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Old 02-28-2012
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Default Allopurinol

i read it might precipitate the attck thus its contraindicated for acute attacks of gout.
What is the mechanism though?
dont delete this post admin!
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Old 02-28-2012
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"Individual gout flares are often triggered by acute increases or decreases in urate levels that may lead to the production, exposure, or shedding of crystals that are not coated with apo B or apo E. This can result from acute alcohol ingestion, acute overindulgence in foods high in purines, rapid weight loss, starvation, trauma, or hemorrhage. Medications that increase uric acid levels via effects on renal tubular transport include diuretics and low-dose aspirin. Gout flares can also result from agents that lower levels of uric acid, including the use of radiocontrast dyes and medications such as allopurinol or uricosurics''
http://emedicine.medscape.com/article/329958-overview
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Old 02-28-2012
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Quote:
Originally Posted by LatinGeorge View Post
"Individual gout flares are often triggered by acute increases or decreases in urate levels that may lead to the production, exposure, or shedding of crystals that are not coated with apo B or apo E. This can result from acute alcohol ingestion, acute overindulgence in foods high in purines, rapid weight loss, starvation, trauma, or hemorrhage. Medications that increase uric acid levels via effects on renal tubular transport include diuretics and low-dose aspirin. Gout flares can also result from agents that lower levels of uric acid, including the use of radiocontrast dyes and medications such as allopurinol or uricosurics''
http://emedicine.medscape.com/article/329958-overview
ok thanks thats what i mentioned.
whats the mechanism
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The mobilization of urates from tissue deposits which lead to fluctuations in the serum uric acid levels may be a possible explanation for these attacks. As far as i understand, the sudden decrease of uric acid, causes a mobilization of urate from its deposits on tissue which exacerbates the acute attack.
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Thanks, LatinGeorge!

@kenlee: Did you even read the link LatinGeorge posted? Everything is in there.

- Clumps or microtophi of highly negatively charged and reactive urate crystals are normally coated with serum proteins (apolipoprotein [apo] E or apo B) that physically inhibit the binding of the crystals to cell receptors.

- Acute increases or DECREASE in urate levels (eg, Allopurinol in acute gout) lead to the production, exposure, or shedding of crystals that are not coated with apo B or apo E.

- Naked urate crystals (not coated with apo B or Apo E) are then believed to interact with intracellular and surface receptors of local dendritic cells and macrophages, serving as a danger signal to activate the innate immune system. --> acute attack of gout
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