Gout: definition, symptoms, causes, diagnosis, treatment

By Cristiano Antonino On May 11, 2023

Although already described by Hippocrates, Celsus and Galen, gout is a disease that still exists today

While in the past it was considered the disease of the rich (Suetonius defines it as ‘morbus dominorum’) because it affected the more affluent social classes due to their lifestyle (it usually begins with large meals with excessive meat or alcohol intake), today we know that it is a disease with a strong genetic component that is only partly linked to environmental factors.

When we talk about gout, we mean a disorder of purine metabolism that leads to increased urate levels in the blood (hyperuricemia).

This condition can lead to the formation of uric acid deposits in various locations, causing swellings called tophi, or acute joint inflammatory attacks with urate deposits in the joints or a kidney disease called gouty nephropathy.

What is gout?

Gout is an acute inflammatory disease that is caused by a deposition of uric acid crystals in the joints and manifests itself – in most cases – with a sudden onset of joint pain, redness and swelling.

The metatarsophalangeal joint of the big toe is most affected, although uric acid can also accumulate in other locations creating so-called tophi, swellings caused by the aggregation of uric acid in the dermis, skin or tendons.

In addition, it is often associated with other pathological conditions, such as obesity, hypercholesterolaemia and hypertriglyceridaemia.

Some triggering factors for acute gouty attacks are alcohol abuse, overeating, prolonged fasting, joint trauma and intense and prolonged exertion.

Thus, an incorrect lifestyle can increase the risk of developing gout, particularly in men and people who are familiar with the disease.

Gout can result from excessive production of uric acid or difficulty in eliminating it.

Uric acid

Uric acid is the waste product of purines (nitrogenous organic substances present in all cells) and is formed in the body from the metabolism of purines, whether endogenous – i.e. produced by the body – or exogenous – i.e. from our diet.

Under normal conditions, uric acid is excreted through the urine, but the body can no longer eliminate it in the event of an increase in blood levels of this substance.

Alterations in the homeostasis of this molecule may depend on various factors, such as alcoholism, obesity, high metabolic turnover (tumour lysis or myeloproliferative diseases), the use of certain drugs (salicides and diuretics) and diets rich in meat, a food that contains many purines.

Certain genetic diseases can also cause hypereuricukaemia, with or without uric acid deposition.

Hypereukaemia

Chronic hypereuraukaemia is an extremely harmful condition for the body: if left untreated, the consequences can be disabling, particularly when cardiovascular, renal and joint complications occur.

One of these consequences is gout

To confirm the presence of hypereuracaemia, the patient undergoes a 5-day purine-restricted diet, with the indication to discontinue any medications that affect uric acid metabolism.

If uric acid values do not fall below the threshold value, this is called hyperuricukaemia.

This can be classified as:

Primary, if it does not depend on acquired diseases;
Secondary, when it results from other pathological conditions or from taking specific drugs.

In summary, the reason why gout arises is the presence of one or both of the following factors:

Excessive purine synthesis, with overproduction of uric acid.
Decreased renal excretion of uric acid.

In the first case, the aetiology is essentially hereditary and is aggravated by increased dietary intake of purine compounds (meat, alcohol).

In the second case, hypereuracaemia is caused by problems with the kidney, which does not function as it should, failing to excrete excess uric acid.

Traditionally, the onset of gout is blamed on excessive food intake.

Although this factor, along with alcoholism, sedentariness and the abuse of certain drugs, is predisposing, its contribution remains marginal in individuals who are not genetically predisposed.

The symptoms of gout are quite specific:

Intense joint pain, almost always in the big toe, which begins acutely with attacks that usually last for a few days and then gradually fade away.
Joint oedema and erythema, which accompany the pain. In addition to the wrists, ankles, heels and knees, the earlobes and kidneys are also sites where uric acid crystals can settle, leading to the formation of tophi. This is particularly the case when the disease evolves into its chronic form.
General malaise and fever are possible.

The tophi are initially salmon-pink in colour, later becoming – in the chronic form – yellowish-white.

Gout can also favour the formation of urinary stones, to the point of impairing – in cases not treated promptly or correctly – kidney function.

Gouty nephropathy

Excessive uric acid accumulation can cause gouty nephropathy.

This disease is an obstructive renal inflammation of the renal tubules and possibly results in acute renal failure.

Diagnosis

Gout is diagnosed by performing specific laboratory tests to assess that the uric acid concentration in blood and urine is within the normal range.

Obviously, suspicion of gout arises in the presence of factors that favour increased production and/or reduced uric acid excretion.

Thanks to the medical history, the doctor will gather the necessary information such as: previous tests, any concomitant diseases, family history, use of medication, food and drink.

At this point, an objective test will look for signs that may suggest the presence of an inflammatory process such as: redness, swelling and pain in the joints.

In this case it may be useful to perform an X-ray, which is necessary to better characterise the bone damage, which occurs in an advanced state of the pathology.

If blood and urine tests show hyperukaemia and the objective test is suggestive of arthritis, the diagnosis can be confirmed with certainty by microscopic analysis of the synovial fluid, which should reveal the presence of needle-shaped uric acid crystals.

Prevention

Although genetic factors are important in the development of the disease, virtuous lifestyle changes can reduce uric acid levels in the body, preventing the onset of the disease.

In particular, we can make certain dietary choices that are particularly effective, such as reducing meat and fish intake, consuming adequate amounts of vitamin C, limiting alcohol consumption and reducing one’s body weight.

Correct fluid intake is also crucial in gout, as it helps prevent kidney stones from forming.

Treatment and therapy

In the acute phase it is necessary to intervene early to reduce the painful symptoms: the doctor will prescribe anti-inflammatory drugs (or steroids) and colchicine.

Once the inflammation has been reduced, the aim of therapy will be to maintain normal uric acid levels to prevent the onset of new attacks, avoiding the formation of new tophi and a chronic evolution of the pathology.

Fundamental, in addition to the use of the appropriate drugs, will be a correct eating style accompanied by the intake of at least 2 litres of water a day (if there are no contraindications), avoiding alcoholic beverages – especially beer – and limiting foods high in purines (meat, fish and legumes).

If this is not enough, drugs will be prescribed to reduce uric acid levels, such as allopurinol, which inhibit uric acid synthesis, and uricosuric drugs such as probenecid or sulfinpyrazone, which promote its elimination.

In the case of gout, drugs that may interfere with purine metabolism should be discontinued.

In any case, therapy with these drugs should begin after the acute picture has resolved.

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