Gout is considered a form of
crystal deposition arthritis, hence the name, gouty arthritis.
Uric acid, a chemical that is found in the serum component of our blood,
is the key to understanding gout. Excessively high levels of uric
acid lead to the deposition of monosodium urate crystals into joints and
certain subcutaneous spaces in the body. To understand the way that acute
gouty attacks occur, let's use a simple example;
Example - As
children, we would make our own rock candy. We'd get a pot of
water and begin to heat it on the stove. As the water warmed, we'd
add sugar. The hotter the water became, the more sugar we could dissolve.
When the water was close to a boil and saturated with sugar, we would
remove it from the heat and allow the sugar to crystallize on a string
as the water cooled.
Acute gouty attacks occur in much the same manner. Most acute
gouty attacks occur in the late
hours of the night. As we sleep, our bodies tend to focus on the primary
metabolic functions such as digestion, breathing, etc. The extremities,
such as the feet tend to cool as a result of this 'lack of attention'.
As they cool, and if the dissolved amount of uric acid is high enough,
the result is the change of uric acid from a liquid to a crystal. The
hallmark symptoms of gout are a) an acute onset of pain and b) an onset
that occurs while you're sleeping in the early hours of the night.
Uric acid is measured in the
serum (liquid) component of our blood. Normal levels for men are
less that 7mg/dl of serum and slightly less for most women. This
level tends to rise in women following menopause. The vast
majority of gout patients are men with an onset during the 4th to 5th
decade of life. If serum uric acid levels
surpass 10mg/dl, the likelihood of a gout attack is very probable.
High levels of uric acid
result from high levels of intake or low levels of excretion of purines. The inability to metabolize purines may be inherited or
acquired. Purines are protein components in foods that are found
commonly in the following foods;
red meats and organ parts (sausage, liver, kidney, tongue, heart)
Dark fillet fish (mackerel, anchovies, sardines, herring and fish roe)
Dairy products (milk, ice cream, cottage cheese)
Individuals who have had
acute gouty attacks should limit their intake of these foods. This
does not mean that they need to completely eliminate them from their
diets, but rather they should consume these foods with moderation. Serum
uric acid is also significantly influenced by the ability of the kidney
to excrete uric acid. Factors that may change normal renal function
may result in limited excretion of uric acid. These factors
include the use of thiazide (HCTZ -hydrochlorthizide) diuretic therapy,
dehydration and renal failure.
Many antihypertensive (blood pressure lowering) medications include HCTZ
and include Dyazide, Maxide, Moduretic, indapamide, Microzideand
Other factors that may contribute to the onset of gout include trauma, the
stress of surgery, emotional stress, fatigue, infection or the use of penicillin.
Treatment of gout and gouty arthritis
The most significant consideration in the treatment of
gout is the frequency of
attacks. Frequent attacks (more than one a year) will result in
progressive erosion of the joint, leading to painful chronic
arthritis. Isolated attacks (less that one a year) lead to minimal
destruction of the joint. The frequency of gouty attacks
determines whether treatment is merely for each attack, or whether daily
medication should be taken to lower levels of serum uric acid.
Treatment of acute attacks
includes the use of prednisone or non-steroidal anti-inflammatory medications such as
Indocin or Clinoril. Control of pain may require a mild narcotic such as
codeine. Other treatment may include Colchicine which yields
dramatic results but carries severe side effects which include nausea
and severe diarrhea. Colchicine is dosed once every two hours until the
desired (or undesired) effects are achieved.
Treatment of recurrent
attacks includes the modifications in diet as previously discussed and
the use of Allopurinal, an inhibitor of uric acid synthesis.
Probenecid and sulfinpyrazone are also used to increase the output of
uric acid by the kidney. Dosing and combination therapy depends
upon the level of serum uric acid which is measured periodically during
therapy. Individuals prone to gouty attacks should also maintain a
high fluid intake to promote the excretion of uric acid and decrease the
tendency to form uric acid stones in the kidney and bladder.
Gouty arthritis is the sequela of multiple untreated attacks that
progressively destroy the cartilage of the joint. Surgical debridement of
a joint with chronic damaged by chronic gout shows depositions of a material
called gouty tophi that resemble cottage cheese. These gout crystals erode
the surface cartilage resulting in premature destruction of the joint.
Debridement of the joint, fusion or joint replacement is often indicated.
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