Deckle Edge Media_Maluti_Issue 1 Winter 2017

Apple a Day
Disease of Kings
& the King of Diseases
the risk of hyperuricemia. Increased production of uric acid is the
result of interference by a product of fructose metabolism in purine
metabolism. This interference has a dual action, both increasing
uric acid and increasing the synthesis of purine. Fructose also
inhibits the excretion of uric acid, apparently by competing with
uric acid for access to the transport protein SLC2A9. The effect of
fructose in reducing excretion of uric acid is increased in people
with a hereditary (genetic) predisposition toward hyperuricemia
and/or gout.
Starvation causes the body to metabolize its own (purine-rich)
tissues for energy. Thus, like a high purine diet, starvation increases
the amount of purine converted to uric acid. A very low calorie
diet without carbohydrate can induce extreme hyperuricemia;
including some carbohydrate (and reducing the protein) reduces
the level of hyperuricemia. Starvation also impairs the ability of
the kidney to excrete uric acid, due to competition for transport
between uric acid and ketones.
By DR. FRANCOIS VAN WYK • 058 622 1691
Gouty arthritis was among the earliest diseases to be recognized as a clinical entity. First identified by the
Egyptians in 2640 BC, podagra (acute gout occurring in the first metatarsophalangeal joint) was later recognized
by Hippocrates in the fifth century BC, who referred to it as “the unwalkable disease”. Some of Hippocrates’s
remarkable clinical perceptions in relation to gout are preserved in aphorisms, which are as true today as
they were 2500 years ago. Hippocrates also noted the link between the disease and an intemperate lifestyle,
referring to podagra as an “arthritis of the rich”, as opposed to rheumatism, an “arthritis of the poor”. It was
called the Disease of Kings and in some eras gout was perceived as socially desirable because of its prevalence
among the politically and socially powerful.
The common cold is well named – but the gout seems instantly to
raise the patient’s social status, comment from the London Times in
1900.
As a GP in Harrismith I have found that gout is synonymous with
pain in single joints. In a significant percentage of cases I have
found that gout is misdiagnosed and therefore the wrong treatment
is given. The so-called “gout mix” is sold over the counter and
although it suppresses pain in the short term it does not provide
a long-term solution. Let’s make the right diagnosis for a lasting
cure.
What is gout?
Gout is caused by the build-up of uric acid in your system. High uric
acid levels can form needle like crystals. The deposited sodium
urate crystals can be regarded as the cause of gouty inflammation,
which is characterized by a warm, red, swollen and painful joint.
What causes high uric acid levels?
Many factors contribute to hyperuricemia (high uric acid levels in
the blood), including genetics, insulin resistance, hypertension,
hypothyroidism, renal insufficiency, obesity, diet, use of certain
medications, and consumption of alcoholic beverages. Of these,
alcohol consumption is the most significant.
Causes of hyperuricemia can be classified into three functional
types: increased production of uric acid, decreased excretion of
uric acid, and mixed type. Causes of increased production include
high levels of purine (found in high concentrations in meat and
meat products) in the diet and increased purine metabolism.
Causes of decreased excretion include kidney disease, certain
drugs, and competition for excretion between uric acid and other
molecules. Mixed causes include high levels of alcohol and/or
fructose in the diet, and starvation.
Increased production of uric acid
A purine-rich diet is a common but minor cause of hyperuricemia.
Diet alone generally is not sufficient to cause hyperuricemia.
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Purine content of foods varies. Foods high in certain purines may
be more potent in exacerbating hyperuricemia.
Hyperuricemia of this type is a common complication of solid
organ transplant. Apart from normal variation (with a genetic
component), tumor lysis syndrome produces extreme levels of uric
acid, mainly leading to renal failure. The Lesch-Nyhan syndrome (a
rare genetic disorder) is also associated with extremely high levels
of uric acid.
Decreased excretion of uric acid
The principal medications that contribute to hyperuricemia by
decreased excretion are the primary antiuricosurics (medication
that decrease uric acid excretion). Other medication and agents
include diuretics, salicylates, nicotinic acid and diclofenac
(Voltaren).
A ketogenic diet impairs the ability of the kidney to excrete uric
acid, due to competition for transport between uric acid and
ketones.
Mixed type
Causes of hyperuricemia that are of mixed type have a dual action,
both increasing production and decreasing excretion of uric acid.
High intake of alcohol (ethanol), a significant cause of hyperuricemia,
has a dual action that is compounded by multiple mechanisms.
Ethanol increases production of uric acid by increasing production
of lactic acid, hence lactic acidosis. Ethanol also increases the
plasma concentrations of hypoxanthine and xanthine (potent
purines) via the acceleration of adenine nucleotide degradation,
and is a possible weak inhibitor of xanthine dehydrogenase.
As a by-product of its fermentation process, beer additionally
contributes purines. Ethanol decreases excretion of uric acid by
promoting dehydration and (rarely) clinical ketoacidosis.
High dietary intake of fructose/sugar contributes significantly to
hyperuricemia. In a large study in the United States, consumption
of four or more sugar-sweetened soft drinks per day increased
Diagnosis of gout
To diagnose gout, the doctor will take a patient’s medical
history, examine the affected joint and do a blood test. He
or she will also ask about:
• Other symptoms
• What medications the patient is taking
• The patient’s diet
• How quickly and intensely the gout attack came on
Details of the attack the doctor is looking for: severity of
pain, length of attack, and joints affected.
The doctor will need to rule out other potential causes of
joint pain and inflammation such as infection, injury or
another type of arthritis. He or she will take a blood test
to measure the level of uric acid in your blood. A high level
of uric acid in your blood doesn’t necessarily mean you
have gout, just as a normal level doesn’t mean you don’t
have it. Your doctor may take an X-ray, ultrasound, CT or
MRI to examine soft tissue and bone. The doctor might also
remove fluid from the affected joint and examine it under a
microscope for uric acid crystals. Finding uric acid crystals
in the joint fluid is the surest way to make a gout diagnosis.
Treatment of an acute attack
Here are the steps for getting the pain and swelling of a
gout attack under control:
• Take an anti-inflammatory medication as soon as possible
– preferably Naproxen/Esomeprazole (Vimovo®), as it
has the lowest cardiovascular risk of all NSAIDS.
• Ice and elevate the joint.
• Drink plenty of fluids (no alcohol or sweet sodas).
• Call your doctor and make an appointment.
• Relax; stress can aggravate gout.
• Ask friends and family to help you with daily tasks.
Despite the sudden onset and intense pain, gout attacks
usually peak and resolve within a week or 10 days and then
disappear completely. The first 36 hours are typically the
worst. However, it’s important that once you have an attack,
you begin working with your doctor to control uric acid
levels and prevent future gout attacks.
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