A Practical Approach To Gout
Current management of an
Conservative treatment measures
To treat gout, your doctor will first
focus on relieving your pain by controlling the joint inflammation. Nonsteroidal
anti-inflammatory drugs (NSAIDs), such as ibuprofen, naproxen sodium, or
indomethacin, are available over-the-counter and are effective in relieving pain
If you cannot take these types of
drugs because you have a peptic ulcer or kidney disease, your doctor may
recommend another anti-inflammatory drug called colchicine.
It has also been very effective in
relieving gout, but can cause diarrhea and other side effects while you are
taking the drug.
Sometimes, corticosteroids such as
prednisone and adrenocorticotropic hormone can be injected directly into the
joint to quickly stop the inflammation.
Corticosteroids can also be taken
orally, but are never used for more than a few days to avoid side effects.
Aspirin and aspirin-related drugs
should be avoided because they only worsen gout.
To prevent future attacks and reduce
your risk of permanent joint damage, your doctor will work on lowering your uric
Sometimes simply losing weight will
reduce these levels.
Doctors recommend that anyone with
gout gets plenty of rest, avoids alcoholic beverages, maintains a healthy
weight, eats only small amounts of purine-rich foods, and drinks plenty of
fluids, such as water.
However, if you have repeated, severe
attacks despite these measures, you may need to take drugs such as
which increase the excretion of uric acid by the kidneys.
These drugs don't work for everyone
and can cause kidney stones. Some people have more success with
allopurinol, which actually blocks the production of urate and can dissolve
kidney stones. However, it too has potential side effects, including a skin rash
and liver damage.
Once you begin to take probenecid,
sulfinpyrazone, or allopurinol, you must continue to take them for life to
prevent the return of gout.
You can dissolve the urate crystals
and relieve pain during an attack by applying hot, then cold compresses.
This is called contrast hydrotherapy,
and doctors recommend that you alternate three-minute hot compresses with
30-second cold compresses.
If you have tophi, you will find that
they will shrink as your uric acid levels come down, and your range of motion
around those joints will improve. However, extremely large tophi may need to be
People with high uric acid levels but
no gout symptoms require no treatment at all unless there is a family history of
gout or kidney stones.
While there is no cure for gout, its
symptoms can be managed through a combination of drug therapy and
Lifestyle changes mean maintaining a
healthy weight, getting plenty of rest, exercising, and drinking plenty of
water, especially if you are taking diuretics for high blood pressure.
If you must drink alcoholic
beverages, drink no more than two ounces in one day. Also avoid foods that are
rich in purine, which produces urate.
These include organ meats, such as
liver, kidney, and sweetbreads; sardines; anchovies; shrimp; red meat; gravies;
dried beans; beer; and wine.
Conservative treatment measures
Patients with gout should be advised
to lose weight, moderate their use of alcohol (especially beer), avoid
dehydration and repetitive trauma, and control hypertension and hyperlipidemia.
A purine-restricted diet may be
unpalatable to many patients and may reduce serum urate levels by only 1 mg/dL.
A more reasonable
is to reduce consumption of fat, cholesterol, and meat (especially organ meats,
which contain high levels of purines).
Patients should also be advised to
drink at least eight glasses of liquids daily to prevent dehydration and help
reduce uric acid levels.
Use of thiazides and loop diuretics
may decrease the clearance of uric acid and reduce plasma volume and therefore
should be discontinued or avoided if possible.
Other drugs, such as low-dose
aspirin, ethambutol hydrochloride (Myambutol), pyrazinamide, and niacin,
decrease uric acid excretion by competing for secretion in renal tubules and
also should be avoided.
Agents for acute episodes
Early treatment to reduce
inflammation and pain is important in an acute attack of gout. The current
pharmacologic options include
indomethacin, are commonly the first medication prescribed to treat acute gout.
Other NSAIDS may be equally effective. NSAIDS are initially prescribed at
maximum dosage and reduced as symptoms subside. The medication should be
continued until pain and inflammation are non-existent for at least 48 hours.
NSAIDS which are COX-2 inhibitors may be useful for patients with
gastrointestinal concerns but their use for acute gout has not been specifically
Colchicine is used to
treat acute flares of gouty arthritis and to prevent recurrent acute attacks.
