Toe the line: Live right to avoid pain of gout
Fred Flintstone had the biggest feet, and he used them to propel his car. I’ll bet a pedicure would have cost him a grand! Fred loved his brontosaurus ribs, and perhaps a few beers at the Water Buffalo Lodge. Did a Stone Age doctor tell Fred he was a prime candidate for gout?
Fred had many risk factors: he was a male between 30-60 years old and overweight. About five million Americans have gout, and its prevalence is increasing.
An acute gout attack causes severe (mean and angry!) pain, usually in one joint. About 80 percent of cases of gout involve the great toe base– to the side of the ball of the foot (a.k.a podagra)– or the knee. This is why folks with a podagra wear flip-flops (and Jimmy Buffet in Margaritaville wouldn’t step on a pop top) because anything– even bed sheets!– can hurt the inflamed joint.
The joint inflammation is red, hot, swollen, and makes life a living Hades. The severity of gout inflammation peaks within 12 to 24 hours, although it takes days to weeks for complete resolution. The redness can extend beyond the joint to mimic a skin infection. Swelling can spread to make a toe look like link sausage (minus the eggs and grits).
The other 20 percent of gout flares can occur in any joint and, rarely, in more than one joint.
Gout flares can be precipitated by trauma, such as simply stubbing the toe on a coffee table. Alcohol consumption can lead to gout, though wine isn’t included in this bar tab of pain. (Yay!) Meat, liver, kidneys, and seafood, which are rich in purines, increase the risk of gout attacks. Fishiest of the fish are high in purines, such as anchovies, sardines, herring, and mackerel. Low-fat dairy products (e.g. low fat yogurt, skim milk) and coffee (not tea, though) seem to lower the risk.
Okay, so what's the deal with purines? Urate crystals deposit in the joint to cause gout, and urate (a.k.a uric acid) is created from purines. All patients with gout have high urate sometime in their lives, though levels can be normal on labs during an acute gout attack. Uric acid increases in the blood because it is overproduced and/or because it is not excreted by the kidneys.
Overproduction of urate can be due to inherited enzyme disorders, cancer, some bone marrow disorders, psoriasis, and obesity. Certain drugs like diuretics, niacin, and warfarin can increase urate production. Fructose can even increase urate. (So much for Fruity Pebbles!)
Decreased kidney clearance of urate can occur in congestive heart failure, chronic kidney disease, lead poisoning, hypothyroidism, and dehydration. I wonder if folks on the Atkins diet have more gout because starvation ketoacidosis (which is why weight loss occurs in this diet) is a cause as well.
Ironically, allopurinol, which is used to lower uric acid levels, can precipitate a gout attack in the first month. For acute attack, colchicine helps treat the gout, although the side effect is diarrhea! Indomethacin can be hard on the stomach but can reduce pain and inflammation as well. Probenecid can be used too, although it interacts with quite a few important medications.
The goal is to reduce the number of gout flares because the joint is destroyed with each attack. Also, weird urate-filled nodules, called tophaceous gout, can pop up on the skin such as over the elbow. Kidney stones and slow functioning kidneys can result from high uric acid.
Joint pain stinks! If there are risk factors for high levels of uric acid, it could be worth a trip to the doc to have it checked out.
High urate doesn’t mean gout will occur, but the realization might help in leading to some lifestyle and medicine changes. Prevention is what it’s all agout.
Dr. Hook cracks a joke or two, but he's an esteemed doctor with an interesting webpage, drjohnhong.com.