Gout, a disease of antiquity, is experiencing a resurgence. In fact, it's been estimated that more than eight million Americans may have the disease. There are several reasons for this. First, more Americans are obese, a significant risk factor for gout.
Second the obesity is often accompanied by other risk factors such as high blood pressure, diabetes, and elevated blood lipids, the combination being known as "the metabolic syndrome."
Finally, there has been an increased availability as well as increased consumption of high fructose containing beverages, another risk factor for gout.
The underlying physiologic reason for gout is the inability of the body to rid itself of uric acid. Uric acid is a byproduct of the metabolism of purines, a major constituent of many foods.
Ordinarily, the kidneys are responsible for the bulk of elimination of uric acid but in gout they cannot keep up with the huge burden of uric acid in the blood.
While most people who experience one or two attacks a year can be managed conservatively, patients who experience repeated attacks or who have markedly elevated levels of serum uric acid (SUA), are candidates for medical treatment.
Medicines such as colchicine, non-steroidal-anti-inflammatory drugs, and steroids are helpful for breaking acute attacks of the disease. For chronic disease where the aim is to lower SUA, medicines such as probenecid, allopurinol, and febuxostat (Uloric) are useful.
However, a small percentage of patients will not respond to these measures. Some patients with long-standing gout develop tophi, collections of uric acid near the skin surface. These are an indication of a tremendous uric acid burden. A new drug called pegloticase (Krystexxa) lowers SUA by converting it to allantoin, an inert ingredient. It is administered intravenously in a dose of 8 mgs intravenously every two weeks and drives the SUA to 0 within 3 months. Tophi "melt away."
The down side is that approximately 25-50 per cent of patients will develop blocking antibodies to the drug and if not recognized, can experience severe infusion reactions.
The way to spot this coming is get a SUA level the morning before a proposed infusion. If the SUA is 4 mgs/dl or higher the patient has developed antibodies and is at high risk for an infusion reaction and should not be given pegloticase. Patients should not receive other SUA lowering therapies along with pegloticase since they may mask the development of antibodies. Patients should be screened for G6PD deficiency since this is a contraindication to receiving pegloticase. Finally, "prepping" a patient with steroids and an antihistamine also lower the risk of infusion reactions.
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