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Gout CPG 2009
Gout CPG 2009
GOUTY
ARTHRITIS
Based on 2009 Philippine Clinical Practice Guidelines for the Management of Gout
Philippine Rheumatology Association
Objectives
Introduction
01 Gouty Arthritis and its
Pathogenesis
Gout Medications
CPG 03 Mechanisms of actions
Recommendations
02 Based on PRA 2008
4
INTRODUCTION
Most uric acid circulates as the urate anion, and serum urate concentrations normally
approach the theoretical limit of serum urate solubility. Human tissues have a very limited
ability to metabolize urate; thus, uric acid must be eliminated by the kidney and the gut
to maintain urate homeostasis.
PURINES
A purine is an aromatic heterocycle
composed of carbon and nitrogen.
Hyperuricemia is defined as serum uric acid (SUA) level exceeding the limit of
urate solubility in the plasma, which is
Sensitivity 92%
Specificity 89%
PHASE 2
Acute Gouty Arthritis
● Lifestyle modifications
● Correct modifiable risk factors
● Start Colchicine 0.5mg BID to prevent future flares for 3-6 months
until normal SUA is achieved
Colchicine
Interferes with the inflammatory process by metaphase arrest
of multiplying Inflammatory Cells
Decreased Inflammation
NSAIDS
Inhibits COX
Inhibits PG synthesis
Reduces Inflammation
Gout Medications
Allopurinol and
Febuxostat
Xanthine Oxidase Inhibitors
Uricosurics
Probenecid inhibits the tubular reabsorption of urate, thus increasing the
urinary excretion of uric acid in the urine and decreasing serum urate
levels.