421 Homburg/Saar, Germany.

Alzheimer's disease (AD) is a devastating brain disorder clinically characterised by progressive loss of characteristic cognitive abilities. Increasing evidence suggests a disturbed copper (Cu) homeostasis to be associated with the pathological processes. In the present study we analysed the plasma Cu levels and cognitive abilities using the Alzheimer's disease Assessment Scale-cognitive subscale (ADAS-cog) in 32 patients with mild to moderate AD. Statistical analysis revealed a negative correlation between plasma Cu levels and cognitive decline (r=-0.49; P<0.01). Patients with low plasma Cu (mean 82 +/- SD 9) had significant higher ADAS-cog values (mean 23 +/- SD 7), than patients with medium plasma Cu (mean 110 +/- SD 7), who exhibited lower ADAS-cog scores (mean 16 +/- SD 4; ANOVA, P<0.0001). Despite the fact that all patients had plasma Cu levels within the physiological range between 65 microg and 165 microg/dL, 87.5% of the patients revealed a significant negative correlation between plasma Cu and ADAS-cog. This finding supports the hypothesis of a mild Cu deficiency in most AD patients.


so, a tangled web, AGAIN 8O ! but so, maybe if they took some copper it would help bring their uric acid down closer to a safer level for cognitive function.

then if we look for links between gout and cognitive disfunction, do these occur together? yes they do, Lesch-Nyhan Disease.

<shortened url>

J Hist Neurosci. 2005 Mar;14(1):1-10.

Lesch-Nyhan Disease.Nyhan WL.
Department of Pediatrics University of California San Diego La Jolla CA 92093-0830, USA. wnyhan@ucsd.edu

The first description of Lesch-Nyhan disease was in 1964; the first two patients were seen in 1963. The disease has caught the imagination of a variety of clinicians and scientists. The clinical picture is striking, combining spasticity, involuntary movements, and cognitive retardation with self-injurious behavior and the manifestations of gout. Biochemically, the overproduction of uric acid--the end product of purine metabolism--was, when measured, the largest ever seen. The disease is now well understood on a molecular basis. Enzyme analysis and mutational analysis have made available a full range of genetic testing, including diagnosis, carrier detection, and prenatal diagnosis. Therapy with allopurinol has been effective for those manifestations the disease shares with gout. Treatment for the neurological and behavioral features of the disease remains elusive.


we have also had a study abstract posted here which says ms and gout don't mix, but here we see that gout and cognitive disorders related to elevated uric acid do mix. so, i think we ms-ers are safe aiming for closer to 300 without great fear of cognitive issures related to uric acid. now d3 on the other hand...

well, just in case anyone is still reading, i like really complicated abstracts like the one below, because they get across how many different interrelated factors affect human function.

<shortened url>
J Nutr Health Aging. 2006 Sep-Oct;10(5):377-85
Effects of nutrients (in food) on the structure and function of the nervous system: update on dietary requirements for brain. Part 1: micronutrients.Bourre JM.
French Academy of Medicine. INSERM, U705 ; CNRS, UMR 7157 ; Universites Paris 7 et 5, Department of Neuro-pharmaco-nutrition. Hopital Fernand Widal, 200, rue du Faubourg Saint-Denis, 75475 Paris cedex 10. jean-marie.bourre@fwidal.inserm.fr

