Gout and high blood uric acid levels (hyperuricaemia)

What are the causes?

The characteristic acute inflammatory arthritis of gout is caused by the deposition of needle-shaped crystals of uric acid (mono-sodium urate) in the joints. Uric acid is a waste product produced in the body that passes through the kidneys into the urine. Some people, due to their genetic makeup, do not excrete adequate amounts of uric acid from their kidneys. Decreased removal of uric acid for kidneys over time leads to a slow but steady increase in the level of uric acid content of their body that may also cause a high blood uric acid level.

Research has shown that in general population there are individuals whose blood uric acid levels are much higher than the range seen in normal persons. While the majority of such individuals may never develop acute gouty arthritis attack, most of them would be candidates for high blood pressure, coronary heart disease, brain ‘stroke’ and kidney damage (discussed below). Such individuals are called hyperuricaemic individuals i.e. those having high blood uric acid levels. While most hyperuricaemic men would never get acute gouty attack, a few of them, especially those with family history of gout would start developing acute gouty arthritis attacks by the age of about 40 years. Interestingly, blood uric acid levels generally falls during acute attack of gout. Therefore, testing blood uric acid for diagnosing an acute joint problem as ‘gouty arthritis’, is not recommended.

Research has also shown that men with gout almost always have several associated diseases – often identified by a term called ‘metabolic syndrome’ that includes obesity, high blood pressure, high cholesterol levels, tendency for developing diabetes and very high risk for getting heart attack and brain ‘stroke’. Research has also shown that high blood uric acid is directly related to poor cardiovascular health causing high blood pressure and damage of blood vessel lining further adding to the cause for early age heart attack and brain ‘stroke’. High blood uric acid is also injurious to kidney tissue. Thus, over a period of time most patients with gout develop slowly progressive kidney damage. It is very important to mention that only a small proportion of persons having high blood uric acid level would ever get actual acute gout attack and gouty arthritis. Most of them will never get gouty attack yet, they are prone to heart attack, brain ‘stroke’ and other features of metabolic syndrome.

In this regard it is important to mention that although high blood uric acid levels are directly toxic to blood vessels and cause high blood pressure. Once that happens, the high blood pressure becomes a permanent feature. Therefore, reducing blood uric acid levels by uric acid lowering drugs do not cause lowering of blood pressure. Such patients would require life-time treatment for high blood pressure with appropriate blood pressure lowering drugs.

How is the diagnosis made?

Acute gouty arthritis attack can be diagnosed by typical clinical symptoms easily recognised by a trained physician. Sudden acute onset of red hot, and very painful swelling at the base of the big toe or any one of the joints in ankle-feet region (described above) where touching even with a soft cloth causes excruciating pain, occurring in a male above 40 years of age, often with family history, and history of similar previous attacks of acute joint problems, should be considered acute gouty arthritis. Such a patient often has some ‘trigger’ (see above) that precipitates the acute attack. He should immediate seek medical attention, preferably from a trained rheumatologist (physicians trained in the evaluation, diagnosis and treatment of joint diseases).

The diagnosis is confirmed by demonstrating uric acid crystals (that look like small needles) in the joint fluid. This procedure is best done by a trained rheumatologist who would also examine the fluid and confirm if uric acid crystals are present in the fluid. It is useful to remember that testing for blood uric acid level does not give the diagnosis of gout. As mentioned above, blood uric acid level is usually normal during acute gouty attack. Therefore, a high blood uric acid level does not necessarily mean that the person has gout, nor does a normal blood uric acid level exclude the possibility of acute gouty arthritis attack. Therefore, the diagnosis of gout should be left to the rheumatologist who would see the clinical picture as well as try to demonstrate uric acid crystals in the joint fluid.

Chronic gouty arthritis affecting several joints in the extremities is even more difficult to diagnose and only well-trained and experienced rheumatologist will be able to diagnose this condition with certainty. Of course chronic tophaseous gout is so striking in appearance that it is easy to diagnose by simply looking at the joints of the patients.

What is the treatment?

Treatment of acute gouty attack requires immediate control of the acute joint symptoms followed by strategies to prevent future possible attacks, and joint and tissue damage due to the deposition of uric acid crystals in the long run. Acute attack is treated with the use of fast acting anti-inflammatory drugs. Commonly used drugs belong to the category of so-called non-steroidal anti-inflammatory drugs (NSAIDs). There are several of them like ibuprofen, diclofenac, naproxen, indomethacin. However, most of them have a major side-effect i.e. severe irritation of the gastrointestinal tract that may even lead to ulcer formation (called peptic ulcer). The newer anti-inflammatory drugs called coxibs (celecoxib, etoricoxib) have much less gastrointestinal toxicity with equal efficacy in controlling acute gouty attack.

A recent report recommends that patients who cannot take NSAIDs (due to allergy or GI disease), one of the best methods for quick relief for acute gouty attack is prescribe prednisolone 35 mg daily for 5 days. It is said to be a highly effective, cheap and safe treatment for acute gouty attack. Injection of depot-preparations of glucocorticoids (e.g. depot-methylprednisolone or triamcinolone acetonide) in the joint itself.After the acute attack subsides, the person must be investigated to find out if he has any underlying renal disease, or he is taking some drugs that cause rise in blood uric acid levels. If the rheumatologist finds a definite cause for high blood uric levels, all efforts must be made to correct it. However, in the majority of such patients no obvious cause is found and such person are labelled as having ‘primary gout’. 

Such persons are advised as follows:

• General positive health practices:
• Dietary precautions (see Appendix – I – above)
• Regular fitness workouts especially aerobic exercises, control of cholesterol, high blood pressure. It is important to reduce weight very gradually as sudden weight loss can also precipitate an acute attack of gout.
• Plenty of fluids on a regular basis.
• Avoid all the drugs that can cause acute gouty attack or raise the blood uric acid levels (aspirin is one of them).

If these measures do not prevent further attacks of gout and blood uric acid remains persistently high, then, under careful guidance of the doctor, uric acid lowering drugs can be instituted. These include allopurinol, sulfinpyrazone, and probenecid. It is important to remember that, if given for the first time in a person who has had acute attacks of gouty arthritis in the past; these drugs may precipitate an acute attack of gout. Therefore, it is necessary to take these drugs under the guidance of the doctor who may prescribe some additional drugs to prevent acute attack of gout during the initiation period with these drugs (e.g. colchicines). Therefore, the bottom-line of treatment of gouty arthritis should be to consult a well-trained and experienced rheumatologist and follow the advice given by him/her. The rheumatologist now have several effective drugs to keep uric acid levels below 5 mg/dL to completely prevent any further attacks of gouty arthritis.