Getting to Know Gout
by Ken Flieger

     Say the word "gout" and some people will think of a bloated
king surveying the remains of a sumptuous feast, wine glass in
hand, swollen foot propped on a pillow--looking for all the world
like the dismal product of a grossly overindulgent life.
     There are a couple of flaws in that conventional image. We
know, for example, that gout doesn't afflict only the privileged
classes and that women, too, are susceptible, though a lot less
than men.
     But still there's a good deal right with that picture. It
correctly reflects that:
     About 90 percent of people afflicted with gout are men over
40.
     Obesity in general, and in particular excessive weight gain
in men between ages 20 and 40, has been shown to increase the
risk of gout. In fact, about half of all gout sufferers are
overweight.
     Alcohol abuse and so-called "binge" drinking are associated
with gout, as is eating purine-rich foods such as brains,
kidneys, liver, sardines, anchovies, and dried beans and peas.
     In addition, careful scientific surveys have shown that
occupational exposure to lead, the use of certain drugs to
control high blood pressure, some surgical procedures, family
history (possibly a genetic predisposition), and trauma are all
linked to an increased risk of gout. Indeed, the prevalence of
gout--the number of gout sufferers for each 100,000 people--is
rising rapidly in the United States and other developed
countries. Some authorities believe the increase is related to
higher living standards.
     Our fanciful image of a gouty Henry VIII (or other bloated
monarch) can't show, however, the one common denominator that
ties together this mixed bag of risk factors: failure of the
metabolic process that controls the amount of uric acid in the
blood. For most people, the process works just fine. But in some
1 million Americans, uric acid metabolism has gone seriously
haywire. As a result, they suffer from gout.
     And suffer they do. An Englishman, Thomas Sydenham, writing
in the 17th century, left this unfortunately all-too-accurate
description of a typical attack of gout:

     The victim goes to bed in good health. About two o'clock in
     the morning, he is awakened by a severe pain in the great
     toe; more rarely in the heel, ankle, or instep. The pain is
     like that of a dislocation. [It] becomes more intense. So
     exquisite and lively meanwhile is the feeling of the part
     affected, that it cannot bear the weight of the bed-clothes
     nor the jar of a person walking in the room. The night is
     passed in torture.
     
A Crystal Culprit
     In spite of the agony and havoc it can cause, uric acid is a
normal constituent of the human body. Ordinarily about one-third
of the uric acid in our system comes from food, especially foods
like those noted earlier that are rich in purines. The rest we
produce ourselves through ordinary metabolism.
     The body converts purines to uric acid. The level of uric
acid in the blood fluctuates in response to diet, fluid intake,
overall health status, and other factors. Men normally have
somewhat more uric acid than women do (although the difference
begins to narrow after menopause), and in both sexes it tends to
increase with advancing age.
     Higher-than-normal amounts of uric acid in the blood, a
condition called hyperuricemia, is quite common and only rarely
warrants medical treatment. On the other hand, sustained
hyperuricemia is the primary risk factor for gout. It's safe to
say that, while not all people with hyperuricemia develop gout,
virtually everyone with gout is hyperuricemic. It works this way:
     At normal and even somewhat elevated levels, uric acid stays
in solution in the blood. It moves through the circulation, gets
filtered by the kidneys, and is excreted in the urine. When,
however, blood uric acid levels rise above a certain
concentration (which varies with temperature and blood acidity),
it forms needle-like crystals that lodge in or around a joint.
     In response to irritation caused by uric acid crystals, the
skin covering the affected area rapidly becomes tight, inflamed,
swollen, and red or purplish. These classical signs of
inflammation, together with sudden and extreme pain (just as
Thomas Sydenham described), strongly suggest an acute attack of
gout. The diagnosis is confirmed by laboratory finding of uric
acid crystals in fluid taken from the affected joint.
     Why is the big toe the most common site for an initial gout
attack? Perhaps because first, the extremities are a bit cooler
than other parts of the body, and uric acid crystals form more
readily at lower temperatures; and second, normal walking and
standing subject the feet to considerable stress. Together, these
factors might explain why the big toe, heel, instep, and Achilles
tendon are among the places that gout attacks first. Other
targets, especially in untreated patients who have recurrent
attacks of gout, are the knee, elbow, wrist, fingers and, less
often, the shoulder, pelvis, spine, and internal organs.
     Gout is classified as a form of arthritis because it is
initially and predominantly a disease of the joints. Other
similar conditions exist; one called flpseudogoutfl is somewhat
milder than true gout and is caused by calcium rather than uric
acid crystals. Infection or trauma to the affected area can mimic
gout and mislead both patients and health professionals. Accurate
diagnosis is essential for appropriate treatment.
     Without treatment, an initial acute attack of gout will run
its painful course within several days or a few weeks, by which
time all outward evidence of the disease disappears. The next
acute attack--50 or more percent of gout sufferers will have a
second attack--may not occur for months or years. Subsequent
attacks, however, are likely to be more frequent, more severe,
and more destructive to joints and other tissue unless the
problem is treated. Over time, uric acid crystals accumulate in
the body, causing gritty, chalky deposits called tophi that are
sometimes visible under the skin, particularly around joints and
in the edges of the ears. Tophi may also form inside bone near
the joints, in the kidneys, and in other organs and tissues,
causing permanent damage. Advances in  treatment, fortunately,
have made this kind of chronic gout extremely rare.

