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Microcrystal synovitis - Monosodium urate crystal deposition esp in joints, kidneys and other soft tissue
caused by chronic hyperuricaemia (urate >450)
typically mono-arthritis (esp 1st MTP in foot)
M=F post 60yrs, pre-men F less
esp african
inc with age
dietary component

Uric acid crystal depostis are tophi which grow and cause bone erosion and painful damage
 
Uric acid is end product of purine metabolism, produced by liver and excreted by kidney
90% gout - due to difficulty excreting urate, 10% due to overproduction
may have hyperuricaemia for 20 yrs before Sx start
 
aSx - urate usually coated with apolipoprotein so don't bind to cell surface, in gout this gets dissolved off and an immune response follows - so Rx recoats the urate and Sx resolve
 
''risk factors''
envt, diet, genetics
obesity and insulin resistance may contribute
drugs - aspirin, diuretic
 
''Clinical criteria''
1st MTP involved
severe joint pain develops over 6-12 hrs
swelling, tender, erythema
self limiting - resolves completely
tophus
 
''Ix''
serum urate not in acute phase (Sx due to acute change in urate level - so dec impt as well), WCC and CRP may be useful acutely
TG LDL - associated with gout
fasting glc
baseline U/E
24 hr urine for urate (over excretors of urate won't respond to uricosuric therapy, most pts with high serum levels are unable to excrete)
?MC&S of joint fluid if thinking sepsis
 
''2ndary gout''
underexcretion - hypothyroid, hyperparathyroid, nephropathy, dehydration, chronic alcohol, drugs (thiazides)
overproduction - diet, obese, high cell turnover, myeloproliferation, psoriasis, chemo, anaemia (haemolytic and pernicious), xs exercize
 
''Treatment'' - do NOT treat aSx hyperuricaemia
''Acute'' therapy - NSAID, Intra-articular steroids, Colchicine, prednisolone (all 2/52 and taper)
''Prophyllaxis'' - if >2 attacks per year (high urate), start >2/52 after acute phase, uricosuric (Probenecid, amlodipine, atorvastatin, Losartin), Xanthine oxidase inhibitors (Allopurinol) aim - minimise morbidity and decrease disabling end organ damage - use with thought  of SE with age
reduce urate load (avoid liver, kidney, seafood, oily fish, yeast)
lifestyle - reduce alcohol and weight
 
''Colchicine''
slow onset action
80% GI SE (usually diarrhoea)
avoid if eGFR <60 (or half dose)

''Allopurinol''
can precipitate attack if start early (<2/52 after acute)
Initial 100mg od and inc till urate <300
cover start with NSAID or colchicine
use if >2 attacks in year, tophi, renal disease, urate stones, on cytotoxics or diuretics

Allopurinol
use if tophi, Xray changes, 2+ attacks /yr, uric acid nephropathy or stones
cover start with NSAID for 1-3/12 - until hyperuricaemia is corrected (to avoid ppt an attack)
if attack on allopurinol keep dose same until resolved and then titrate up
SE - rash diarrhoea nausea
also .... lots !
 
alternative -
Febuxostat (beware liver disease and CCF)
Probenecid - fewer SE, less effective, avoid if renal stones / impaired, on aspirin and with CCF as need to drink lots
Other drugs (above) are all mildly uricosuric
 
Diet
liver, kidney, red meat, herring, sardines, salmon
tomatoes, celery, new potatoes, spinach, strawberries
Caviar, Beer,
 
10% initial presentation is polyarticular (esp elderly women with renal impariment)
In time attacks are generally less severe but more frequent and prolonged
more proximal and polyarticular
 
Renal stones
more common in gout esp pure uric acid stones
leads to renal impairment
 
Tophi
acute gout linked to mental health issues - renal failure and arthritis
documented in all tissues except brain