What is gout?
A chronic disease which involves deposition of monosodium urate crystals into soft tissue, joints and kidney
What is the most important determinate of developing gout?
Serum uric acid concentration
-Incidence of gout increased exponentially when uric acid levels are >0.54mmol
BUT acute gout can occur with normal serum
What is uric acid?
Uric acid is the by product of purine metabolism that occurs in the liver
Purine sources are endogenous and dietary
What factors increase uric acid?
Eating purine rich foods such as
- Seafood
- Meat
- Alcohol (esp beer and spirits)
- Fructose sweetened drinks
Disorders of high cell turnover
- Haem malignancies
- Psoarisis
Anything that blocks renal excretion of uric acid
What can disrupt kidney uric acid excretion?
Drugs:
- Thiazide diuretics (common 2ndary gout)
- Loop diurectics
- Cyclosporins
Conditions: (are risk factors for gout))
- DM
- HTN
- Dyslipidemia
- CKD
- Obesity (because high insulin levels)
- Sepsis
- Dehydration
How does acute gout present?
Monoarticular (1st MTP or other part of foot)
- Red
- Swollen
- severe pain
- joint mobility may be limited
But can subside within days to weeks
How does chronic gout present?
- Can be oligoarticular or polyarticular
- Can have symmetrical involvement of small joints of hands (can mimic rheumatoid and psoriatic arthritis)
- Gouty tophi
- elbows (olecranon bursae)
- knees (prepatellar bursae)
- peripheral joints (fingers & toes)
What is the pathogenesis of chronic gout?
Recurrent attacks
Urate crystals deposit in soft tissue, joints, kidneys
Leads to joint arthritis and chronic kidney disease
What investigations would you do for gout?
a) Joint aspirate
b) Xrays
- show soft tissue swelling
- punched out lesions- erosions
c) serum uric acid concentration- but not diagnostic
What is the management of acute gout?
- NSAIDS: naproxen, ibuprofen, indomethacin
OR - Prednisone: 15-30mg PO for 3-5 days
OR
3.Corticosteroid injections: local max two sites
OR - Colchicine: 1mg PO initially then 500mcg 1 hour later as a single one-day course
What is required for definitive diagnosis of gout?
Joint aspirate
- show monosodium urate crystals
- negative birefringent and needle shaped
Once definite diagnosis made, diagnostic aspiration not needed for recurrent attacks
What is the management of chronic gout?
- First line urate lowering therapy
- Allopurinol monotherapy
- Allopurinol + Probenecid - Second line (when Allopurinol counter-indicated)
- Probenecid
- Febuxostat
What is the mechanism of action of allopurinol?
Xanthine oxidase inhibitor
Which inhibits the synthesis of uric acid
Purine–>hypoxanthine–>xanthine–>uric acid
What are symptoms of intolerance to allopurinol?
Rashes- maculapapular
Hepatotoxicity
Allopurinol hypersensitivity syndrome: fever, rash, hepatitis
When you have started patient on allopurinol, what needs to be measured and titrated?
In the first month the dose of allopurinol should be titrated with serum uric acid concentration
What is the target serum uric acid concentration for treatment with allopurinol?
- Serum Uric acid <0.36mmol/L
- If tophi present then target <0.30mmol/L
What is important in patient education when starting chronic gout treatment?
Life long adherence
The risk of flares when starting or increasing urate lowering therapy
What is the dose of allopurinol?
50mg PO daily for 4 weeks
- Then increase the dose by 50mg every 2-4 weeks Or
- Increase by 100mg every 4 weeks
BUT max dose 900mg daily
=To achieve the target uric acid concentration
If a patient has a acute flare whilst on chronic gout management how should it be treated?
Continue urate lowering therapy (allopurinol etc)
Add tx for acute gout flare (NSAID, colchicine, prednisone)
As there is a high risk of flares when starting or increasing urate lowering therapy, what can you do to minimise this risk?
Flare prophylaxis
- Colchicine 500mg daily once or BD OR
- NSAID PO OR
- Prednisone 5mg PO daily
Prophylaxis should be used for at least 6 months