Treatment
     As with most illnesses, effective treatment of gout depends
on a correct diagnosis. Gout can be unequivocally diagnosed by
telltale uric acid crystals in joint fluid. But appropriate
treatment is often started after a "clinical" diagnosis based on
painfully obvious signs and symptoms and other relevant factors,
such as the patient's uric acid level, age, weight, gender, diet,
and alcohol use. If this picture adds up to a strong suspicion of
gout, treatment can be started with the immediate goal of
arresting the acute attack.
     Acute gout is treated with drugs that block the inflammatory
reaction. One of the oldest agents known to be effective against
acute gout is colchicine, which comes from a common European
plant, the autumn crocus, and is marketed in this country
primarily as a generic drug. An English clergyman, Sidney Smith,
said a century and a half ago that he had only to go into his
garden and hold out his gouty toe to the plant to obtain a prompt
cure. This may have been an exaggeration, but a rapid response to
colchicine suggests that the patient does indeed have gout.
     This old, powerful remedy is now used less often than it
once was because it can be quite toxic, causing nausea, vomiting,
diarrhea, and stomach cramps when taken by mouth and severe (even
fatal) blood disorders when taken intravenously. Moreover, modern
agents, specifically nonsteroidal anti-inflammatory drugs
(NSAIDs) are highly effective against acute gout and less toxic
than colchicine. To treat an acute case of gout, the first choice
of many physicians is the NSAID Indocin (and other brands of
indomethacin). Naprosyn (naproxen) is another NSAID commonly used
in acute gout.
     Steroid drugs, such as Deltasone (and other brands of
prednisone) and Acthar (and other brands of adrenocorticotropic
hormone), may be used if NSAIDs fail to control an acute attack.
Steroids may be taken by mouth or by injection into the
bloodstream or muscle.
     Drug treatment usually relieves the symptoms of acute gout
within 48 hours. Subsequent treatment, which may well be
lifelong, is aimed at preventing further attacks by controlling
uric acid in the blood--keeping it below concentrations at which
crystals can form. Two main treatment approaches are used, in
some cases simultaneously.
     One approach is to slow the rate at which the body produces
uric acid. Zyloprim (allopurinol) has been approved for the
treatment of gout and is frequently prescribed for gout patients
who have uric acid kidney stones or other kidney problems. Side
effects include skin rash and upset stomach, both of which
usually subside as the body becomes used to the drug. Zyloprim
makes some patients drowsy, so they need to be cautious about
driving or using machinery.
     The other approach to controlling gout following an initial
acute attack is to increase the amount of uric acid excreted in
urine. Two so-called uricosuric drugs commonly used for this are
Benemid (probenecid) and Anturane (sulfinpyrazone), both approved
by FDA for gout treatment. In addition to lowering blood uric 
acid levels, these drugs help dissolve deposits of uric acid
crystals around joints and in other tissue. Zyloprim is also used
to dissolve tophaceous gout in uric acid over-producers.
Uricosurics can cause nausea, stomach upset, headache, and a
potentially serious skin rash.
     Drugs to control uric acid levels may, paradoxically,
prolong an acute attack. For this reason, Benemid, Anturane and
Zyloprim are not used during the acute stage of gout. They may,
in fact, induce gout flare-ups during the early part of long-term
use. Accordingly, colchicine in a dose low enough to avoid toxic
side effects is sometimes prescribed to prevent acute attacks
during this phase of treatment.

Common-Sense Measures
     Better understanding of what gout is, what causes it, and
how to treat it has perhaps dispelled some of the traditional
myths about what has been erroneously called "the disease of
kings." Then, too, folk wisdom about gout, coupled with good
science and medicine, points to measures that prudent people can
take to prevent or at least lessen the severity of the condition.
     Many authorities and the Arthritis Foundation, which
supports research and public service programs relating to gout,
advocate weight control as a logical aid to gout prevention. They
point out, however, that people who are overweight should get
professional guidance in planning a weight-reduction program,
because fasting or severe dieting can actually increase uric acid
levels.
     Experts generally agree that people with gout can eat pretty
much what they want, within limits. People who have kidney stones
caused by uric acid may need to avoid purine-rich foods. But this
problem can usually be handled effectively with drug treatment.
     Curbing alcohol use and avoiding "binge" drinking can reduce
the likelihood of acute attacks. So can drinking six or eight
glasses of water a day, which dilutes uric acid and aids its
removal by the kidneys. Some medicines--in particular the
thiazide diuretics ("water pills") used to control high blood
pressure--tend to increase uric acid levels. A gout patient
taking one of these drugs may have to switch to another type of
diuretic or blood pressure medicine.
     Finally, although uncommon, it might be helpful to find out
if an environmental or occupational exposure to lead is playing a
role in a patient's problem with gout.
     While a cure for gout--a treatment that gets rid of the
condition once and for all--isn't on the horizon, reliable and
effective ways of diagnosing gout and keeping it under control
constitute one of the more impressive success stories of modern
medical science.
     There may be no sure-fire way to keep a person from having
that first agonizing attack, but prompt treatment can minimize
the risk of further attacks and virtually rule out the damaging
and crippling effects of chronic gouty arthritis. 

Ken Flieger is a writer in Washington, D.C.