Crystal Arthropathy

Crystal Arthropathy

Gouty Arthritis

·        Prevalence: ½ - 1%, male:female = 5:1. Common in Maori and Polynesian populations. Most people with hyperuricaemia don‟t have gout

·        Family history common

·        Types:

o  Acute Gout:

§  Severe pain, redness and swelling, may be febrile

§  Differential of acute gout: septic arthritis or haemarthrosis

o  Chronic Recurrent Gout: 

§  Urate deposits with inflammatory cells surrounding them (tophi) in avascular areas: pinna, infra-patella and Achilles tendons, joints, eye, etc Þ chronic tophaceous gout = gouty tophi

§  Bone erosion and loss of cartilage

·        Distribution:

o  Acute gouty arthritis is usually monoarticular

o  Affects MTP joint of the great toe in 75% of cases

o  Ankles and knees involved after recurrent attacks

o  Fingers, wrists and elbows affected late

·        Pathogenesis:

o  Uric acid is the last step in the breakdown of purines 

o   Hyperuricaemia (uric acid > 0.41 mmol/L) ® deposition of monosodium urate crystals (MSU) in joints (and viscera, especially the kidney) ® chemotactic to leukocytes and activate complement ® accumulation of neutrophils and macrophages ® erosion, inflammation, secondary OA 

o  May be precipitated by trauma, surgery, starvation, infection and diuretics 

o  Hyperuricaemia results from ­ turnover or ¯ excretion

o  Causes of ¯ excretion:

§  Primary gout 

§  Renal failure ® hyperuricaemia which rarely ® gout

§  Hypertension

§  Primary hypoparathyroidism

§  Hypothyroidism

§  ­Lactic acid production (eg from ETOH)

o   ­ Cell turnover (®­turnover of purines) due to:

§  Lymphoma, leukaemia, severe psoriasis, haemolysis, muscle necrosis

§  Disorders of purine synthesis (eg Lesch-Nyhan syndrome)

o   Hyperuricaemia can also cause renal failure eg cytotoxic treatment

·        Diagnosis: 

o   Needle shaped, negatively birefringent urate crystals in tissues and synovial fluid (serum urate not always ­) – also neutrophils (+ ingested crystals)

o   ­ESR

o   Check renal function and BP

o   X-rays: in early stages may only show soft tissue swelling

·        Treatment:

o   Acute: 

§  NSAID (eg ibuprofen, Naproxen, indometacin, not aspirin) – but problematic in renal failure and heart failure (® fluid retention). Also contra-indicated if on anticoagulants (® GI bleed) 

§  Colchicine

o   Prevention: 

§  Avoid purine-rich foods (offal, oily fish, beer), ¯ obesity and excess alcohol (which is why it used to be called the „disease of kings‟) 

§  No aspirin: salicylates competes with uric acid for excretion ® ­serum urate

§  Long term („interval‟) treatment: Allopurinol:

·        Xanthine-oxidase inhibitor ® ¯serum urate 

·        But not during an acute attack – wait three weeks. Mobilises gouty tophi ® ­systemic urate ® precipitates acute gout. Use with colchicine cover 

·        SE: rash, fever, ¯WCC 

·        Allopurinol can also be used during chemotherapy for leukaemia/lymphoma/myeloma to prevent gout from ­purines

·        Also uricosuric drugs (® ­excretion): probenecid or sulfinpyrazone

Pseudogout

·        = Calcium Pyrophosphate Deposition (CPPD)

·        Onset in 30s

·        Deposition of chalky white crystalline material – usually calcium pyrophosphate 

·        ® Chondrocalcinosis: deposition in articular cartilage ® calcification on x-ray

·        Predominantly large joints (especially the knees)

·        Aspirate: positively birefringent rhomboid shaped crystals

·        In some there are signs of hyperparathyroidism and haemochromatosis