Crystal Arthropathy
·
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
§ ÂLactic
acid production (eg from ETOH)
o  Cell
turnover (®Âturnover 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
Â) – also neutrophils (+ ingested crystals)
o ÂESR
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 ® Âserum
urate
§ Long term („interval‟) treatment: Allopurinol:
· Xanthine-oxidase inhibitor ® ¯serum urate
· But not during an acute attack – wait three weeks. Mobilises gouty tophi ® Âsystemic 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 Âpurines
·
Also uricosuric drugs (® Âexcretion):
probenecid or sulfinpyrazone
·
= 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
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