Gout is a term used to describe a whole range of arthritis caused due to deposition of various microcrystals in joint (Mono sodium Urate (MSU) crystals, Calcium pyrophosphate dehydrate crystals (CPPD), Calcium hydroxyl apatite crystals (HA), and Calcium oxalate (CaOx) crystals). The commonest of these which is often used synonomusly with gout is due to Mono sodium Urate deposition.

It has following features either singly or in combination:

1. Hyper Uricemia or excess of Uric acid: Uric acid is the final break down of purine metabolism in humans. Normally two third to three fourths of urate is excreted in urine and rest is secreted in intestine. Normal levels of uric acid in humans are 3.0 – 7.0 mg /dl, and a value greater than 7.0 mg /dl is termed as hyperuricemia.

2. Attacks of acute, typically monoarticular (single joint involvement), inflammatory arthritis.

3. tophaceous deposition of urate crystals in and around joints.

4. Interstial deposition of urate crystals in renal parenchyma

5. Urolithiasis (stone)

The hall mark of gout is acute attack of painful arthritis involving one joint usually great toe or knee. The first attack begins explosively and is very painful. The agonizing pain is accompanied by signs of intense inflammation – swelling, redness, warmth, equisite tenderness, and occasionally low grade fever. If untreated, the attack usually peaks 24 – 48 hrs after the first symptoms and subsidies within 7 – 10 days. The skin over the involved part may come off as the episode resolves. Any factor that either increases or decreases the serum urate level may precipitate an attack. Some of the provocative factors include – stress, trauma, infection, hospitalization, surgery, starvation, weight reduction, hyperalimentation, excessive food intake, alcohol and medications.

Some individual face only a single attack in their lifetime, others experience recuurence. Although the interval between the first and second attack may be over 40 years, three fourts have a second attack within 2 years. The term interval gout or intercritical gout describes the periods between attacks of acute arthritis when the individual has no joint complaints. Chronic gout is a term used for persistent polyarticular low grade pain with acute or subacute inflammation.


A definitive diagnosis requires aspiration of the involved joint or tissue and demonstration of intracellular monososdium crystals in synovail fluid polymorphonuclear leukocytes or in tophaceous aggregates. Using polarized microscopy, the strong negative birefrigent needle shaped crystals can be demonstrated.


Once the diagnosis of gouty arthritis is secure, the choice of therapeutic agents includes colchicines, non steroidal antiinflamatory drugs (NSAID’s) or intraarticular glucocorticoids.

Colchicine is given in oral dose of 0.6 mg every hour until improvement occurs, or gastrointestinal side effect occurs or 10 dose have been given without any relief occurs ( in which case the diagnosis needs to be questioned) Colchicine is highly effective but about 80 percent develop abdominall pain, diarrhea and nausea. Colchicine can also be given intravenously but the approach is risky.

NSAID’s are started when the diagnosis is not sure and usually begins with highest dose of the chosen agent. Intaraticular steroids may be used in patients who cannot take orally or are refractory to colchicine.

Treatment of Hyperuricemia

It si begun only when all the acute symptoms have subsided and the urate levels are constantly high. The aim is to keep urate levels below 5 mg/dl. The treatment includes dietary modification and specific urate lowering agents. Most commonly used agent is an enzyme inhibitor of xanthine oxidase (nvolved in purine metabolism) known as Allopurinol.

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