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Myths about gout are hampering its treatment

The prevalence of gout is increasing worldwide. It has become the most common cause of inflammatory arthritis in men, and its prevalence in postmenopausal women continues to rise. This increase is due to changes in diet and lifestyle, increased use of certain diuretics and increasing obesity.

Developed countries have a higher burden of gout than developing countries. But in the developing world – and particularly in Africa – where countries have experienced a rapid epidemiological transition and increases in non-communicable chronic diseases such as obesity, there is an increasing risk.

Gout is a form of arthritis that happens when too little uric acid is excreted from the body and then forms crystals in and around joints in the body. Uric acid forms when proteins called purines break down in the body. Although essential for a normal metabolism, excess uric acid is excreted from the body mainly via the kidneys into urine.

Many patients with gout struggle to control the disease. The crystals cause acute attacks of pain, heat, redness and swelling in these joints, which can be painful and debilitating. Over time, chronic gout occurs when lumps or “tophi” develop on the elbows, earlobes, fingers, knees, ankles and toes. Eventually the joints become deformed.

But both gout and tophi can disappear if they are properly treated. Many doctors and patients are, however, unsure of the best treatment. This results in poor patient education, patients taking treatment “on and off” rather than daily as prescribed, doctors using the wrong medicine, or at the wrong dosage (frequently too little) and perhaps not being aware of interactions between drugs, and poorly addressed lifestyle factors.

Myths and facts about gout

There are several incorrect common beliefs about gout.

One of the most popular is that gout only affects the big toe. But this is not true. The first gout attack usually occurs in the lower limb (knee, ankle or big toe), but later almost any joint can be affected.

It is also often reported that the underlying problem for most gout sufferers is that their bodies produce too much uric acid. But this is not true. More than 90% of gout sufferers get rid of too little uric acid in their kidneys. This poor renal secretion of uric acid can be the result of kidney problems, high blood pressure, excess alcohol consumption or medication – for example diuretics (water reduction tablets) or drugs used to treat TB infection. In addition, certain genes result in too little uric acid being secreted from the body, and thus increase the risk of gout.

Another common belief is that acidic foods cause gout. But acidic foods such as tomatoes and oranges cannot cause or worsen gout.

Rather, foods high in purines can increase the risk of gout, particularly in someone who is secreting too little uric acid. Some foods have a very high purine content. These include seafoods such as mussels, lobster, sardines and salmon, as well as beer, bacon, liver, sweetbreads, turkey, veal, and high fructose corn syrup. High fructose corn syrup is often found in processed foods such as soft drinks, chips and biscuits, syrups, chutneys and sauces.

There are certain foods that are protective of gout. These include coffee, low-fat dairy products and particularly yoghurt, high doses of vitamin C, cherry or lemon juice, soya and lentils.

Although any type of alcohol inhibits uric acid secretion and should be avoided in patients with gout, beer is a “double hit” because it is rich in guanosine, which adds to the body’s purine load.

The best treatment

Patients with gout often have other illnesses. Elevated uric acid and gout are frequently associated with the metabolic syndrome – a cluster of diseases consisting of diabetes, high blood pressure, high cholesterol and obesity, leading to heart attacks and kidney failure.

But that does not mean that everyone with a raised blood-uric acid level needs treatment for gout. Many people with high uric acid levels never develop gout. Even patients who have one attack of gout may not need treatment to reduce the uric acid levels. They should consider a lifestyle change, such as altering their diet, losing weight and drinking more water.

The “gold standard” to diagnose an acute attack of gout is to remove some fluid from the joint with a needle and syringe, and examine this under a microscope for uric acid crystals. If this cannot be done, certain typical symptoms and signs seen together are highly suggestive of gout, and a diagnosis can be made. Joint ultrasound or dual energy CT scan images show gout very well.

Non-steroidal anti-inflammatories are the best treatment for an acute gout attack unless the person has kidney problems or stomach ulcers. Patients who cannot use these anti-inflammatories require corticosteroids, either injected into the joint or taken as tablets (otherwise known as prednisone).

A patient with numerous acute attacks, or tophi, requires drugs called allopurinol that lower the uric acid level in the body. But these prevent attacks of gout rather than treating an attack.

In the first six months of using allopurinol, gout attacks can occur more frequently. Understanding this, and having anti-inflammatories on hand, is important.

It is important that patients do not stop or alter the dosage of medication as it may result in the uric acid level returning to its initial level. They may get “stuck” in this cycle of stop-and-start treatment and the gout will steadily get worse. But with consistent use over time, once the uric acid level drops, acute attacks will stop and tophi will be disappear. This may takes months or years in a patient with many tophi.

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