Gout is a form of arthritis. Like other types of arthritis, it causes pain and swelling in the joints.
Gout develops in some people who chronically have a condition called “hyperuricemia,” meaning high levels of a substance called urate (also known as uric acid) in the blood.
Urate can form crystals that build up in different parts of the body, causing symptoms.
Not everyone with hyperuricemia develops gout; up to two-thirds of people with hyperuricemia never have any symptoms, although it is unclear why this is.
In some people, urate crystals may form that can lead to kidney stones and other problems with kidney function. Gout usually develops in adulthood and is rare in children.
It commonly develops earlier in adult men (often between the ages of 30 and 45) than in women (usually after age 55); it is particularly common in people older than 65 regardless of gender.
Pacific Island populations, particularly those of Polynesian descent, have a high prevalence of hyperuricaemia and gout.
This is because of an inherently higher urate level among these populations with a demonstrated genetic predisposition.
Risk factors
There are several medical conditions and lifestyle factors that increase a person’s risk of developing gout, including:
- Obesity;
- High blood pressure;
- Chronic kidney disease;
- Overeating or prolonged fasting;
- Consuming excessive amounts of alcohol (particularly beer, whiskey, gin, vodka, or rum) on a regular basis;
- Consuming large amounts of meat or seafood;
- Consuming beverages containing high fructose corn syrup (such as non-diet sodas); and
- Taking medications that affect blood levels of urate (especially diuretics).
In people already diagnosed with gout (referred to as “established gout”), there are also certain characteristics that increase the risk of repeated gout flares. These include:
- Injury or recent surgery;
- Fasting;
- Consuming excessive amounts of alcohol (wine may also be implicated as a risk for additional gout flares in people who have had prior flares);
- Overeating;
- Taking medications that induce sudden changes in blood urate levels; and
- Dehydration.
Symptoms
Gout flares (also called gout attacks) are sudden episodes of severe joint pain, usually involving redness, swelling, and tenderness of the joint.
Although a gout flare typically affects a single joint, some people develop several inflamed joints at the same time.
The pain and inflammation usually reach peak intensity within 12 to 24 hours and generally improve completely within a few days to several weeks, even if untreated.
It is not clear how the body “turns off” a gout flare. The inflammation is precipitated by the deposition of uric acid crystals in the lining of the joint (synovial lining) and the fluid within the joint.
Intense joint inflammation occurs when white blood cells recognise these crystals as foreign material and engulf the crystals of uric acid and release chemicals that promote inflammation.
The resulting inflammation causes pain, heat, and redness of the joint associated with gout flare
People who have repeated gout flares or persistent hyperuricemia for many years can develop Tophaceous gout.
This term describes the accumulation of large numbers of urate crystals in masses called “tophi”.
People with this form of gout develop tophi in joints, bursae (the fluid-filled sacs that cushion and protect tissues), bones and cartilage, or under the skin.
Tophi may cause erosion of the bone and eventually joint damage and deformity (called gouty arthropathy).
Developing tophi near the small joints of the feet or fingers can cause physical changes that can not only be distressing (due to the cosmetic appearance) but also contribute to restricted movement and disability.
Tophi are usually not painful or tender.
Kidney related complications
Normally, the kidneys filter urate in the blood and excrete it from the body through urine. In people with gout, urate crystals can build up in the kidney or other parts of the urinary tract, leading to kidney stones.
If a stone gets large enough, it can block one of the ureters (the tubes that carry urine from the kidney to the bladder and out of the body). Kidney stones caused by urate crystals occur in approximately 15 per cent of people with gout. This compares with an 8 per cent risk of kidney stones in people without gout.
Diagnosing gout
The best way to diagnose gout is for a doctor to examine the fluid lining the affected joint (synovial fluid) under a microscope to look for urate crystals.
To do this, he or she uses a needle and syringe to withdraw a small amount of fluid from inside the joint.
Tophi located just beneath the skin can also be sampled with a needle to diagnose tophaceous gout.
If it is not possible to do a synovial fluid analysis, your doctor will consider your history, symptoms, physical exam, and blood test results.
Among the criteria for suspecting gout are:
- Rapidly developing pain and inflammation initially involving one joint at a time, especially the joint at the base of the large toe, however any joint may be involved;
- Complete resolution of symptoms between flares; and
- High levels of urate in the blood (this is most accurate for diagnosis after a gout flare resolves because urate levels may be within normal limits during the flare).
Treatment of gout flares
The goal of treatment of gout flares is to reduce your pain, inflammation, and the accompanying disability quickly and safely.