The objective of this update is to give an overview of the effects of dietary nutrients on the structure and certain functions of the brain. As any other organ, the brain is elaborated from substances present in the diet (sometimes exclusively, for vitamins, minerals, essential amino-acids and essential fatty acids, including omega- 3 polyunsaturated fatty acids). However, for long it was not fully accepted that food can have an influence on brain structure, and thus on its function, including cognitive and intellectuals. In fact, most micronutrients (vitamins and trace-elements) have been directly evaluated in the setting of cerebral functioning. For instance, to produce energy, the use of glucose by nervous tissue implies the presence of vitamin B1; this vitamin modulates cognitive performance, especially in the elderly. Vitamin B9 preserves brain during its development and memory during ageing. Vitamin B6 is likely to benefit in treating premenstrual depression. Vitamins B6 and B12, among others, are directly involved in the synthesis of some neurotransmitters. Vitamin B12 delays the onset of signs of dementia (and blood abnormalities), provided it is administered in a precise clinical timing window, before the onset of the first symptoms. Supplementation with cobalamin improves cerebral and cognitive functions in the elderly; it frequently improves the functioning of factors related to the frontal lobe, as well as the language function of those with cognitive disorders. Adolescents who have a borderline level of vitamin B12 develop signs of cognitive changes. In the brain, the nerve endings contain the highest concentrations of vitamin C in the human body (after the suprarenal glands). Vitamin D (or certain of its analogues) could be of interest in the prevention of various aspects of neurodegenerative or neuroimmune diseases. Among the various vitamin E components (tocopherols and tocotrienols), only alpha-tocopherol is actively uptaken by the brain and is directly involved in nervous membranes protection. Even vitamin K has been involved in nervous tissue biochemistry. Iron is necessary to ensure oxygenation and to produce energy in the cerebral parenchyma (via cytochrome oxidase), and for the synthesis of neurotransmitters and myelin; iron deficiency is found in children with attention-deficit/hyperactivity disorder. Iron concentrations in the umbilical artery are critical during the development of the foetus, and in relation with the IQ in the child; infantile anaemia with its associated iron deficiency is linked to perturbation of the development of cognitive functions. Iron deficiency anaemia is common, particularly in women, and is associated, for instance, with apathy, depression and rapid fatigue when exercising. Lithium importance, at least in psychiatry, is known for a long time. Magnesium plays important roles in all the major metabolisms: in oxidation-reduction and in ionic regulation, among others. Zinc participates among others in the perception of taste. An unbalanced copper metabolism homeostasis (due to dietary deficiency) could be linked to Alzheimer disease. The iodine provided by the thyroid hormone ensures the energy metabolism of the cerebral cells; the dietary reduction of iodine during pregnancy induces severe cerebral dysfunction, actually leading to cretinism. Among many mechanisms, manganese, copper, and zinc participate in enzymatic mechanisms that protect against free radicals, toxic derivatives of oxygen. More specifically, the full genetic potential of the child for physical growth ad mental development may be compromised due to deficiency (even subclinical) of micronutrients. Children and adolescents with poor nutritional status are exposed to alterations of mental and behavioural functions that can be corrected by dietary measures, but only to certain extend. Indeed, nutrient composition and meal pattern can exert either immediate or long-term effects, beneficial or adverse. Brain diseases during aging can also be due to failure for protective mechanism, due to dietary deficiencies, for instance in anti-oxidants and nutrients (trace elements, vitamins, non essential micronutrients such as polyphenols) related with protection against free radicals. Macronutrients are presented in the accompanying paper.


if you read all this, congrats! can't believe you lasted. anyway what do ppl think?
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Postby LisaBee » Wed Jan 10, 2007 6:10 pm

I'm a bit perplexed. I've read abstracts on PubMed indicating lower, not higher, uric acid is observed in patients with neurodegenerative diseases compared to controls. Just two recent examples are below, one is for Alzheimer's and another is BSE.

I think in some cardiovascular diseases uric acid is elevated, as NHE's article indicated. I wonder if other factors relating to cardiovascular disease, such as reduced blood flowin the brain, could be causing cognitive effects and the elevated uric acid is just along for the ride. That is a total guess on my part though.

It is a very interesting area. The inverse relationship between MS and gout that has been demonstrated in an epidemiological survey (Hooper et al. 1998) is one of the biggest areas that has remained largely unexplored in MS research, especially since increasing uric acid in mice suppressed EAE and also promoted recovery in animals already with active disease. (See Scott et al 2002 and Spitsin et al. 2002). It is one of the rare cases where there is actual human epidemiological evidence and studies in the MS animal model possibly support each other. There is an additional study in which Copaxone was shown to raise uric acid and it was suggested as one of the mechanisms of actions of Copaxone. Yet, other than one 2004 German review article, I can find nothing specifically published on uric acid and MS since 2002. That was five years ago!

Here's the Alzheimer's one:

1: Int J Geriatr Psychiatry. 2006 Apr;21(4):344-8. Links
Decreased plasma antioxidants in patients with Alzheimer's disease.Kim TS, Pae CU, Yoon SJ, Jang WY, Lee NJ, Kim JJ, Lee SJ, Lee C, Paik IH, Lee CU.
Department of Psychiatry, Kangnam St. Mary's Hospital, The Catholic University of Korea, College of Medicine, Seoul, Korea.

