Gout.

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Introduction:

Introduction

Diagnosis

Purine metabolism

Diagnosis

Management

Introduction: Gout is a common arthritis caused by deposition of monosodium urate crystals within

joints after chronic hyperuricaemia. It affects 1–2% of adults in developed countries& is the most common inflammatory

arthritis in men. Epidemiological data are consistent with a rise in prevalence of gout. Diet / genetic polymorphisms of renal transporters of urate seem to be the main causal

factors of primary gout. Gout & hyperuricaemia are associated with HT, DM, metabolic syndrome, renal &

CVD. NSAIDs& colchicine remain the most widely recommended drugs to treat acute attacks. Oral corticosteroids could be an alternative to these drugs.

Introduction: Interleukin 1β is a pivotal mediator of acute gout&could become

a therapeutic target. When serum uric acid is lowered below monosodium urate

saturation point, the crystals dissolve & gout can be cured. Patient education, appropriate lifestyle advice, treatment of

comorbidities are an important part of management.

1977 ACR criteria for acute gout 1977 ACR criteria for acute gout

The presence of characteristic urate crystals in the joint fluid, or a The presence of characteristic urate crystals in the joint fluid, or a tophus proved to contain urate crystals by chemical means or tophus proved to contain urate crystals by chemical means or polarized light microscopy, or the presence of 6 of the following polarized light microscopy, or the presence of 6 of the following 12 clinical, lab radio features12 clinical, lab radio features

1977 ACR criteria for acute gout 1977 ACR criteria for acute gout 1. More than one attack of acute arthritis 1. More than one attack of acute arthritis 2. Maximum inflammation developed within 1 day 2. Maximum inflammation developed within 1 day 3. Monoarthritis attack 3. Monoarthritis attack 4. Redness observed over joints 4. Redness observed over joints 5. First metatarsophalangeal joint painful or swollen 5. First metatarsophalangeal joint painful or swollen 6. Unilateral first metatarsophalangeal joint attack 6. Unilateral first metatarsophalangeal joint attack 7. Unilateral tarsal joint attack 7. Unilateral tarsal joint attack 8. Tophus (proven or suspected) 8. Tophus (proven or suspected) 9. Hyperuricemia 9. Hyperuricemia 10. Asymmetric swelling within a joint on x ray/exam 10. Asymmetric swelling within a joint on x ray/exam 11. Subcortical cysts without erosions on x ray 11. Subcortical cysts without erosions on x ray 12. Monosodium urate monohydrate microcrystals in joint fluid 12. Monosodium urate monohydrate microcrystals in joint fluid during attack during attack 13. Joint fluid culture negative for organisms during attack 13. Joint fluid culture negative for organisms during attack

Gout: acute attack trt

Cochicin.

NSAIDs

steroids

0·5 mg three times daily

Favored if no C/Is&for 1–2 ws.

Paranteral &oral pred

Rest/Ice

SteoidesColchicin/NSAIDs

Toxic effects of colchicine:

Macrolides

cyclosporine verapamil

RF/HF ElderlyToxic effects of colchicine

Statins

Urate - lowering therapy:

Tophi

Uric acid stones

Indicated in:Indicated in:

Recurrent attacks

Chronic arthropathy

Non-drug Management:

Stop diuretics

Dietary changes

Include:Include:

Stop alcohol weight loss

Dietary advices:

FructoseRed meat/sea food.

Avoid:Avoid:

Beer Spirits

Starting urate -lowering drugs:

- Started 1-2 weeks after resolution of the acute attack.

- Colchicin or NSAIDs for 3-6 months.

Should be treated without interruption of urate-lowering therapy.

Urate lowering drugs:

Prevention of acute flares during maintenance trt:

Flares

Urate-lowering drugs: Allopurinol: XOI. The dose increased until a uric acid conc of 3-3.5 or maximum of

300-800 mgm are achieved. Dose is reduced in patients with RF. Side-effects are rare& include cutaneous intolerance, in

2%,usually in 3 weeks with mortality of 20%.

Cutaneous S/Es of Allopurinol increased with:

RF

Co-diurtics use

ReChalenge

High dose

Urate-lowering drugs: Rasburicase Off –label monthly infusions of rasburicase have been eff

ective in patients with severe gout not treatable with allopurinol.

A pegylated uricase—less antigenic& longer half-life—is under development.

FDA-approved for Tumor Lysis Syndrome High cost.

Urate-lowering drugs: Febuxostat

Febuxostat is a novel XOI; 80-120 mg/ day are more effective than allopurinol 300 mg/day.

Dose adjustment is not necessary in mild renal failure. Side-eff ects include raised liver enzyme activity and a small

increase in the rate of serious cardiovascular events, precludes use in patients with ischaemic or CHF.

Uricosuric agents Probenecid, sulfinpyrazone,benzbromarone Can be used as second-line therapy for patients with

underexcretion of uric acid. Fluid intake should be increased/ urine pH maintained above

6 to prevent development of uric acid stones. Benzbromarone, a powerful uricosuric drug, is more active

than allopurinol taken at the maximum allowed dose for patients with moderate renal failure.

Hepatotoxic.

Gout & RF: Interaction between allopurinol/azathioprine/ 6-MP Mycophenolate mofetil has no effect on uricaemia &not

metabolised by XO, can be used in place of ciclosporin or tacrolimus, which both raise serum urate.

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