Crystal Arthritis: Gout

Question 1

Definition

Answer 1

Inflammatory arthritis: Chronically high blood uric acid. Monosodium urate crystals are deposited in the joint causing it to become hot = most commonly in first metatarsophalangeal joint (MTP) = Swollen and painful

Question 2

Epidemiology

Answer 2

Male
Increases with age (rare under 20) : 40-60

Question 3

Risk factors

Answer 3

Obesity
Purine rich diet: meat, seafood, alcohol
Cytotoxic drugs
Lesch-Nyhan syndrome: X-linked
Severe psoriasis
CKD
Diuretics
Pyrazinamide
Lead toxicity

Question 4

What food can be anti-gout?

Answer 4

Dairy

Question 5

Aetiology

Answer 5

Urate overproduction (10%)
- Increased consumption
- Chemotherapy
- Obesity
- Psoriasis (increased cell turnover)
Reduced excretion of urate (90%)
- CKD
- Dehydration
- Alcohol consumption
- Diuretics/Aspirin

Question 6

Pathophysiology

Answer 6

Urate = metabolite of purine synthesis and the incidence of gout increases with hyperuricaemia (uric acid > 0.45 mmol/L)
However the incidence can occur at completely normal urate levels
Uric acid has limited solubility in the blood. When there is too much uric acid in the blood it can become a urate iron + bind to sodium, leading to the formation of monosodium urate crystals which deposits in areas with slow blood flow, including joints and kidney tubules

Question 7

Signs

Answer 7

Joint inflammation: tenderness, erythema and swelling (sudden onset of hot, red, swollen toe)
Monoarticular or oligoarticular (≤ 4 joints):
- 1st MTP most commonly affected in a first presentation (70%);
- The ankle, wrist and knee are also commonly affected
Gouty tophi: nodular masses of urate crystals form, usually as a late complication
- Small joints + connective tissue of the hands (DIP)

Question 8

Why does gout tend to attack joints in extremities

Answer 8

Temperatures in feet and hands can be low enough to precipitate urate from plasma. This tophi typically form in the helix of the ear, fingertips

Question 9

Diagnosis

Answer 9

Exclude septic arthritis
Joint aspiration + polarised light microscopy: (GOLD STANDARD)
- No bacterial growth
- NEGATIVE BIFRINGENT NEEDLE SHAPED CRYSTALS
Joint x-ray:
- Earliest signs = bone effusions with relatively preserved joint space
- lytic lesions in the bone
- punched out erosions
- erosions can have sclerotic borders with over hanging edges
- absence of periarticular osteopenia (unlike rheumatoid arthritis)
Serum urate:
- Usually taken 4-6 weeks after the attack resolves as levels may be falsely low/normal during the attack as the urate is deposited within the joint. Hyperuricaemia does not confirm gout, nor does normal levels exclude gout

Question 10

Treatment

Answer 10

Acute:
- NSAIDS (FIRST LINE) + PPI
- Colchicine (when NSAIDS CI or in renal insufficiency)
- Corticosteroids: intra-articular (SECOND LINE)
Prevention:
- Xanthine oxidase inhibitor = ALLOPURINOL (FIRST LINE)
- FEBUXOSTATE (SECOND LINE)
* should begin 2 weeks after attack, if already on continue during attack *
Refractory cases: if ULT monotherapy options above do not achieve serum uric acid target
- Uricosuric agent: SULFINPYRAZONE or PROBENECID if normal renal function
- BENZBROMARONE if renal insufficiency
These drugs increase the excretion of uric acid in the urine

Question 11

Complications

Answer 11

Urate nephrolithiasis