Gout is a type of arthropathy that results from the formation of crystals. Gout may occur from either the over-production of uric acid (the cause of most cases) or the under-excretion of uric acid.1,2
Uric acid, which the kidneys excrete, is an end product of purine metabolism.2 Normal values of serum uric acid are 6 mg/dL or less in women and 7 mg/dL or less in men. However, elevated levels do not always correlate with an acute gout attack. Levels greater than 6 mg/dL simply increase one’s risk of a gout attack.
When the level of uric acid becomes too great, the uric acid level will eventually reach a point where it can no longer dissolve and will precipitate out into crystals. When they enter tissue, gouty crystals will cause a foreign body type reaction.1,2 An inflammatory response starts and the body sends the Marines as the first line of attack. These white blood cells engulf the crystals but due to the sharp needle-like form of the crystals, these cells are easily injured and destroyed, releasing their toxic insides. These chemicals cause an even greater inflammatory response and the vicious cycle continues.
Gout is more common in men than in women and does not usually occur before the age of 30. Gout in women usually occurs after menopause.1,2
There are four stages to gout. These stages are as follows:
1. Asymptomatic hyperuricemia
2. Acute gouty arthritis
3. Intercritical gout
4. Chronic tophaceous gout
Tophi are the pathognomonic hallmark of gout. These tophi can appear in joint cartilage, ligaments, tendons and soft tissues. If left untreated, superficial areas of tophi formation can ulcerate and lead to a secondary infection.1,2 Note that the big toe joint is by far the most common location for gout, occurring in 50 percent of acute attacks and up to 90 percent of patients with long-term involvement.1,2
In the acute phase of gout, patients will present with exquisite pain and tenderness.1,2 The pain may be so severe that a simple sheet on top of the area produces excruciating pain. Other symptoms include redness, swelling and increased temperature of the skin. Note that the first attack may involve one joint with subsequent attacks becoming oligoarticular.4
Following an acute attack, a latent period may follow with no signs or symptoms. This may develop 72 to 96 hours after the initial attack and can last weeks to years.
In the chronic phase of gout, patients may exhibit a chalky appearance of tophi in the tissues.1,2 Ulcerations with secondary infection can occur during this phase if gout goes untreated.
The best way to make a diagnosis is to take a sample of the joint fluid and examine it under a microscope.1,2 The crystals appear needle shaped as I noted previously and if one views the crystals under a polarizing light, they will display negative birefringence. Another method of diagnosis is by looking at the affected area under X-ray. It is common to see erosive changes to the bones at that joint level. These characteristic changes may look like punched out areas with an overhanging piece of bone, known as Martel’s sign.
The best treatment is with strict diet control.1-3 Numerous foods may spur on a gout attack. They include meats (red meat in particular), certain seafood, foods high in fat and alcohol (especially red wines).
In contrast, some data shows that vitamin C, cherries and coffee may actually reduce serum uric acid levels.3
The following medications may be effective for gout.
• Colchicine (Colcrys, Takeda Pharmaceuticals) is helpful for the acute phase but has heavy side effects.
• Allopurinol blocks the production of uric acid and one can use it more for prevention and for the chronic phase.
• Indomethacin (Indocin, Lundbeck) is a type of non-steroidal anti-inflammatory drug that patients can use during the acute phase.
• Probenecid (Probalan) increases the excretion of urate.
Consider surgical treatment if the joint involvement is severe from the destructive nature of gout.
1. Coughlin M, Mann R, Saltzman C (eds). Surgery of the Foot and Ankle, eighth edition. Mosby Elsevier, Philadelphia, 2007.
2. Kumar V, Abbas AK, Fausto N, Mitchell R. Robbins Basic Pathology, eighth edition. Saunders, Philadelphia, 2007.
3. Schumacher R, Chen L. The practical management of gout. Cleve Clin J Med. 2008; 75(Suppl 5):S22-25.
4. Doherty M. New insights into the epidemiology of gout. Rheumatology. 2009; 48(Suppl 2):ii2-ii8.