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Uric acid, which is the final product of purine nucleoside metabolism, is a strong peroxynitrite scavenger. Several studies report on lower serum uric acid levels in multiple sclerosis. In this study, we investigated serum uric acid levels before and after high-dose methylprednisolone treatment (intravenous 1 g/day/5 days) in multiple sclerosis patients. Blood samples from 25 definite multiple sclerosis patients (11 male and 14 female) before and after methylprednisolone treatment (days 0, 6 and 30) and from 20 healthy donors (9 male and 11 female) were analyzed. Serum uric acid levels were measured using a quantitative enzymatic assay (Elitech diagnostics, Sees, France) according to the manufacturer's protocol, and the results were standardized using a commercial uric acid standard solution. We observed significantly increased serum uric acid levels 1 day after the termination of the therapy (day 6). These differences were sustained for 30 days after starting treatment (during remission period). Mean serum uric acid levels were significantly higher in the control group. These results suggest that increasing the uric acid concentration may represent one of the possible mechanisms of action of methylprednisolone in multiple sclerosis.
next bit is from "http://en.wikipedia.org/wiki/Methylprednisolone"
Methylprednisolone (molecular weight 374.4 is a synthetic glucocorticoid drug which is usually taken orally. It's chemical name is pregna-1,4-diene-3,20 -dione, 11,17,21-trihydroxy-6-methyl-,(6α, 11β)- and its chemical formula is C22H30O5.
Like most adrenocortical steroids, methylprednisolone is typically used for its anti-inflammatory purposes. However, glucocorticoids have a wide range of effects, including changes to metabolism and immune responses. The list of medical conditions for which methlyprednisolone is rather large, and is similar to other corticosteroids such as prednisolone. Common uses includes arthritis therapy and short-term treatment of bronchial inflammation due to various respiratory diseases. It is used both in the treatment of acute periods and long-term controlling of autoimmune diseases, most notably SLE.
Methylprednisolone has serious side effects if taken long-term, including weight gain, glaucoma, osteoporosis and psychosis, especially when overdosed. The most serious side effect occurs after the kidneys cease natural production of cortisone, which methylprednisolone will replace. Abrupt cessation of the drug after this occurs can result in a condition known as Addisonian crisis, which can be fatal. To prevent this, the drug is usually prescribed with a tapering dosage, including a pre-dosed "dose pack" detailing a specific number of pills to take as designated times over a six day period.
Alternative treatments to many of the conditions currently indicated for methlyprednisolone are actively being researched. Additionally, new drugs such as budesonide are being created, which provide similar benefits but without the adrenal suppression problems.
***jimmy wonders if this is why liver extract has been used in some earlier ms treatment protocols...***
hi again, i know there have been many more postings about uric acid on more recent threads than this one, but here's an update. when i said above that my level was normal, "luckily", that was before i knew that there was a "normal range" normal, as opposed to an "ms average" and a "healthy controls average". now i know that i've been stuck at or below the ms average the whole time since diagnosis. in spite of trying to up the high purine foods.
i've just made the connection, (though i might have run across it before unawares) that zinc status and uric acid have a relationship. and since my zinc has been quite a bit lower than the bottom end of the normal range, i had a quick scout for connections between zinc and UA, with this result:
Quote:
Effect of Zinc Deficiency on Urinary Excretion of Nitrogenous Compounds and Liver Amino Acid-catabolizing Enzymes in Rats
The effect of dietary zinc deficiency in rats on the levels of urinary nitrogen, urea, uric acid, and creatinine was studied. Zinc deficiency substantially increased urinary excretion of total nitrogen. The amount of urea excretion of zinc-deficient rats was approximately 42 and 87% more than that of zinc-supplemented pair-fed and ad libitum-fed rats, respectively. Zinc-deficient rats also showed significantly higher excretion of uric acid. No difference was observed in creatinine excretion between zinc-deficient and zinc-supplemented groups. Further studies demonstrated that zinc-deficient rats had increased activities of liver tryptophan pyrrolase and arginase. The activities of liver threonine dehydratase and serine dehydratase were unaffected by zinc deficiency. Overall findings support in principle the concept that zinc deficiency results in an increased protein catabolism and also indicate that the hepatic amino aciddegrading enzymes may be one of the possible regulating sites involved in the protein metabolism of rats.
if i have anything in common with rats, hopefully all this zinc supplementing i've been doing will show up in my next UA result too. hope so!
Joined: Sep 11, 2007 Posts: 507 Location: southern California
Posted: Tue May 13, 2008 5:18 pm Post subject:
Thanks for the zinc connection, JL. You always connect the dots
I hopped on the inosine bus at the beginning of our MS tour. I'd read all about the antioxidant, peroxynitrite-inhibited benefits of increasing uric acid in MSers. Interesting side note, Copaxone increases uric acid, and some think this is a large part of how it works in RRMS. Interferons do not change serum UA levels.
