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hiyas, i have had all these sources posted to the uric acid page on wikipedia for quite some time now, but for those who don't have access to read source full-text, here are some excerpts:
MS patients were found to have significantly lower serum uric acid levels (193.89 ± 49.05 µmol/l; mean value ±SD) in comparison with healthy donors (292.7 ± 58.65 µmol/l; P = 0.000) and OIND (jimmy: "other inflammatory neuro disease") patients (242.7 ± 46.66 µmol/l; P = 0.001). We found that MS patients with relapse had significantly lower serum uric acid levels (161.49 ± 23.61 µmol/l) than MS patients with remission (234.39 ± 41.96 µmol/l; P = 0.000) and more over, MS patients with BBB disruption had significantly lower serum uric acid levels (163.95 ± 26.07 µmol/l) than those with normal BBB (252.48 ± 25.94 µmol/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.
The overlap between uric acid levels in those with and without gout is shown in a study in which the lowest level in a gouty subject was 6 mg/dL, while the highest uric acid in a nongouty person was 9.5 mg/dL.
citation:
Seegmiller JE, Laster L, and Howell RR, “Biochemistry of Uric Acid and its Relation to Gout,” N Engl J Med, 1983, 268:712-6
You are correct Jimmy wife's levels are quite low as you mention, I am waiting the inosine from USA and will give her this week in order to increase her uric acid above 200µmol/L!
And I thought 2.9mg/dL is normal...
We had his uric acid levels tested at start, which were low (below 3.6 mg) He is now high/normal (around 8 mg) He has blood work every 3 months, and this is part of the test. He has had a good year...no relapse, no progression. He was taking 2mg daily, now is taking 1mg. We'll have levels checked again in June.
that is really great that he's had a good year re: relapse and progression! and really smart to have quarterly bloodwork.
i guess he's still safe from gout, if one can go as high as 9.5 and not have it
Joined: Jul 28, 2005 Posts: 1272 Location: Sydney, Australia
Posted: Mon Apr 21, 2008 3:03 am Post subject:
I had a blood test last Monday, and just got the results back.
One thing that was a question in my mind is how quickly the effect of inosine was on my Uric acid, and if I could control it at all. So, on the day, I took 1.5g in the morning and another 1.5g a few hours before the blood draw (normally I take 1g twice a day). I know a sample size of one isnt too much to go off, but the results indicate that it may of had an effect.
My previous 3 results have been (Units are mmol/L, with a reference range of 0.20 to 0.46):
16/05/06 0.27
05/01/07 0.43
01/10/07 0.38
My last result was:
15/04/08 0.47
The first reading I had after my MS Dx was below the reference range (i.e. below 0.2). For my next test, I may try skipping the inosine for the day, and maybe the day before.
CURE I believe optimal dose is 2mg and less if you can't have frequent blood tests, it's better to incease gradually your uric acid rather take huge inosine doses and be in risk of gout.
One week before I started wife's daily inosine supps, first days 1gr, now she takes 2grs.
Hope it will work as does in animals (mices, pigs).
so sounds like cure is right on track at 1mg 2x per day in the normal routine. i will keep this in mind for if i ever get around to taking inosine myself :S
maybe one more crappy result will tip me over the edge?
Purinergic modulation of microglial cell activation :
Abstract Microglial cells are resident macrophages in the brain and their activation is an important part of the brain immune response and the pathology of the major CNS diseases. Microglial activation is triggered by pathological signals and is characterized by morphological changes, proliferation, phagocytosis and the secretion of various cytokines and inflammatory mediators, which could be both destructive and protective for the nervous tissue. Purines are one of the most important mediators which regulate different aspects of microglial function. They could be released to the extracellular space from neurons, astrocytes and from the microglia itself, upon physiological neuronal activity and in response to pathological stimuli and cellular damage. Microglial activation is regulated by various subtypes of nucleotide (P2X, P2Y) and adenosine (A1, A2A and A3) receptors, which control ionic conductances, membrane potential, gene transcription, the production of inflammatory mediators and cell survival. Among them, the role of P2X7 receptors is especially well delineated, but P2X4, various P2Y, A1, A2A and A3 receptors also powerfully participate in the microglial response. The pathological role of microglial purine receptors has also been demonstrated in disease models; e.g., in ischemia, sclerosis multiplex and neuropathic pain. Due to their upregulation and selective activation under pathological conditions, they provide new avenues in the treatment of neurodegenerative and neuroinflammatory illnesses.
Receptor-Mediated Interaction Between the Sympathetic Nervous System and Immune System in Inflammation
(1) Department of Surgery, UMD-New Jersey Medical School, Newark, NJ, 07103
Abstract The sympathetic nervous system plays a central role in establishing communication between the central nervous system and the immune system during inflammation. Inflammation activates the sympathetic nervous system, which causes release of the transmitters of the sympathetic nerv-ous system in the periphery. The transmitters of the sympathetic nervous system are the cate-cholamines noradrenaline and adrenaline and the purines ATP, adenosine, and inosine. Once these transmitters are released, they stimulate both presynaptic receptors on nerve terminals and post-synaptic receptors on immune cells. The receptors that are sensitive to catecholamines are termed adrenoceptors, whereas the receptors that bind purines are called purinoceptors. Stimulation of the presynaptic receptors exerts an autoregulatory effect on the release of transmitters. Ligation of the postsynaptic receptors on inflammatory cells modulates the inflammatory ac-tivities of these cells. The present review summarizes some of the most important aspects of the current state of knowledge about the interactions between the sympathetic nervous system and the immune system during inflammation with a special emphasis on the role of adreno and purinoceptors.
so sounds like cure is right on track at 1mg 2x per day in the normal routine. i will keep this in mind for if i ever get around to taking inosine myself :S
maybe one more crappy result will tip me over the edge?
Just for your info Jimmy wife's uric acid levels are now at 344 µmol/L (5.8 mg/dL) exactly double than before a month with 2X1gr/day inosine supplementation, which means her levels are in the "optimal for MS without inducing gout" zone - PERFECT!
I start give her 1gr/day every other day in case her levels go sky high.
My problem now is that I can't lower her hepatic enzymes although she takes all the antioxidants, choline, sylibum, dandelion etc next week (hope) I'll receive the N-acetyl cysteine that helps liver function!
But she had blood tests 6 days after a bacterial (or virus) infection, could this be the reason for the levated enzymes?
Where are you Cheerleader when I need you, what did you do with your husband to lower his liver enzymes?
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