This treatment is usually short-term and limited to the duration of the flare. Deciding which medication to use is based upon several factors, including your risk of bleeding, kidney health, and whether you have a past history of an ulcer in the stomach or small intestine.
Anti-inflammatory medications are the best treatment for gout flares. They are most effective when started early in the course of a flare.
If you have a history of gout, your clinician can give you medication to keep on hand in the event of a flare. This is important because early treatment is key in minimizing the amount of time it takes to decrease the pain, severity, and duration of a flare.
Non-steroidal anti-inflammatory drugs — (NSAIDs) work to reduce swelling in a joint. They include ibuprofen (sample brand names: Advil, Motrin), naproxen, indomethacin, and celecoxib
Colchicine may be prescribed for a gout flare instead of an NSAID. Colchicine does not increase the risk of ulcers, has no known interaction with anticoagulants (“blood thinners”), and, in proper doses, does not affect kidney function.
However, colchicine can have bothersome side effects when given in excess, including diarrhea, nausea, vomiting, and crampy abdominal pain.
Colchicine therapy seems to be most effective when started within 24 hours of the first symptoms of a gout flare. Your doctor will tell you what dose you should take if you have a flare
Steroids, also known as glucocorticoids such as prednisone can be given to people with impaired kidney function or at increased risk for bleeding, as well those with multiple affected joints or who cannot take NSAIDs or colchicine.
Certain people are generally not candidates for glucocorticoid treatment, including those who have poorly controlled diabetes, in whom infection is a concern, or who cannot tolerate steroids for some other reason.
Long term urate lowering therapy
Over time, medications and lifestyle changes can lower urate levels and, as a result, prevent or reverse urate crystal deposits that can cause joint damage, disability, kidney stone formation, and possibly kidney damage.
People who have one or more of these complications are especially encouraged to take a urate-lowering treatment.
The goal of urate-lowering therapy is to achieve and maintain blood urate levels below a specific level.
In practice, the recommended goal for most people with gout is less than 6mg/100mL (360 micromol/L), except in people with tophaceous or severe gout, in which case the suggested goal is less than 5mg/dL (300 micromol/L).
Not everyone with gout will require urate-lowering therapy. If you only have rare or mild flares, you may be able to manage your gout by treating the flares as they happen.
However, if you have frequent, prolonged, painful, or disabling gout flares, joint damage, or tophi, will likely need urate-lowering therapy.
Medications lower urate levels in one of three ways: they increase urate excretion by the kidneys; they decrease the body’s production of urate; or they break down urate.
Urate-lowering therapy is usually started after a gout flare has resolved. People who take their medication regularly and maintain urate levels below the target range over months to years eventually experience fewer flares; sometimes, flares stop altogether.
Doctors recommend that preventive therapy be continued if needed to maintain blood urate levels in the goal range indefinitely; stopping treatment is commonly associated with a return to hyperuricemia and recurrence of gout.
Medications that lower urate levels and are commonly prescribed include Allopurinol (brand names: Alloprim, Zyloprim) and Febuxostat (brand names: Uloric, Adenuric) work by preventing the formation of urate.
Allopurinol is the most commonly used drug for lowering urate levels in people with gout.
Allopurinol can cause side effects, including skin reactions (rash), lowered white blood cell and platelet counts, diarrhea, and fever, although these problems occur in only a small percentage of people.
Dietary changes
Improving your diet may reduce the frequency of gout flares. Foods and beverages that are high in purines should be avoided since purines are converted in the body to urice acid.
Foods rich in purines include:
- Beer and grain liquors (like vodka and whiskey);
- Red meat, lamb, and pork;
- Organ meats, such as liver, kidneys, and glandular meats like the thymus or pancreas (you may hear them called sweetbreads);
- Seafood, especially shellfish like shrimp, lobster, mussels, anchovies, and sardines; and
- High-fructose products like soda and some juices, cereal, ice cream, candy, and fast food.
Because obesity is a risk factor for gout, as well as for many other health conditions, losing weight (if you are overweight) is an important goal. However, extreme or “fad” diets are not recommended.
Changes in diet are often recommended along with urate-lowering medications.
Changing your diet alone is unlikely to lower blood urate levels by more than about 15 per cent, even if you make major changes to your diet.
On the other hand, if you lose weight in addition to changing your diet, it is possible to see more significant improvements in urate control, along with benefits to your general health.
- DR ANOSHIA MCCAIG is a general practitioner at Oceania Hospitals Pte Ltd. The views expressed are the author’s and do not reflect the views of this newspaper.
