Gout has been a defined medical illness since the days of Hippocrates in the 5th century B.C. It’s known as “the disease of kings and the king of diseases.” Triggered by an excess of uric acid in the body, the initial symptoms result from the formation of needle-like crystals in the joints. It’s these sharp crystals that inflame the joint tissue and lead to the acute attacks of gout.
Gout afflicts an estimated 840 out of 100,000 people. In relative terms, gout accounts for about 5% of all cases of arthritis. Interestingly, gout and its complications occur more commonly and at a younger age in males. And, there’s a strong association with obesity, hypertension, elevated cholesterol and triglycerides, and diabetes. The proximal joint of the big toe (known as the first MTP joint for you medical types) is the initial joint affected in 50% of the cases followed in frequency by other lower extremity joints. This presentation of gout is called podagra. Over 90% of patients who present with acute polyarticular gout have a history of podagra. So, you can see why it’s a shoe in for disease of the month!
The word, Gout, derives from a 2000 year old term “gutta” which referred to arthritis at the base of the big toe. However, it wasn’t until 1684 that uric acid crystals were first seen under the microscope by Antonj van Leeuwenhoek. Two centuries ago, gout was associated with “high living and superior social status” and longevity. That prominent men of the times such as Benjamin Franklin and Thomas Jefferson were gout sufferers helped to foster this misconstrued logic. Furthermore, in 18th century England, the average life expectancy was about 30 years old. Gout is 10 times more prevalent in folks over the age of 45, so once again, misconstrued logic associated it with longevity. And even in an 1861 medical reference, “Gunn’s New Domestic Physician: Home Book of Health”, the etiology of excess uric acid is proffered as “high living, the free use of acid and fermented liquors, and an idle or sedentary habit of living.”
The reason for the elevated uric acid levels that may ultimately lead to gout is multifactorial. The excess can be caused by an increased production of uric acid by the body, by an under-elimination of uric acid by the kidneys, or by an increased intake of foods containing purines which are metabolized by our bodies into uric acid. Dried peas and beans, certain meats, and seafood are particularly high in purines. Hearts, herring, mussels, smelt, sardines and sweetbreads are very high in purines. Followed by anchovies, grouse, mutton, kidneys, goose, and haddock. So, here’s ANOTHER reason to avoid these disgusting foods! Also, alcoholic beverages may also significantly increase uric acid levels and precipitate gout attacks. Now that we’ve crystallized our thoughts, let’s move on.
Since blood levels of uric acid in people with acute gout attacks can be transiently normal or even low, the definitive diagnosis depends on finding uric acid crystals in the joint fluid during an attack. Several other forms of arthritis can mimic gout. I’ve recently had a patient who was convinced he had gout because of foot pain. . .only to find out after extensive testing that he had tendonitis. Additionally, there are many people who have perpetually high blood levels of uric acid, but they never experience acute gout. The solubility of uric acid in the serum is about 7 mg/dl. The risk of gout attack increases with increasing uric acid levels above this mark, though some people with very high serum levels will never have a gout attack. Go figure! So even if you toe the line with good health habits, you could still fall prey to the disease. Conversely, you could eat, drink, and be a merry couch potato and always have a best (and painless) foot to put forward.
An acute gouty attack commonly occurs at night and can be triggered by stressful events, alcohol, drugs (esp. diuretics), or other acute illnesses. An early acute gout attack usually subsides within 3 to 10 days, even without treatment. And, thankfully, months or even years may pass before another gouty attack. Between attacks, a person has normal joint function and no symptoms. However, there is a chronic form of gout as well. Chronic tophaceous gout is the most disabling form of gout. It generally takes over 10 years to develop and causes permanent damage to the affected joints–and sometimes to the kidneys-since uric acid kidney stones can form, and uric acid crystals can clog kidney tubules. . .leading to kidney failure.
Treatments:
In the 1860s, therapeutic advice included sequential cold water immersions of the affected body parts throughout the day, proper regard to diet, and in extreme cases, use of Jimson leaf poultices. . . .
In 2002, thankfully there are more sophisticated and effective treatments available. Acute episodes respond to nonsteroidal anti-inflammatory drugs such as Ibuprofen 800 mg three times per day, or Indomethacin 25–50 mg four times per day until symptoms resolve. Steroids, either orally, intravenously, or intra-articularly may be used to counter severe inflammation.
High dose Colchicine, once the clear drug of choice for acute gout attacks, is now generally discouraged because of the high incidence of GI side effects in the oral form, and serious toxicities (such as myopathy, neuropathy, and aplastic anemia) associated with its IV use. However, the low dose, oral form of Colchicine is well-tolerated and can be an effective prophylactic agent in people with early gout and recurrent acute episodes. And, finally, there are uric acid lowering agents such as allopurinol and probenecid that can be appropriately used in select patient populations. One specific use for allopurinol is in cancer chemotherapy patients, since the destruction of tumor masses can suddenly release extremely high levels of uric acid into the blood stream. Longterm use of either of these agents must be monitored carefully, since they can adversely affect the liver, bone marrow, and/or kidneys if not used properly and under scheduled supervision.
Okay, I know your brain is tired by now, but no discussion on gout would be complete without including the following first-person account of a gout attack. Those of you who suffer such episodes will feel vindicated that your miseries are vividly described. And, those of us who have never had such experiences, will consider the sparing a blessing. Thanks for joining me in my joint effort this week.
Dr Thomas Sydenham, himself a gout sufferer, wrote a vivid (now famous) description of an acute gout attack in 1683. “The victim goes to bed and sleeps in good health. About 2 o’clock in the morning, he is awakened by a severe pain in the great toe; more rarely in the heel, ankle, or instep. This pain is like that of a dislocation, and yet the parts feel as if cold water were poured over them. . . The pain which at first moderate becomes more intense. . .Now it is a violent stretching and tearing of the ligaments–now it is a gnawing pain and now a pressure and tightening. So exquisite and lively meanwhile is the feeling of the part affected, that it cannot bear the weight of bedclothes nor the jar of a person walking in the room.”
Stephen L. Hines, M.D.
April 2002