OBJECTIVES: It has been suggested that oxidative injuries have an important role in the pathogenesis of Alzheimer's disease (AD). In this study, we assess whether the plasma levels of albumin, bilirubin, and uric acid would be altered in the AD patients compared to those of the healthy controls. Furthermore, we tried to find the correlations between plasma antioxidant levels and the cognitive function in AD patients. METHODS: The plasma albumin, bilirubin, and uric acid levels were measured by standard methods in 101 AD patients and 101 healthy controls. The Korean version of the Mini Mental Status Examination (MMSE-K) was used to evaluate the cognitive functions of AD patients. RESULTS: A significant reduction in the albumin, bilirubin, and uric acid levels in the AD group was found compared to those of the control group. The scores of MMSE-K showed the positive correlation with albumin level in the AD group after adjusting confounding factors such as body mass index, gender and age. CONCLUSION: This study showed that oxidative injuries could be involved in the pathogenesis of AD, as well as indicating that some antioxidant might be associated with the cognitive functions in AD. Copyright (c) 2006 John Wiley & Sons, Ltd.

^^^^^^^^^^^^
And the BSE one:
^^^^^^^^^^^^^

PMID: 16534775 [PubMed - indexed for MEDLINE]

: Exp Neurol. 2004 Nov;190(1):233-44. Links
BSE and vCJD cause disturbance to uric acid levels.Lekishvili T, Sassoon J, Thompsett AR, Green A, Ironside JW, Brown DR.
Department of Biology and Biochemistry, University of Bath, Claverton Down, Bath, BA2 7AY, UK.

Bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-Jakob disease (vCJD) are two new members of the family of neurodegenerative conditions termed prion diseases. Oxidative damage has been shown to occur in prion diseases and is potentially responsible for the rapid neurodegeneration that is central to the pathogenesis of these diseases. An important nonenzymatic antioxidant in the brain is uric acid. Analysis of uric acid in the brain and cerebrospinal fluid (CSF) of cases of BSE and CJD showed a specific reduction in CSF levels for both BSE and variant CJD, but not sporadic CJD. Further studies based on cell culture experiments suggested that uric acid in the brain was produced by microglia. Uric acid was also shown to inhibit neurotoxicity of a prion protein peptide, production of the abnormal prion protein isoform (PrP(Sc)) by infected cells, and polymerization of recombinant prion protein. These findings suggest that changes in uric acid may aid differential diagnosis of vCJD. Uric acid could be used to inhibit cell death or PrP(Sc) formation in prion disease.

PMID: 15473996 [PubMed - indexed for MEDLINE]
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Postby CureOrBust » Wed Jan 10, 2007 7:03 pm

LisaBee wrote:It is one of the rare cases where there is actual human epidemiological evidence and studies in the MS animal model possibly support each other. There is an additional study in which Copaxone was shown to raise uric acid and it was suggested as one of the mechanisms of actions of Copaxone. Yet, other than one 2004 German review article, I can find nothing specifically published on uric acid and MS since 2002. That was five years ago!

This article was a human trail with inosine from 2001 to 2004.
Therapeutic value of serum uric acid levels increasing in the treatment of multiple sclerosis

The full copy of the article is floating about
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this bowl is too small!

Postby jimmylegs » Wed Jan 10, 2007 8:31 pm

hi i agree it's not the most clear thing in the world, yikes! anyway i think at the end of the day the answer is finding out which bowl of uric acid porridge is just right.
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food and function

Postby jimmylegs » Thu Jan 11, 2007 7:55 am

just re-reading the big fancy abstract above and enjoying things like:

However, for long it was not fully accepted that food can have an influence on brain structure ...most micronutrients (vitamins and trace-elements) have been directly evaluated in the setting of cerebral functioning... the use of glucose by nervous tissue implies the presence of vitamin B1... Vitamins B6 and B12, among others, are directly involved in the synthesis of some neurotransmitters... Adolescents who have a borderline level of vitamin B12 develop signs of cognitive changes. In the brain, the nerve endings contain the highest concentrations of vitamin C in the human body (after the suprarenal glands). Vitamin D (or certain of its analogues) could be of interest in the prevention of various aspects of neurodegenerative or neuroimmune diseases. Among the various vitamin E components (tocopherols and tocotrienols), only alpha-tocopherol is actively uptaken by the brain and is directly involved in nervous membranes protection. Even vitamin K has been involved in nervous tissue biochemistry. Iron is necessary... for the synthesis of neurotransmitters and myelin... Iron deficiency anaemia is common, particularly in women... Magnesium plays important roles in all the major metabolisms: in oxidation-reduction... Among many mechanisms, manganese, copper, and zinc participate in enzymatic mechanisms that protect against free radicals... Indeed, nutrient composition and meal pattern can exert either immediate or long-term effects, beneficial or adverse.
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Postby LisaBee » Thu Jan 11, 2007 5:14 pm

Thanks, Cure!