Colchicine does not cure gout or take the place of other medicines that lower
the amount of uric acid in the body. It prevents or relieves gout attacks by
reducing inflammation. Colchicine may be used in 2 ways: some people take small
amounts of it regularly for months or years, while others take large amounts of
colchicine during a short period of time (several hours).
adrenocorticotropic hormone can be used for patients who cannot take NSAIDS
or colchicine. Patients with acute gout typically receive daily doses of
prednisone (20-40mg) or its equivalent for 3 to 4 days, then it is tapered
gradually over one to two weeks. ACTH is administered as an intramuscular
injection (an initial dose and subsequent doses over several days as needed).
(brand name - Zyloprim) is prescribed for chronic gout or gouty arthritis
and works by affecting the system that manufactures uric acid in the body. It is
used to prevent gout attacks, not to treat them once they occur.
Probenecid (brand names -
Benemid, Probalan) is prescribed for chronic gout and gouty arthritis. It is
used to prevent attacks related to gout, not treat them once they occur. It acts
on the kidneys to help the body eliminate uric acid. Probenecid is known as a
ColBenemid (other brand names are
Col-Probenecid and Proben-C) is a gout medication that contains Probenecid,
which is a uricosuric agent, and Colchicine, which has anti-gout properties.
name - Anturane) is also known as a uricosuric agent and is used to treat
gouty arthritis. It works by lowering the amount of uric acid in your blood,
preventing gout attacks. The drug helps prevent attacks but is not used to treat
an attack once it has started.
Losartan, (brand names - Cozaar and
Hyzaar), is not specifically a gout medication but is an angiotensin II receptor
antagonist, antihypertensive drug that may help control uric acid levels.
Fenofibrate, (brand name - Tricor), is not a specific gout medication but it a
lipid-lowering drug that may help uric acid levels.
Analgesic painkillers are also used
to relieve the intense pain of gout. All of the aforementioned drugs can be used
in combination, to control symptoms, prevent future attacks, and maintain
healthy uric acid levels.
Acute Gouty Arthritis
Three treatments currently available
for acute gouty arthritis attacks are nonsteroidal anti-inflammatory drugs
(NSAIDs), colchicine and corticosteroids.
NSAIDs -Indomethacin (Indocin) and
Corticosteroids - Prednisone,
Triamcinolone acetonide and Corticotropin
NSAIDs. These rapid-acting drugs
are currently the most favored treatment for acute gout attacks.
NSAIDs have become first-line
therapy for acute episodes because of the many side effects experienced with
colchicine and its lack of efficacy if administered beyond 24 hours after
onset of an attack.
Any NSAID is effective for acute
attacks, but agents with a short half-life (eg, indomethacin (Indocin),
ibuprofen) are most popular because of their rapid onset of action.
Use of NSAIDs should be avoided or
monitored carefully in patients with preexisting renal dysfunction or a
history of gastrointestinal bleeding. Also, because these agents affect
platelet function, they should not be given to patients who have a bleeding
propensity or are receiving anticoagulation therapy.
All NSAIDs can have serious
gastrointestinal side effects, including bleeding and ulceration.
These drugs should therefore be
used with caution in patients with a history of peptic ulcer disease,
congestive heart failure or chronic renal failure.
Discretion should be used in giving
NSAIDs to patients who are allergic to aspirin or have asthma or nasal polyps.
Whether use of the newer
cyclooxygenase-2 inhibitors will be beneficial or safer in such patients is
yet to be determined. These are a relatively new type of anti-inflammatory
drug that are currently under scrutiny. By inhibition of cyclooxygenase-2, the
vicious cycle of inflammation and pain caused by gout is impeded. COX-2
expression in monocytes has been suggested to be induced in response to urate
Colchicine. This agent is an
effective alternative to NSAIDs in the treatment of acute gouty arthritis.
Colchicine is most beneficial when
it is given in the first 12 to 36 hours of an attack. It apparently exerts its
effect by inhibiting the phagocytosis of uric acid and blocking the release of
Colchicine has anti-inflammatory
activity but no analgesic activity.
Colchicine can be given orally or
Colchicine can be given
intravenously, if the oral route is not available or gastrointestinal side
effects have to be avoided.
Intravenous administration has been
associated with an increased risk of toxic side effects, including bone marrow
suppression and renal or hepatic cell damage.
However, intravenous colchicine
therapy is generally unnecessary for an acute flare of gout, and when
administered incorrectly, it can cause bone marrow toxicity and irritation of
the soft tissues and veins.
After intravenous therapy,
administration of additional oral colchicine must be avoided for a full week,
according to manufacturers' recommendations.
