Gout -revisited Shrenik Shah. definition Monosodium urate (MSU) crystal deposition  episodic and later persistent joint inflammation and tophi All MSU.

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GOUT Disease caused by tissue deposition of Monosodium urate crystals as a result of supersatuaration of extra cellular fluid with MSU.
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Presentation transcript:

Gout -revisited Shrenik Shah

definition Monosodium urate (MSU) crystal deposition  episodic and later persistent joint inflammation and tophi All MSU crystal deposition- broader definition EULAR- European League Against Rheumatism –guidelines

TOPHACEOUS GOUT

Diagnosis Clinical features and hyperuricaemia- inaccurate way of diagnosis MSU crystals in synovial fluid (SF)-gold std. Regular microscope- polarized MSU- needle-acicular, strong birefringence CPPD- rhomboidal, parallelepipedic,acicular- absent/weak birefirngence

MSU CRYSTALS –PLAIN AND POLARISED MICROSCOPY

Diagnosis 2 All SF drained from undiagnosed arthrpathies Aspirating asymptomatic knees / first MTP jts Palpable tophi- needling Tissue samples- fixed in alcohol / freezing

PODAGRA

Clinical Diagnosis Recurrent episodes of acute arthritis of first MTP joint (podagra)  Gout D/D- infections/ psoriatic arthritis/ CPPD Less typical location of first gouty attack-50% Tarsum, ankle, knee, wrist Arthritis of TM jt, AC jt, manubriosternal, sternoclavicualr, sacroiliac,pubic symphysis, or hip joints, lumbar spine or flexor tenosynovitis with CTS Polyarticular, additive/ less acute /persistent Confused : septic arthritis/ spondylodiscitis / RA / tumours

Hyperuricemia SUA  0.5% develop Gout in 1 year > 9 mg  4.9% Any articular manifestation –mistaken for gout Absense of high SUA  disregard gout SUA levels may be normal during acute attack due to high renal excretion Gouty attack if urate lowering therapy without colchicine prophylaxis / anytime during therapy before crystals are dissolved

Approach ACR criteria, Rome and N Y criteria when compared with MSU crystal identification- poor in under an over diagnosis D/D- CPPD, RA and OA-poor Ongoing inflammation and crystal deposition Erroneous diagnosis- lifelong urate lowering drugs

Future perspectives- USG Visualize crystal deposits Double contour sign- hyperechoic enhancement of the outer surface of hyaline cartilage Soft and hard tophi Hyperechoic spots within SF

USG

Management Normalising of SUA levels  dissolution of crystals SUA normal indefinitely to avoid forming new crystals and return of gout Bouts of arthritis- clinical presentaion, after the start of therapy until crystals dissolve or indefinately in improperly treated/ untreated patients Causes –evaluated Associated- metabolic syndrome( arterial hypertension, hyperlipidemia, obesity or glucose intolerance - treated

Reducing uricemia to eliminate urate crystals SUA<6 mg. lower the level- sooner clearance 9/10 signal joints with gout< 10 yrs were free of crystals after 1 yr of SUA lowering therapy and remaining one by 18 months Crystals can be found in SF samples from never inflamed joints and periarticular structures of patients of asymptomatic hyperuriceamia Rx only after gouty attack has subsided Prophylactic colchicine

Allopurinol Inexpensive, safe and effective Refractory if SUA not < 6 mg 300 mg- fixed dosage? Max 800 mg mg may be necessary in many Lack of compliance  allopurinol failure S creatinine >2  avoid NSAIDs, reduce allopurinal

Allopurinol 2 Hypersensitivity syndrome-lethal DRESS syndrome-drug rash with eosinophilia and systemic symtoms Stevens –Johnson syndrome Azathioprine- metabolism same. Coadministration causes toxicity Reduction of SUA  improves renal insufficiency and reduces BP in adolescents with hypertension

Uricosuric drugs Probenecid mg h/o renal calculi- caution- alkanise urine and plenty of fluids Difficult allopurinol refractory patients- combine allopurinol with uricosuric drugs

Newer drugs Febuxostat- nonpurine selective inhibitor of XO- for allopurinol intolerance and renal failure cases Uricase- degrades uric acid to allantoin- soluble and easily eliminated- treating tumor lysis syndrome- Losartan and clofibrate- reduces SUA along with BP and lipids

NSAIDs Indomethacin -50 mg tds Etoricoxib -120mg od Naproxen- 500mg bd Prednisolone-35 mg daily short courses of steroids  rebound attack hence prophylactic colchicine Intraarticular steroids- small doses- infection ruled out

Colchicine Formerlt daignostic aid Frequent side effects- high dose EULAR guidelines- max of 3 tabs of 0.5 mg in first 24 hours for acute gout 0.5 mg BD in older patients 0.5 mg OD in renal and hepatic abnormalities Acute GI, myelotoxicity, myotoxicity after prolonged use

Dietary and life style factors Evaluation of metabolic syndrome- high BP, insulin resistance, dyslipidemia, abdominal obesity, comorbid conditions Independent CVS risk factor- increased risk factor for MI, fatal coronary heart disease, level of association rises with severity of Gout Hypocaloric diet, reduced intake of purine rich foods, alcohol, sugar sweetened soft drinks

SUA increasing Medication Diuretics Low dose aspirin Cyclosporin Pyrazinamide, ethambutol Nicotinic acid Cytostatic agents

Case studies

Case 1

Case 2

X ray USG

PRE AND POST TREATMENT

Case 3

Tophaceous gout