I don't know why it didn't come up in my search. I couldn't download the article but I found the Pubmed abstract with the info you provided, it looks like a study by Toncev (2006) open label (I guess), administering inosine at 1-2 g daily. Duration of the the study was decent, mean of 37 months. Total of 64 patients, 32 treated subjects and 32 controls matched on age, gender, duration of disease and disability. Significantly lower relapse rate in the inosine treated group, significantly lower EDSS score in the treated group, and no adverse effects in the treated group.

Hats off to this study author. Somebody did it! Of course, it isn't blinded and may have other flaws, but given the side effects of the CRABs, those trials weren't truly blinded either in my opinion. My next burning question is - is insosine better than a CRAB?? It is certainly much much cheaper and easier to take. Is it safer? Don't know. That would, as always, take more study. Here it is - yet more fun abstracts for Jimmylegs!
^^^^^^^^^^^^^^^

: Vojnosanit Pregl. 2006 Oct;63(10):879-82. Links
Therapeutic value of serum uric acid levels increasing in the treatment of multiple sclerosis.Toncev G.
Clinical Center Kragujevac, Center of Neurology, Kragujevac, Srbija.

BACKGROUND/AIM: Uric acid was successfully used in both, prevention and treatment of the animal model of multiple sclerosis (MS). Recently it has been shown that inosine, a ribosylated precursor of uric acid, might be used to elevate serum uric acid levels in MS patients. The aim of this study was to evaluate the safety and efficacy of oral inosine as a single drug treatment in patients with MS. METHOD: We administered inosine orally to 32 MS patients from 2001-2004 year at doses from 1-2 g daily (given twice) depending on the pretreatment serum uric acid levels. The mean follow-up interval was 37.69+/-6.55 months. The other 32 MS patients, without any treatment except for a relapse period (matched by age, sex, duration of disease and functional disability), were used as controls. The follow-up interval of these patients was 36.39 +/- 2.68 months. The neurological disability was evaluated by the Expanded Disability Status Scale score (EDSS). RESULTS: During the observed period the treated MS patients were found to have the lower relapses rate than the non-treated MS patients (Chi-square test, p = 0.001). None of the patients have showed any adverse effect of inosine treatment. The non-treated MS patients were found to have a higher increasing in the mean EDSS score than the treated ones (two-way ANOVA-repeated measures/factor times, p = 0.025). CONCLUSION: Our results suggested that the treatment approaches based on the elevation of serum uric acid levels might prove beneficial for some MS patients.

PMID: 17121380 [PubMed - in process]
^^^^^^^^^^^^^^^
Here's an earlier paper by the same author leading into the later study...


^^^^^^^^^^^^^^

1: Eur J Neurol. 2002 May;9(3):221-6. Links
Serum uric acid levels in multiple sclerosis patients correlate with activity of disease and blood-brain barrier dysfunction.Toncev G, Milicic B, Toncev S, Samardzic G.
Center of Neurology, Clinical Hospital Center Kragujevac, Svetozara Markovica, Yugoslavia. gtoncev@ptt.yu