Experts are divided about whether
to use colchicine or an NSAID to treat inflammation. Colchicine, while highly
effective for acute gout, is often not well tolerated.
For 50% to 80% of patients, it can
cause gastrointestinal side effects before the attack is relieved. Colchicine
requires dose adjustment for renally compromised and elderly patients.
Even low-dose daily therapy for
prophylaxis can be associated with severe adverse effects. Drug interactions
must also be considered—concomitant erythromycin, simvastatin, or cyclosporine
therapy can alter colchicine's metabolism, predisposing patients to adverse
(glucocorticoid) and salt-retaining (mineralocorticoid) properties.
Glucocorticoids cause profound and varied metabolic effects. In addition,
these agents modify the body's immune response to diverse stimuli.
Oral corticosteroids may be used
for patients with gout or pseudo gout who cannot tolerate NSAIDs. Although
there have been case reports of adrenal crisis related to multiple
interarticular injections of steroids for gout, this has not been clearly
Monarthric gout responds well to
corticosteroids given by intra-articular injection.
Systemic corticosteroids (e.g.,
prednisone [Deltasone], in a dosage of 20 to 30 mg per day) are used only when
NSAIDs and colchicine are not effective or are contraindicated.
Long-term therapy is not indicated
for a single attack of gout.
However, it may be reasonable to
identify precipitating factors and to obtain a 24-hour urine collection to
determine creatinine clearance and excretion of uric acid.
Treatment with allopurinol or a
uricosuric drug should be considered in patients who have at least two
episodes of gout in 1 year.
Asymptomatic hyperuricemia does not
usually produce adverse effects before the development of gout and, therefore,
does not require treatment. However, it may be advisable to determine the
cause of the hyperuricemia.
Urate-lowering therapy should not
be prescribed without concomitant use of an NSAID or low-dose colchicine.
Serum urate levels may fluctuate during the initiation of such therapy and
induce a gouty flare or prolong an ongoing attack.
Long-term therapy should not be
initiated until the patient has returned to baseline in terms of nutrition,
activity level, and medication use. Beginning therapy before that time may
actually exacerbate a flare or prolong an existing episode.
Glucocorticoid therapy, either
oral or parenteral, is effective in patients who are unable to take or
tolerate NSAIDs and colchicine.
Side effects of this regimen are
rare but may include glucose intolerance, electrolyte shifts, hypertension,
and increased susceptibility to infection. A symptom flare may occur after
tapering of corticosteroid therapy.
Intra-articular steroids are
useful in patients with multiple medical problems, involvement of only a few
joints, or contraindications to other therapies.
A postinjection flare caused by
the steroid crystals themselves may occur but is usually short-lived. This
approach has been particularly successful in postoperative patients with a
single affected joint who are unable to take oral medications.
Corticotropin (ACTH) (an
exogenously produced corticotropin that stimulates the adrenal cortex to
secrete cortisol, corticosterone, and several androgens) is still an option
for treating gout.
Although this agent has been
shown to be as effective as indomethacin, it carries a higher risk of
rebound attacks, and multiple injections may be required. Some investigators
have reported efficacy in acute attacks, especially in patients with
multiple medical conditions.
Prevention of Recurrent Attacks
Hyperuricemic therapy should be
initiated in patients with frequent gout attacks, tophi or urate nephropathy.
A low dosage of an NSAID or
colchicine is effective in preventing acute gouty attacks.
Hyperuricemic drug therapy should not
be started until an acute attack of gouty arthritis has ended, because of the
risk of increased mobilization of uric acid stores. A reasonable goal is to
reduce the serum uric acid concentration to less than 6 mg per dL (360 µmol per
Reduction of serum uric acid levels
to normal is the goal of treatment designed to prevent acute attacks of gout.
When attacks of gout recur despite
conservative measures (eg, dietary modifications, reduction in alcohol
consumption), treatment with urate-lowering agents is indicated.
The two classes of medications
available for reducing serum urate levels are :
In most cases, lifetime treatment
with one of these agents is indicated.
These agents decrease the serum uric
acid level by increasing renal excretion.
Therapy with uricosuric agents is
generally recommended for patients less than 60 years of age who have normal
renal function, under-excretion of uric acid (<700 mg/24 hr), and no history of
Although 24-hour uric acid
measurement is not required in all patients with gout, it may be useful when
uricosuric drug therapy is being considered.
