GOUT

Introduction
Crystal associated disease can be
primary(true) or secondary.
Crystals:
Monosodium urate
monohydrate[GOUT],
Calcium pyrophosphate dihydrates,
Basic calcium phosphates
Cholestrol
Calcium oxalates

GOUT
True crystal deposition disease
Results in deposition of monosodium urate
crystals in the joints and soft tissues, with
accompanying inflammation and degenerative
consequences
Primary hereditary error of purine metabolism
{Male}
Secondary drugs that inhibit uric acid excretion
or increase rate of cell death or renal impairment
{Women}

Hyperuricaemia
Diminshed renal excretion(common)
Inherited isolated renal tubuler defect(underexcretors)
Renal failure
Chronic drug therapy:-Thiazide and loop diuretics,
low dose asprin, cyclosporin, pyrazinamide
Lead toxicity
Alcohol
Lactic acidosis
Hyperparathyroidsm
Myxedema

 Increase production
Increase turnover:--Chronic myeloproliferative or
lymphoproliferative disorders
Increase synthesis:--Idiopathic(common)
Enzyme defect---HGPRT and Gluc 6 phosphatase def
PRPP overactivity

Risk factors
Obesity
High alcohol
Type IV hyperlipoprotenemia,
hypertension, IHD
Unidentified tissue factors

Stages of classic gout

1. Asymptomatic hyperuricemia
2. Acute intermittent gout
3. Advanced gout (chronic tophaceous
gout)

Acute Gout
1st MTPPodagra
Painrapid, progressing, worst pain night/
early morning
Tender
Redness and swelling
Self limiting in 514 days
Fever, malaise, skin changes
Bursitis, tenosynovitis, cellulitis
Petite or cluster attacks..rare polyarticular.

 Acute attacks can be precipitated:

Increased alcohol consumption (especially beer)
Trauma
Use of diuretics
Dehydration
Cyclosporine
Diet (organ meat, shellfish)
Drugs that can lead to sudden changes
(increase or decrease) in urate levels, such as
hypouricemic agents

Intercritical
Asymptomatic between attack
Varies
Gradually decreases, more number
of joints, more severe

Chronic trophaceous Gout

Large MSUM crystals deposits
produce irregular firm nodules
tophi(white)
Ulcer---White gritty discharge--inflammation
Deformity and functional impairment

Other complication
Urolithiasis (uric acid) ppt by purine
overproduction, uricosuric drugs,
defects in tubular reabsorption ,
dehydration, low pH of urine
Chronic urate nephropathyMSUM
deposit inflammation , fibrosis,
glomerulosclerosis and sec
pyelonephritis

Investigation
CBC, ESR, Serum lipids
Joint aspirate/bursa/tophus---neutrophils
and MSUM crystals(polarisation microscope:
needle shaped and negatively birefringent)
Serum uric acid(6mg/dL)
24 hr urinary uric acid excretion(800mg)
RFT
Imaging: osteoarthritis to gouty erosions
SCORING8

Management

Recommendations From the 2012 American College of

Rheumatology Guidelines for Management of Gout
ACR recommends a comprehensive treatment plan for the management of gout,
including both nonpharmacologic and pharmacologic approaches
Patient education including diet and lifestyle modifications is recommended
along with the following pharmacologic approaches for the management of gout

Acute Gout Flares

Gout Flare Prophylaxis

Chronic Gout Management

Treat an acute gout

flare with
pharmacologic
therapy (NSAIDs,
corticosteroids, or
colchicine) within
24 hours of onset2

For gout attack prophylaxis, initiate

low-dose colchicine or low-dose
NSAIDs when initiating uratelowering therapy (ULT)2
Anti-inflammatory prophylaxis
should be continued from
initiation of ULT for the greater of2:
At least 6 months, or

When initiating ULT, begin

anti-inflammatory gout flare
prophylaxis1
Initiate first-line ULT, febuxostat
or allopurinol, or if at least one of
these is contraindicated or not
tolerated, probenecid can be used
to treat to sUA target of <6 mg/dL1
sUA should be monitored
regularly (every 2-5 weeks) during
ULT titration, then every 6 months
once target sUA is achieved1

Following achievement of
target serum urate, for
3 months in patients without
tophi or 6 months in patients
with tophi on physical exam

Acute Attack
Indomethacin(25-50mg tid), Naproxen (825mg ;
275mg 8th hrlyLD 250mg bid), Sulindac(200mg
bid), Diclofenac(50mgQID),ibuprofen(800mg tid),
celecoxib
Colchicine 1/1.2mg loading 0.5mg/0.6mg 6 th
hrly until symptoms abate(LD0.6mg OD or BID)
Corticosteroids : Prednisone 0.5mg/kg/day 510days and stop-2-5days taper in 7-10 days
-----LD-10mg/day
Triamcinolone60mg IM/IA

Hypouricaemic agentsLong term

management

Recurrent attack
Tophi
Evidence of bone and joint damage
Associated renal disease
Elevated uric acid and gout

Hypouricaemic agentsLong term

management
Xanthine oxidase inhibitor
Allopurinol 100mg-300mg OD xanthine
oxidase inhibitor titrated until uric acid<
6mg/dL ;6weekly-----6months
SE: rash, GI symtoms, headache, urticaria,
interstitial nephritis, hypersenstivity reaction.
Febuxostat 40-80mg OD
SE: include nausea, diarrhea, arthralgia,
headache, increased hepatic serum enzyme
levels and rash

 Uricosuric agents:
Probenecid 0.5-1g 12th hrly---alternate first line
Sulfinpyrazone 100mg 8th hrly, fenofibrate,
losartan
Note: Never use with asprin
CI: Over producers
renal impairment
Urolithiasis

 Pegloticase: severe refractory case of

gout or intolerance hypouricaemic
agents
Recombinantmodified
mammalianurate oxidase (uricase)
it metabolisesuric acidtoallantoin
For adult patients 8 mg given as an
intravenous infusion every two
weeks.

Others
ACTH---25-40IU S/C---NPO
Anakinra: IL -1 inhibitorNot
approved
Canakinumab

Differential dx:
1. Crystal-induced arthritis:
CPPD
Hydroxyapatite
Calcium oxalate

2. Infectious arthritis
3. Systemic diseases:
Psoriatic arthritis
RA
Reactive arthritis