Over the last two or three decades, scientists’ knowledge of gout has greatly increased. In turn, the medical management of the gout sufferer has vastly improved. Gout has not been eradicated and probably never will be, but the treatment is so much better that the illness has become far less severe.
Gout is one of the oldest ailments known to medicine. Indeed Hippocrates, the physician of ancient Greece known as the father of medicine, was acquainted with the malady more than 2400 years ago and called it “the unwalkable disease.”
Many famous people have been sufferers including Kublai Khan, Erasmus, Alexander the Great. Queen Anne, Francis Bacon, Lord Beaver brook, Oliver Cromwell, Charles Darwin, Benjamin Franklin, Henry VIII (you might have guessed), Sir Isaac Newton, John Wesley, and Cardinal Wolsey, to name just a few.
An Olympic marathon has been won by a gout sufferer – in between attacks.
WHO GETS IT?
The popular concept of the gout sufferer as an overweight middle-aged to an elderly man of affluence who over-eats and over-drinks is not really accurate and is exaggerated. Many people who are lean and live frugal lives suffer also from gout. Diet and living habits are secondary factors. Gout can occur at any age and in either sex but about 95 percent of cases are male. The first attack comes usually in middle age.
The disease is not uncommon but estimates of its occurrence vary. At least 1 percent of the population have gout and some observers estimate the incidence to up to 4 percent.
WHAT IS IT?
At this stage, gout should be defined. It is an inborn error of metabolism whereby uric acid levels in the body are higher than normal and the acid crystallizes out in joints.
An “inborn error of metabolism”? This occurs in a person born with a relative inability to handle certain foods or parts of foods. This inability leads to the over-production of uric acid, and the excess at times can become deposited in joints, thus producing acute painful gouty arthritis. Everybody has uric acid in the bloodstream but gout sufferers have more than normal. Apart from becoming deposited in joints, the acid can crystallize out under the skin and also in the kidneys.
In severe cases, before modern methods of treatment, it would crystallize in the kidneys and thus block the flow of urine. This led to kidney failure, which was a common cause of death in gout patients before the 1940s and 1950s.
The medical term for an abnormally high blood level of uric acid is hyperuricemia (there are causes of hyperuricemia other than gout but these will not be discussed here).
Certain foods contain high proportions of substances that are precursors of uric acid. Gout sufferers should try to avoid these foods (which is almost impossible) or take them in small quantities.
In addition, they should also keep up a high fluid intake, which has both a diluting and flushing effect on the uric acid – dehydration tends to produce crystallization of uric acid in the kidneys, and kidney-stones of the acid might form.
FOODS TO BE AVOIDED
- Brussels sprouts
- Heart Kidney
- Fish roe
- Meat extracts
- Red wine
THE ACUTE ATTACK
The typical presentation of gout is the sudden onset of pain in a joint. The pain is severe and intense, lt may occur in any joint (except the jaw, for some strange reason) but the commonest to be affected is the joint between the big toe and the foot.
The joint becomes red, hot and swollen and acutely tender to touch.
The first attack, if untreated, may continue for several days; or it may subside in a few hours, but this is unusual. The attack can come on at any time and under any circumstances. Not uncommonly it awakes the patient in the early morning hours.
Acute attacks can be brought on by any type of upset to the body, such as an injury or by over-eating and over-drinking. Any infection, even a cold or sore throat, can sometimes trigger off an attack. Changes in the weather, stress, and worry, and unaccustomed exercise are other triggers. However, sometimes attacks occur for no apparent reason at all.
Occasionally a patient will feel a little “off” in the stomach before an attack. Others notice that they tend to pass more urine. Some perspire or just feel vaguely unwell.
A kidney-stone may be passed before an attack. This is usually very painful. Any such stone should be kept for analysis; in gout, they are generally uric acid stones.
After the attack the patient seems to return to normal health; however, the hyperuricemia will persist.
Once you have gout you always have it, so you must keep it under control.
Complications of chronic gout and chronic gouty arthritis can occur when the underlying hyperuricemia is left untreated; there may be increasing frequency and severity of the acute attacks, and this in turn can lead to more joint changes, bringing on permanent deformity and pain. The joints affected are usually the same as those in the acute attacks but in time other joints can become involved. Feet, ankles, knees, elbows, hands, shoulders, hips, and spine may all be affected.
Another complication is the formation of lumps of uric acid. These lumps most commonly occur alongside joints but also can occur under the skin around the nose and ears. They are very unsightly but fortunately are rarely seen nowadays. Crystals can also deposit and affect the heart muscle, but again this is very rare.
As you will now realize there are two aspects – the acute attack and what happens after the acute attack.
Sometimes the pain of an acute attack is so severe that an injection of a narcotic drug is warranted, but in most cases, the newer anti-inflammatory drugs settle the attack down within a few days. Rest, of course, is also important.
The drugs most commonly used are indomethacin, cortisone, phenylbutazone and colchicine. All are effective but may have side effects in some patients, particularly when used in the fairly high doses necessary to control the acute attack.
The side effects are mainly on the stomach and some patients develop nausea and vomiting and diarrhea. Fortunately, these symptoms disappear when the drug is withdrawn or the dosage reduced.
The duration of treatment, the dosage of the tablets, and response are critical and variable and require good judgment and careful assessment by the doctor.
After the acute attack has settled the aim is to prevent a recurrence. Nowadays sufferers are very fortunate in having available two groups of drugs which if taken on a longterm basis greatly reduce the likelihood of further attacks.
The first “preventative” is a drug called probenecid; this acts on the kidneys making them excrete excess uric acid, which is passed out in the urine. Thus gout subjects taking probenecid excrete much more uric acid than normal people.
The other drug is called allopurinol, and this acts differently. It produces a block in the pathway of uric acid production, and so lowers the level of acid in the body not by working through the kidneys but by working in the metabolic food centers (mainly the liver). So the gout subject who takes allopurinol just does not make as much uric acid.
Both drugs are very effective and fairly free of side effects. The choice is a matter of judgment, and sometimes complex tests are used to help decide.
The other advice given to gout subjects (note this use of the word “subjects” now, rather than “patients” or “sufferers”) is to keep up a good fluid intake.
The gout subject is told that his medication will continue indefinitely. At variable intervals, the blood uric acid level is measured and the dosage adjusted accordingly.
Acute attacks can occur while the subject is taking preventive tablets but they are far less common and far less severe.
The longterm approach must be stressed. The subject must fully understand what his doctor is doing and co-operate; the rapport between doctor and subject is essential. It is true to say that gout cannot be cured but it can be so well controlled that the subject can lead a normal life in every way and have a normal life expectancy – remember the marathon runner.
Medical scientists are still investigating the metabolic pathways that lead to over-production of uric acid. This research is now getting down to complex and intricate biochemical and molecular levels.
There have been several studies attempting to link gout and coronary artery disease. So far there is really nothing conclusive but one study has shown that coronary artery disease patients have higher uric acid levels than average. Perhaps there are dietary factors in common to both conditions. Excess of rich foods, fatty foods, and alcohol certainly are bad for both conditions but to what extent they are causative factors is still not known.
However, gout subjects should avoid excesses and if necessary modify their living and eating habits.