Niloufer Sultan Ali ( Family Medicine Division, Community Health Sciences, Aga Khan University, Karachi. )
Gout is a condition which is characterized by the deposition of monosodium urate crystals in the joints or soft tissue. The disease mainly affects males in third to fifth decades of life.
There are four phases of gout:
(i) Asymptomatic hyper uricemia
(ii) Acute gouty arthritis.
(iii) Inter critical gout.
(iv) Chronic tophaceous gout.
1) Asymptomatic hyperuricemia
It is the term used for an abnormally high serum urate level without gouty arthritis or nephrolithiasis, level of >7 mg per dl. This does not require treatment but urate levels should be lowered by dietary changes and weight reduction1.
ii) Acute gout it s characterized by a sudden onset of pain, erythema, limited range of movements and swelling of the metatarsophalyngeal joint1,2.
iii) Inter critical gout
After recovery from acute gouty arthritis the patient becomes asymptomatic and this phase is known as “inter critical gout”1. During this phase secondary causes of hyperuricemia should be explored by reviewing drug history, purine rich foods, alcohol consumption and weight should be reduced.
iv) Chronic tophaceous gout
Tophi are chalky deposits of sodium urate. The most common sites are the joints of the hands and feet. The rate of urate deposition and tophi formation correlates with the duration and severity of hyperuricemia2.
A confirmatory diagnosis needs aspiration and examination of synovial fluid which shows presence of monosodium urate crystals1.
Under polarized light microscopy, urate crystals are bright, needle shaped and yellow. Even under conventional light microscope needle shaped urate crystals are seen2.
Urate-lowering therapy should not be initiated until the acute attack has completely resolved, since the subsequent rapid decrease in serum urate levels has been shown to exacerbate the gouty attack4.
Allopurinol (Zyloric) is currently the only readily available inhibitor of uric acid synthesis. It causes a detectable decrease in the serum urate level within the first 24 hours after administration and an expected maximum reduction within two weeks after initiation of therapy. indications for the use of allopurihol are chronic tophaceous “erosive” gouty arthritis; secondary hyperuricemia related to the use of cytolytics in treatment of hematologic malignancies and gout complicated by renal disease or renal calculi1,4.
Allopurinol may be. given in a single daily dose of 300 mg. This is the average effective dosage necessary for patients with normal renal function. Frequently, allopurinol therapy is initiated at a dosage of 100 mg per day and increased in increments of 50 to. 100 mg per day every two weeks until the patient’s urate level is less than 6 mg per dL. Side effects from allopurinol include rash, gastrointestinal problems, headache, urticaria and interstitial nephritis.
1. Mark DH, Lori BS, Jeffrey AA, et al. Gout and Hvperuricemia. American Family Physician, 1999;59:925-34.
2. Kelly W, Wortmann RL. Crystal-associated synovitis. Gout and hyperuricemia. In: Kelly WN, ed. Text-hook of rheumatology. 4th ed. Philadelphia: Saunders, 1993:1340-51.
3. Alloway JA, Moriarty Mi, Hoogland YT, et al, Comparison of triamcinolone acetonide with indomethacin in the treatment of acute gouty arthritis. J. Rheumatol., 1993;20:1 11-13.
4. Modellin M, Erckson A, Enzenauer R. Variability of treatment for gouty arthritis between rheumatologists and primary care physicians. J. Clin Rheumatol., 1997;3:24-27.