GOUT: THE DISEASE OF KINGS
- Ben Levinson
- Mar 6
- 5 min read
INTRODUCTION
Well, gout is not really the disease of kings, at least not anymore. These days people of all classes are susceptible to the ravages of this painful malady.
The purpose of this article is to review the disease from its history, its cause, symptoms and treatment. The word gout comes from the Latin Term gutta which means ‘drop’ as it was thought that diseased material was deposited or ‘dropped’ in the joints. It was likely the best observation that could be made at the time, because gout does disfigure joints and deposits a yellowish-white substance called tophi under the skin.
HISTORY
The original description of gout came from ancient Egypt in 2640 BC in the Ebers Papyrus. Hippocrates later called it the ‘unwalkable disease’(1). History has been peppered with many famous people who suffered from gout. Sir. Issac Newton and Benjamin Franklin to name a couple. In a legendary story of Sir. Issac Newton, when he could not find chalk to give a lecture, he would tap his finger joint on the blackboard and use the tophi in that was exposed to write. If one attends a production of the Broadway show and movie 1776, the actor who plays Benjamin Franklin at the Continental Congress is constantly in pain from gout, raising his leg to seek some relief. And it is a very painful disease when one has a gout attack.
In the 1700s and 1800s uric acid crystals were noted in the tophi of patients with gout cementing the idea that changes in uric acid in the body will predispose it to gout. These changes are particularly associated with food and drink that elevate uric acid. Particular culprits that increase purines are foods that are high in a substance that is called a ‘purine’ which is typically found in very expensive foods, hence the moniker ‘disease of kings’. Purines are one a class of biochemicals that make up DNA, the other being pyrimidines. In addition, alcohol will increase uric acid in the blood.
CAUSE
The common cause of gout is the accumulation of crystals of uric acid formed by the breakdown of purines and inability of the kidneys to excrete sufficient amounts of it to prevent its excess in the blood. In this case the uric acid will crystallize in a joint forming a tophus. For reasons that are as yet unclear, these tophi tend to form in the big right toe although as mentioned before with Issac Newton, can also be found anywhere in the body, such as the foot, ankle, midtarsal, knee, wrist, finger, and elbow (3). When they accumulate, inflammation forms around them and it is this inflammation that causes terrible pain. For many people, the pain is so severe that nothing can touch the area, even a light sheet placed over the area or a mild wind will cause great pain.
It is worthwhile to mention that there is a form of gout called saturnine gout which is the result of lead contamination typically seen in people who work in the paint industry, are exposed to lead paint, or drink moonshine from contaminated stills (2). In these cases, the lead will cause kidney toxicity and decrease uric acid excretion. Thus, it is important to consider evaluation of lead levels when evaluating a person for gout.
In addition, people undergoing certain typers of chemotherapy can have gout attack due to increased levels of purines caused by cellular destruction,
DIAGNOSIS
A sudden painful swelling of the big toe or any joint, particularly those mentioned above, typically that will wake someone from sleep, will bring a person to a health care provider. The best way to make the diagnosis is to insert a needle into the affected joint (using a local anesthetic of course) and remove some of the joint fluid. This is then examined in a lab for the characteristic uric acid crystals. For those who have had multiple attacks, an X-ray of the affected area can reveal a finding in bone called ‘punched-out erosions’ more commonly known as ‘rat-bite’ lesions. Sometimes, one can also see evidence of the tophi in the joint. Further examination may be done with an MRI or CT of the affected joint which can show clearer signs of the tophi. The healthcare provider may also order blood levels of uric acid.
The results can be very misleading because after a gout attack the levels could be normal. Therefore, it is important to monitor uric acid over a period of time to obtain accurate data. In this regard, gout is caused not so much by an increase in uric acid in the blood, but by an abrupt change in uric acid levels due to increased accumulation of uric acid or decreased excretion by the kidneys or both.
TREATMENT
‘First things first’ is a good way to approach gout as it is both an acute and chronic condition. Reduction of pain and inflammation is the initial approach. To do this, the health care provider may prescribe a drug known as colchicine. Other practitioners may use one of the NSAIDS such as naprosyn or indomethacin, both of which should be taken with food to avoid stomach upset. The pain reduction may take a couple of days. Some podiatrists and orthopedic surgeons will inject steroid and a local anesthetic directly into the joint which will provide expedited relief.
Once the acute period is over, a decision has to be made on how to treat the condition. After the first attack, the provider might opt to attempt conservative treatment with a gout friendly diet, no alcohol and monitoring of the uric acid. In addition, Vitamin C may be included as this helps with uric acid excretion. If this fails, then a more aggressive approach to reducing uric acid will be undertaken.
A second gout attack after a conservative approach would likely mean that addition of medication. Typically, this will begin with a goal to reduce the uric acid level in the blood stream to less than 6 milligrams per deciliter. In order to achieve this, the first line of treatment will be to begin a course of treatment with a drug called allopurinol. Allopurinol will inhibit the enzyme xanthine oxidase that converts hypoxanthine to xanthine and xanthine to uric acid. Inhibition of this enzyme is responsible for the effects of allopurinol (4).
Earlier it was mentioned that it is the change in uric acid levels that leads to a gout attack by accumulation of uric acid crystals. Allopurinol will cause the change ultimately to reach the desired goal of less than 6 milligrams per deciliter. However, in this transition period, as uric acid levels in the blood change, the possibility of an acute attack is present. To prevent such an attack, providers will also prescribe colchicine for a few months along with the allopurinol until the uric acid in the blood stabilizes.
Since allopurinol can cause unwanted side effects, such as tingling in the arms and legs, providers may switch to alternative medications such as febuxostat (5) which help reduce uric acid. In addition, there are several other alternatives to allopurinol that the provider may prescribe.
Lifestyle is also a very important factor in treatment. Exercise, hydration and a gout friendly diet as well as reduction or elimination of alcohol all play a significant role in prevention of future attacks.
If there are several tophi confined to a single or a couple of joints, the provider may recommend surgical removal or other more invasive procedures depending on joint damage and pain (6). This is usually reserved for the more severe situations where non-surgical treatment has failed.
1. BHATTACHARJEE, S. (2009), A brief history of gout. International Journal of Rheumatic Diseases, 12: 61-63. https://doi.org/10.1111/j.1756-185X.2009.01381.x
2. Poór G, Mituszova M. Saturnine gout. Baillieres Clin Rheumatol. 1989 Apr;3(1):51-61. doi: 10.1016/s0950-3579(89)80035-4. PMID: 2661030.
3. Grassi W, De Angelis R. Clinical features of gout. Reumatismo. 2012 Jan 19;63(4):238-45. doi: 10.4081/reumatismo.2011.238. PMID: 22303530.
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