Aging Begins at 30

Gout Occurs in Elderly Women As Well As Men

Gout is a mixture of some or all of the following: a raised blood uric acid, acute or chronic joint disease, chalky deposits (tophi) near the joint or ear cartilage, kidney disease and stones. Uric acid is a breakdown product of proteins. It is raised because of over production or more frequently from poor kidney excretion. About 9% of the population have raised uric acids; most do not have gout. Uric acid is maximally soluble at 7 mgms/100 cc. Above this uric acid crystal deposits in cartilage and joint tissues. It causes irritation and migration of white blood cells whose chemicals set up "angry" inflammation. Crystals occur in the urine as gravel or stones. The red dust is like blood. About 30% of gout patients have it in the family.

Usually gout affects a 52-year-old man whose blood uric acid started rising at 20. Uric acid sinks during the day and is concentrated in the feet during sleep dehydration so he wakes at 3 a.m. with excruciating pain in his big toe, called podagra, literally a foot seizure. The inflamed joint is purpley-red, swollen, shiny with peeling of the overlying skin. The weight of bed clothes or jarring by someone walking nearby causes agonizing pain. Pain lasts for days or until effective treatment. Gout can be triggered by minor injuries, surgery, excess alcohol, or various drugs, (sulfa, ergot, and Vitamin B12). There may be fever of 102° with chills and a raised white count. About a third have had preceding kidney back pain. About 7% never have another attack.

Secondary gout can occur from big tissue turnover in the treatment of leukemia and lymph node tumors. High blood pressure is a common with gout. Treatment with water pills in post-menopausal women will concentrate uric acid and result in gout. This type has equalized the sex incidence of gout over 65.

Diagnosis is by removing fluid from an affected joint or tophus and identifying urate crystals under a polarized-light microscope.

Until recently treatment of the acute attack employed the drug colchicine, an extract of corms of autumn crocus. Colchicine blocks reaction of white cells to uric acid and white cell recruitment reducing inflammation and pain. The dramatic response is considered to confirm the diagnosis. Colchicine is excreted by the kidneys and the function of the kidneys in 80-year-olds is half the function in young adults. The curative dose is close to the toxic dose so many physicians prefer to use nonsteroidal drugs like indomethacin, or occasionally cortisone-like drugs.

Attacks can be prevented by reducing body uric acid but there is no permanent cure. Aspirin will work if you take 15 tablets or more daily. Small doses make gout worse. Probenecid (Benemid) and sulfinpyrazone (Anturane) increase urinary excretion of uric acid but aspirin interferes. Allopurinol (Zyloprim) reduces the body's production rate of uric acid. These drugs are begun after a second attack within a year. They can make gout attack worse. Continued indefinitely, they lower the risk of subsequent attacks.

Gout sufferers need to drink at least half a gallon of fluids daily and heavy alcohol intake should be avoided. Diet is important to lose weight, starvation or very low calorie crash diets can provoke an attack of gout.

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See related Patient Topics Bones, Joints and Muscles or Gout and Pseudogout.

See related Provider Topics Bones, Joints and Muscles or Gout and Pseudogout.

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