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Understanding Gout (Vatarakta)

Dr. Vikram Dev Singh

Gout is an inflammatory response to the deposition of MSUM crystals in the soft tissues of the joints manifesting as acute arthritis, synovitis, tophaceous deposits, renal disease and hypertension. Hyperuricaemia (Serum uric acid concentration greater than 7.0 mg/dl in males and 6.0 mg/dl in females) is the major determinant of risk of developing gout. This is a brief presentation on gout and its Ayurvedic management.

In crystal induced arthropathies, generally three types of crystal deposits are seen:

1. Monosodium urate monohydrate (MSUM) causing gout;
2. Calcium pyrophosphate dihydrate (CPPD) causing pseudogout; and
3. Calcium hydroxy appatite causing musculoskeletal symptoms like bursitis and tendinitis.

Of these MSUM is the most inflammatory crystal.

Gout
Gout is an inflammatory response to the deposition of MSUM crystals in the soft tissues of the joints manifesting as acute arthritis, synovitis, tophaceous deposits, renal disease and hypertension. Hyperuricaemia (Serum uric acid concentration greater than 7.0 mg/dl in males and 6.0 mg/dl in females) is the major determinant of risk of developing gout.

Pathogenesis
Uric acid is the waste product of purine metabolism. Approximately 70% of it is excreted daily by kidneys and rest from GI tract. If a person either produces excessive amount of uric acid or is unable to excrete as much as normal, the uric acid levels rise in the blood causing hyperuricaemia.

Provocative factors include use of diuretics, alcohol, dietary excess (purine load), surgery, trauma, sepsis, stress, starvation and dehydration. This excess uric acid in blood reacts with sodium to form a salt called MSUM (Monosodium urate monohydrate). These crystals deposit in the soft tissues of the joints causing irritation and erosion of the involved joint and cartilage by virtue of their surface active and mechanical properties causing gout. In gout, 10-15% of cases show increased production of uric acid and 80-90% exhibit impaired uric acid excretion.

Clinical features
1. Asymptomatic hyper-uricaemia: - Only 10% of the hyperuricaemics develop gout and in rest 10%, it may be an incidental finding which needs close observation but no active treatment as such.

2. Acute gout: - Gout is rare in children and premenopausal females. In males the peak age of onset of gout is between fourth and fifth decade of life. The most classic site for the first attack in 70% of cases is first metatarsophalangeal joint (Big toe). The rest may get their first attack at ankles, knees, wrists, elbows and small joints of hands and feet.

The first attack is usually monoarticular and is seldom associated with residual disability. The affected joint and surrounding tissues are red, hot, swollen, tender with shiny overlying skin and extremely painful. Mild fever with chills may be associated alongwith leucocytosis and raised ESR in severely acute attacks. If left untreated the attack of acute gout starts improving in a week or two and the skin over the joint may undergo desquamation.

3. Intercritical gout: - Between acute attacks there may be symptom free periods ranging from several months to several years. But with time, these symptom free periods decrease and the number of sites involved increase. The recurrent attacks may lead to the erosion of the affected joint causing articulating bones fuse, and the joint becomes immovable.

4. Tophaceous gout (Chronic gout): - Tophi are massive accumulations of microcrystals of uric acid and amorphous urates surrounded by histiocytes, giant cells and fibrosis.

Tophi appear as firm, nodular or fusiform swellings developing at the great toe, feet, hand joints and olecranon. Tophus at the helix of ear though classic, is uncommon.

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