I've been taking 2g of inosine pretty much every day for the last 3 to 4 years and this didn't stop my last 2 relapses but these were, I aver, stimulated by drugs/infrared sauna use...What dose do others suggest for inosine? _________________ 1st traceable symptoms Jan 01, last edss by doctor 6.5. Feeling better on capsaicin, scutellaria, salvia, high dose curcumin
GG cure or bust takes inosine too but i'm not sure what dosage, although i'm pretty sure that's been posted in the past - maybe he'll notice this thread and re-post
i haven't been taking any inosine, just tried to eat more high purine foods but it hasn't worked to raise my serum UA yet.
maybe with the zinc deficiency addressed it will climb. if not, i think inosine supplementation will be in my future!
Joined: Jul 28, 2005 Posts: 1135 Location: Sydney, Australia
Posted: Thu May 15, 2008 5:17 am Post subject:
jimmylegs wrote:
GG cure or bust takes inosine too but i'm not sure what dosage, although i'm pretty sure that's been posted in the past - maybe he'll notice this thread and re-post
I also take 2g a day normally, and it hasn't stopped me from having relapses either. However, since starting (3+y ago) my uric acid levels have been in the high normal range. On my last blood test, I took 3g on that day, and I just pushed over into above normal.
Before I started taking inosine, my uric acid was below the reference range considered normal by the processing lab.
gibbledygook wrote:
What dose do others suggest for inosine?
In the study I have, done in serbia, they were given 1g-2g given daily, dependent on their starting uric acid levels.
it will be interesting to see whether my zinc supplementation can help boost the uric acid level when i next get some bloodwork done. i wonder if anyone has ever looked at dietary or supplementary zinc absorption and levels, in patients supplementing with inosine?
My wife takes the last 5 months 50mg zinc daily and this hasn't increase her uric acid levels!
On the other hand inosine isn't a medicine so why you expect from it to completely stop your relapses, it helps with one or other way but seems very optimistic if it could stop relapses!
interesting, has she been supplementing inosine too? if so, in what amounts and for how long? what was her UA level before, and what is it now?
i'm also curious as to your wife's zinc level prior to supplementing 50mg per day for 5 months? was she actually deficient? what is her zinc level now?
i'm asking in order to assess starting and ending levels of zinc and UA in your wife's case, for comparison to my case once i have some current post-zinc-treatment bloodwork.
it looks like a complicated bit of reading to back up these statements succinctly with easy abstracts, but in the meantime:
Quote:
Multiple Sclerosis
Recommendation Test Serum Uric Acid Levels
"...Uric acid levels should be monitored and, if low, raised by supplemental molybdenum and reducing any copper toxicity..."
Copper Toxicity
"Since high levels of copper in the body or diet may result in molybdenum insufficiency and cause low uric acid levels, reducing copper toxicity can result in normalizing uric acid and molybdenum levels..."
"Zinc and manganese with vitamin C remove copper from the tissues..."
Approximately 12% of Americans do not consume the estimated average requirement for zinc and could be at risk for zinc deficiency. Since zinc has proposed antioxidant function, inadequate zinc consumption may lead to an enhanced susceptibility to oxidative stress through several mechanisms, including altered antioxidant defenses. In this study, we hypothesized that dietary zinc restriction would result in lower antioxidant status and increased oxidative damage.
Collectively, zinc deficiency increased oxidative stress, which may be partially explained by increased CYP activity and reductions in hepatic alpha-tocopherol and gamma-tocopherol and in plasma uric acid.
interesting, has she been supplementing inosine too? if so, in what amounts and for how long? what was her UA level before, and what is it now?
i'm also curious as to your wife's zinc level prior to supplementing 50mg per day for 5 months? was she actually deficient? what is her zinc level now?
i'm asking in order to assess starting and ending levels of zinc and UA in your wife's case, for comparison to my case once i have some current post-zinc-treatment bloodwork.
cheers
Her UA levels were quite low 2.9 (1.9-7) but probably in the "normal" MS range.
She hasn't had ever a zinc test but I guess it is at least normal if not above.
There is a zinc taste test that every one can do by himself but haven't tried it yet.
This Saturday she has her blood tests for UA, B, D, hormones, hepatic enzymes etc so I'll tell you.
I expect her UA to be @ 4.5-5 range.
Go for it Jimmylegs! As I keep saying...what in the hell do you have to lose??? And gee, it just might help (as it has for my daughter and you!) Someone just might find that proverbial needle in the haystack. Why not you?
Joined: Feb 10, 2006 Posts: 305 Location: Northern Virginia
Posted: Wed May 21, 2008 8:37 pm Post subject: ...... annnnnndddd
bromley wrote:
ABX has worked for Sarah and some others
..... and who has had a long-term sustained reversal of disability on Avonex, Betaseron, Copaxone or Rebif?
Has anyone done better than Sarah on one of those.
I honestly don't understand what seems to me to be a double standard. I'm not looking for an argument and my typing can't express my quizical feeling. I just want to be clear that I'm not trying to be a smart ***.
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is a synthetic glucocorticoid drug which is usually taken orally. It's chemical name is pregna-1,4-diene-3,20 -dione, 11,17,21-trihydroxy-6-methyl-,(6α, 11β)- and its chemical formula is C22H30O5.
