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.
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
The presence of characteristic urate crystals in the joint fluid, or a tophus proved to contain urate crystals by chemical means or polarized light microscopy, or the presence of 6 of the following 12 clinical, lab radio features
1977 ACR criteria for acute gout
1. More than one attack of acute arthritis
2. Maximum inflammation developed within 1 day
3. Monoarthritis attack
4. Redness observed over joints
5. First metatarsophalangeal joint painful or swollen
6. Unilateral first metatarsophalangeal joint attack
7. Unilateral tarsal joint attack
8. Tophus (proven or suspected)
10. Asymmetric swelling within a joint on x ray/exam
11. Subcortical cysts without erosions on x ray
12. Monosodium urate monohydrate microcrystals in joint fluid 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 Steoides Colchicin/ NSAIDs
Toxic effects of colchicine: Macrolides cyclosporine verapamil RF/HF Elderly Toxic effects of colchicine Statins
Dietary advices: Fructose Red meat/sea food. 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:
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 Re Chalenge 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
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.
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.
Gout & RF:
Interaction between allopurinol/azathioprine/ 6-MP
Mycophenolate mofetil has no effect on uricaemia ¬ metabolised by XO, can be used in place of ciclosporin or tacrolimus, which both raise serum urate.