Several findings suggest lower levels of serum uric acid in multiple sclerosis (MS) patients. The aim of this study is to investigate relationships of uric acid serum levels in relapse-remitting (RR) MS patients with clinical activity of disease and blood-brain barrier (BBB) condition. Sixty-three definite RRMS patients and 40 controls divided into two groups: 20 healthy donors and 20 patients with other inflammatory neurological diseases (OINDs) were analysed. By using a quantitative enzymatic assay according to the manufacture's protocol and a commercial uric acid standard solution, serum uric acid levels were measured and the results were standardized. To investigate BBB function, magnetic resonance imaging after administration of gadolinium was used. MS patients were found to have significantly lower serum uric acid levels (193.89 +/- 49.05 micromol/l; mean value +/-SD) in comparison with healthy donors (292.7 +/- 58.65 micromol/l; P=0.000) and OIND patients (242.7 +/- 46.66 micromol/l; P=0.001). We found that MS patients with relapse had significantly lower serum uric acid levels (161.49 +/- 23.61 micromol/l) than MS patients with remission (234.39 +/- 41.96 micromol/l; P=0.000) and more over, MS patients with BBB disruption had significantly lower serum uric acid levels (163.95 +/- 26.07 micromol/l) than those with normal BBB (252.48 +/- 25.94 micromol/l; P=0.000). Further, we also found that serum uric acid level independently correlated with disease activity, BBB disruption, and gender. These results indicate that lower uric acid levels in MS patients are associated with relapse and suggest that uric acid might be beneficial in the treatment of MS.
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more abstracts

Postby jimmylegs » Thu Jan 11, 2007 5:52 pm

heya, thanks hehehe i think i must have read all these already lol
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Re: Attn: Jimmylegs Re: Uric Acid

Postby NHE » Fri Jan 12, 2007 8:56 am

Thanks for all of the insightful discussion. It has certainly sparked my interest. It seems that having levels which are "just right" are the key. I checked the results of my last blood test which I get done once a year when I renew my Avonex prescription and I did not see uric acid listed. The test results included a CBC, a Comp. Metabolic Panel, and a Lipid Panel. Is there a specific test that must be requested for uric acid and/or is it typically included within a broad panel of tests such that I can maximize the amount of information I get back from my blood work?

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testing your bowl

Postby jimmylegs » Fri Jan 12, 2007 10:24 am

hey NHE glad you got something out of it.

i don't think uric acid typically comes in a panel of associated tests.

on my results it comes back as "ua" sort of like how creatinine comes back as "cr"... they like to save ink or paper space or something (or just try to confuse ppl hehe).

here's the lab info from the resource i use, which typically tells you when there is a group of associated tests to be done:
http://labtestsonline.org/understanding/analytes/uric_acid/test.html but it just has uric acid by itself.
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let's start a lobby

Postby jimmylegs » Fri Jan 12, 2007 10:31 am

i think we should set about initiating a protocol for a standard panel of testing for ms patients that includes markers like D3, B-complex, uric acid, etc etc. so that you get baseline information on your status before you ever start taking your rebif or avonex or whatever!

we can write a letter in common, and all sign it, and then all send it to our respective ms clinics!
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Re: Attn: Jimmylegs Re: Uric Acid

Postby NHE » Fri Jan 12, 2007 10:35 am

Thanks. Here's another article I found. Although this was a really small sample size, it seems that men and women might differ somewhat in their uric acid levels associated with MS attacks.
    Serum uric acid levels in optic neuritis
    Mult Scler. 2004 Jun;10(3):278-80.

    Uric acid, an antioxidant, is reduced in multiple sclerosis (MS). Patients with gout have a reduced incidence of MS. Optic neuritis (ON), often the first manifestation of MS, is not known to be associated with reduced uric acid. Patients with recent onset of ON were investigated to determine whether uric acid levels were reduced at presentation. Twenty-one patients with ON were included, 17 females and 4 males. The mean (SD) serum uric acid in the ON female group was 184.4 (±55.1) mmol/L (range, 116- 309 mmol/L), whilst in the control group it was 235.2 (±50.2) mmol/L (range, 172- 381 mmol/L). The difference was statistically significant (x2 = 8.93, P = 0.003). In the small male cohort, mean (SD) serum uric acid was 305 (±52.1) mmol/L, whilst in the control group it was 328 (±80.4) mmol/L. These differences were not statistically significant. Reduced antioxidant reserve is possibly an early patho genic mechanism in inflammatory demyelination, and raises the possibility that low uric acid levels could be an indicator of disease activity. Since optic neuropathies of other causes were not investigated, future research needs to determine whether low uric acid represents a unique feature of optic neuritis or is seen in other optic neuropathies.

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4??

Postby jimmylegs » Fri Jan 12, 2007 10:43 am

hey there, yea i don't think the male sample size was big enough for them to draw conclusions about statistical significance, or lack thereof. but that doesn't mean there aren't differences between men and women. it would be interesting to see a nice 20 million patient study on that bad-boy hehehe
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