Introduction
Understanding gout:
Not just acute joint attacks
Understanding gout, and consequently managing it, has always been demanding for clinicians
but greater knowledge of disease pathogenesis, more sophisticated diagnostic modalities,
and an increasing array of therapeutic options is diminishing this challenge
Frédéric Lioté MD PhD
Professor of
Rheumatology,
University Paris
Diderot; Rheumatology
Department, Viggo
Petersen Centre,
Lariboisière Hospital,
Paris, France
Gout is one of the most common human
joint diseases, 3–10-times more frequent
than rheumatoid arthritis. It is one of the few
chronic diseases that when properly treated with
a hypouricaemic drug, can easily lead to a ‘cure
under treatment’. The difficulty lies in the clinical
inertia of the attending physician and the patient’s
compliance. Most patients are treated on an
outpatient basis, but they often come to hospital
emergency rooms for gout attacks, which is a great
place to get the patient back in control.
What is gout?
It is a disease of overload of the body with uric
acid salts – urates – that form microcrystals in
and around joints, or even in the skin or other
structures. These microcrystals can lead to very
characteristic acute arthritis. Gout is not just acute
joint attacks. 1
How are urate microcrystals formed?
The main cause is hyperuricaemia, that is, an excess
of serum uric acid (sUA) in the blood. The upper
value of normal uricaemia in both sexes is 360µmol/l
or 6.0mg/dl. Above this level, in about one in ten
patients, the excess sUA/hyperuricaemia precipitates
as microcrystals. This phenomenon is reversible,
which is reassuring for the patient, the doctor and
the pharmacist: if the uricaemia is reduced below
6.0mg/dl (300µmol/l), the crystals dissolve.
How is hyperuricemia established?
It is simple: gout is mainly of genetic origin. 2 The
excess uric acid is a result of reduced urinary
elimination and enhanced intestinal absorption.
Uric acid is filtered through the glomerulus and
partially reabsorbed through the renal tubule,
before being secreted and eliminated in the urine.
Uric acid transporters, such as URAT1 in the renal
tubule and ABG2 in the intestine and renal tubule,
are involved. They can have abnormal activity and
reabsorb too much, for example, for URAT1. The
uric acid ‘bathtub’ then overflows and leads to
crystallisation of the uric acid.
Are there other factors besides the genetic
component?
Environmental/dietary factors are often involved:
high purine foods (meat, seafood, etc), purines from
other sources, such as beer with or without alcohol,
and excess fructose (for example, from sweetened
carbonated drinks). 3
Comorbidities and their treatment reduce uric
acid elimination including: chronic kidney failure
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