Two common uricosuric agents are :
probenecid (Benemid, Benuryl) and
Sulfinpyrazone has an antiplatelet effect that may be beneficial for
patients with a cardiac condition who are unable to take low-dose aspirin.
The major side effects of these
drugs--hypersensitivity reactions and an increased risk of uric acid
nephro-lithiasis - may be avoided by alkalization of the urine. However, this
process involves use of additional medications, which may decrease patient
Sulfinpyrazone is a uricosuric agent
that is related to phenylbutazone.
Because it can act as an antiplatelet
drug, it should be used cautiously in patients who are anticoagulated or have
Sulfinpyrazone can also cause
gastrointestinal problems. Thus, caution should also be exercised in giving this
drug to patients with peptic ulcer disease.
(Benemid) and sulfinpyrazone (Anturane) are used in patients who are considered
underexcretors of uric acid. Uricosuric drugs should not be given to patients
with a urine output of less than 1 mL per minute, a creatinine clearance of less
than 50 mL per minute (0.84 mL per second) or a history of renal calculi. The
physiologic decline in renal function that occurs with aging frequently limits
the use of uricosuric agents.
Probenecid, it is important to note
that the drug also blocks the tubular secretion of other organic acids. This may
result in increased plasma concentrations of penicillins, cephalosporins,
sulfonamides and indomethacin.
Allopurinol (Purinol, Zyloprim)
decreases uric acid production by inhibiting the enzyme xanthine oxidase.
Dosage adjustments are necessary in
patients with impaired creatinine clearance.
The increased risk of precipitating
an acute attack during drug initiation can be decreased by starting with a
dosage of 50 to 100 mg/day.
In addition, medications such as
azathioprine (Imuran) and mercaptopurine (Purinethol) are inactivated by
Allopurinol is indicated in patients
with a history of nephrolithiasis, renal impairment, and an inadequate response
to uricosuric drug therapy. Most patients with tophaceous gout need allopurinol
It is also indicated in patients with
myeloproliferative disease who are undergoing chemotherapy and in those with
hyperuricemia due to HGPRT deficiency or PRPP synthetase overactivity.
Patients with cancer and gout are at
risk for drug interactions because allopurinol can affect the metabolism of some
cancer therapies. In addition, cancer patients may be taking drugs that will
elevate uric acid levels, potentially precipitating gout.
Allopurinol. As a xanthine oxidase
inhibitor, allopurinol (Zyloprim) impairs the conversion of hypoxanthine to
xanthine and the conversion of xanthine to uric acid. The effect of the drug
depends on the dosage.
Allopurinol in a dosage of 300 mg per
day has been reported to reduce serum urate concentrations to less than 7 mg per
dL (420 µmol per L)
Allopurinol is the drug of choice in
patients with severe tophaceous deposits and in patients with a history of
impaired renal function (creatinine clearance of less than 50 mL per minute
[0.84 mL per second]), uric acid nephropathy or nephrolithiasis.
The drug is also preferred as a
pretreatment agent to protect against uric acid nephropathy in patients with
lymphoproliferative or myeloproliferative disorders.
The side effects of allopurinol
include skin rash (e.g., Stevens-Johnson syndrome and toxic epidermal
necrolysis), leukopenia and gastrointestinal disturbances. The initiation of
allopurinol therapy can also precipitate an acute gout attack. The dosage of
allopurinol should be adjusted in patients with renal impairment.
Because flares may occur during a
fall in serum urate levels, low doses of either colchicine or an NSAID may be
effective in preventing acute attacks of gout. Such treatment should be started
before the initiation of urate-lowering therapy. Colchicine can reduce
recurrence of gouty flares regardless of the serum uric acid level.
Gouty arthritis is the culmination of
a number of physiologic mechanisms that ultimately result in deposition of uric
acid within joints and soft tissues.
Decreased uric acid clearance through
the kidney is the most common cause of gout. Tophaceous gout occurs in less than
10% of patients.
Acute episodes are treated with
NSAIDs or colchicine.
Low-dose therapy with these agents
can also prevent recurrent attacks. Most patients with gout need long-term
treatment with either uricosuric agents or xanthine oxidase inhibitors.
General treatment recommendations
The above opinionated
views and information serves to educated and informed consumer . The
information provided herein should not be used during any medical emergency or
for the diagnosis or treatment of any medical condition. .It should not replaced
professional advise and consultation. A licensed physician should be
consulted for diagnosis and treatment of any and all medical conditions