Gout is a common cause of arthritis affecting more than 8 million Americans. Although it affects men more than women, there appears to be an increasing incidence of the disease in post-menopausal women. The incidence overall appears to be increasing as a result of the epidemic of obesity, hypertension, diabetes, and elevated lipids, all of which are associated with gout.
Gout, in 90 per cent of cases, is caused by the inability of the kidneys to get rid of urate. In the other 10 per cent, there is an overproduction of urate.
Animals other than humans don’t get gout because they have an enzyme called uricase which breaks urate down and allows the animal to excrete it. Human beings, on the other hand, lack this enzyme and therefore are unable to excrete urate (uric acid) appropriately. This leads to accumulation of uric acid crystals in the joints and other organ systems.
Gout typically occurs in three stages. The first stage is what is called “asymptomatic hyperuricemia.” Asymptomatic hyperuricemia is characterized by elevate blood uric acid levels without attacks of gout. The higher the blood uric acid level is, though, the greater likelihood of an eventual attack.
The second phase or stage is termed “acute intermittent gout”. During this stage, patients have attacks of gout but after the attack is over, they are relatively symptom free. The danger here is that chronic inflammation persists despite the absence of symptoms.
The third stage is called “chronic tophaceous gout.” In this phase, patients have chronic pain due to repeated attacks of gout with an increasing burden of urate accumulation in the joints, kidneys, and other organs systems. Patients develop “ tophi” which are deposits of inflammatory cells, uric acid crystals and fibrin. Gradual destruction of the joints occurs with the development of crippling deformity. Tophi can cause lumps on finger joints in addition to other areas.
The treatment of gouty arthritis consists of a two-fold approach with relief of the acute attack accompanied by attempts to lower the urate burden.
Acute attacks can be treated with colchicine, non-steroidal anti-inflammatory drugs, and steroids. The latter can be given either orally or directly into the affected joint.
Drugs that lower uric acid need to be used for the chronic treatment of gout. These drugs, when initiated, need to be accompanied by gout prophylaxis in the form of daily doses of either colchicine or non-steroidal anti-inflammatory drugs, for at least six months. The reason is this: as urate shifts as a result of the effect of uric acid lowering drugs, there is a predisposition to acute attacks.
Drugs used to lower uric acid consist of medicines that make patients urinate out their uric acid (probenecid), medicines that suppress uric acid production ( allopurinol, febuxostat [Uloric]), and uricolytic drugs. An example of the latter is pegloticase (Krystexxa), which converts uric acid to allantoin, an inert ingredient that is then excreted.
Counseling a patient in regards to lifestyle and diet also plays a role in the comprehensive approach to gout.
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