Gout Treatment Medications and Lifestyle Adju…

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Gout / Treatment of Gout

Treatment of Gout
Acute Gout Attack
The goal of treatment during an acute gout
attack is suppression of inflammation and
control of pain. It is important to note, that if a
patient is not on uric acid lowering therapy at
the time of an acute attack – then this is not the
time to initiate such therapy. However, if a
patient is on uric acid lowering therapy at the
time of an acute attack, it should not be
discontinued.

Treatment of pain and inflammation can be

achieved with NSAIDs, colchicine, or
corticosteroids (systemic or intra-articular). The
choice of which treatment is the right one for a
particular patient should be made on the basis of
the patient’s co-morbid medical conditions,
other medications, and side effect profile.

1. NSAIDS: Commonly used NSAIDs during

an acute gout attack include ibuprofen
800 mg three to four times daily or
indomethacin 25 to 50 mg four times daily.
Treatment should be discontinued when
symptoms resolve.
2. Colchicine: Intravenous colchicine is
associated with serious toxicities and side
effects, so it should be used as an oral
formulation only. High dose oral colchicine
(1.2 mg followed by 0.6 mg every hour for
6 doses) is generally poorly tolerated
because of GI side effects. Lower doses are
 much better received and may be used in
combination with NSAIDs.
3. Corticosteroids: In patients with
contraindications to NSAID use,
corticosteroids are the next choice.
Corticosteroids can be administered as an
injection into the effected joint (intra-
articular steroids) or given systemically
(orally, such as prednisone or medrol).
Intra-articular steriods are useful if only
one or two joints are affected and the
treating physician is proficient in injecting
those joints. Oral corticosteroids can be
used starting at 30-40 mg daily tapering
over 10-14 days.

Treatment: Uric Acid

Lowering Therapy

Indications

Patients who have multiple episodes of acute

gout attacks per year or who have tophi on exam
are candidates for uric acid lowering therapy.
Use of uric acid lowering agents will reduce the
frequency of gout attacks and over time, reduce
tophi formation, and diminish the risk of joint
destruction. The following are indications for
uric acid lowering therapy:

tophi or chronic arthritis on exam

failure of colchicine prophylaxis of acute
gouty arthritis
renal stones
Prior to chemotherapy as prophylaxis of
tumor lysis syndrome
Extremely high levels of serum uric acid
(>12 mg/dl)

Uric acid is the end product of purine (nucleic

acid component of DNA) metabolism and is
produced normally by the body during tissue
remodeling and breakdown. About 20% of uric
acid is derived from purines ingested in food.
Causes of hyperuricemia can be divided into two
major categories: decreased clearance of uric
acid from the kidney and increased synthesis of
uric acid.

Decreased renal clearance – (90% of

patients)

Intrinsic kidney disease

 heart disease causing decreased blood
flow to the kidney
drugs (loop diuretics, low dose aspirin,
cyclosporin)
genetic predisposition
age related decrease in glomerulofiltration
rate

Increased uric acid synthesis

Dietary indiscretions
Genetic predisposition
Increased tissue turnover–tumors,
lymphoproliferative disorders
Stress induced increased turnover of ATP
Alcohol induced turnover of ATP

All patients should be encouraged to modify

their lifestyle including limiting alcohol intake,
encouraging weight loss where appropriate and
decreasing food rich in purines. Co-morbid
medical conditions should also be controlled
including hypertension, diabetes and
hyperlipidemia.

Foods High in Purines

 Very High – Hearts, herring , mussels,
yeast , smelt, sardines, sweetbreads
Moderately High – Anchovies,
grouse,mutton, veal, bacon, liver salmon,
turkey, kidneys, partridge, trout, goose,
haddock, pheasant, scallops

Medication Options for Uric Acid

Lowering

It is important to note that whenever

starting a uric acid lowering
treatment, there is a risk of
precipitating a gout flare. A plan
should be in place for management if
this occurs. This generally can be
avoided with the co-administration of
prophylactic medications (steroids,
colchicine, NSAIDs) along with the
uric acid lowering therapy.

Probenecid

Probenecid may be given to patients with

decreased clearance of uric acid by the kidney
and normal renal function. In general its use
should be limited to patients under the age of
60. Probenecid acts by inhibiting reabsorption of
uric acid in the proximal tubules of the kidney.
Starting dose is at 500 mg to 1000 mg daily and
increased to 1500 mg to 2000 mg as needed.
Occasionally higher doses are needed.
Probenecid may precipitate renal stone
formation and good oral hydration should be
encouraged. Probenecid is contraindicated in
patients with renal stones (including calcium and
uric acid stones) and in patients with urate
nephropathy. Probenecid given inappropriately
to patients with hyperuricemia due to
overproduction of uric acid can cause renal
stones and urate nephropathy.

uricosuric
decreases uric acid reabsorption at the
proximal renal tubules
useful in patients with decreased renal
clearance of uric acid
can only be used if creatinine clearance
>40 cc/min
must have 24 hour urine for uric acid <800
mg/dl
can be used in renal failure
increased risk of renal stones
Allopurinol

Allopurinol is a well tolerated, inexpensive,

and commonly used uric acid lowering agent.
Allopurinol can be started at doses as low as 100
mg daily (100 mg qod if creatinine clearance <
10 cc/min) and titrated by 100 mg every 10-14
days to achieve a serum uric acid level of 4-5
mg/dl. Liver tests, blood counts, and renal
function and should be monitored while on
therapy. Toxicites include rash, hepatoxicity,
bone marrow suppression and severe
hypersensitivity reactions. Medication
interactions can occur with allopurinol, warfarin,
and theophylline and levels should be
monitored. Allopurinol should be avoided
in patients on azathiprine, 6-mercaptopurine
and cyclophosphamide because of risk for bone
marrow toxicity.

xanthine oxidase inhibitor

prevents production of uric acid
useful in both patients with increased
synthesis and decreased clearance of uric
acid
no 24 hour urine needed
can be used in renal failure
rarely associated with bone marrow
 suppression, hepatotoxicity, and
hypersensitivity reactions

Febuxostat

In 2009, the FDA approved the use of a new

xanthine oxidase inhibitor, febuxostat, for the
treatment of hyperuricemia in gout. It
has demonstrated a dose-dependent decreasee
in serum uric acid (daily doses 80mg or 120mg).
Its efficacy has been demonstrated in patients
with mild or moderate renal impairment and
gout. However, it can cause abnormalities in
liver function tests and routine monitoring of
bloodwork is recommended. Similar to
allopurinol, there are interactions of febuxostat
with azathioprine, 6MP, and theophylline.

xanthine oxidase inhibitor

prevents production of uric acid
useful in both patients with increased
synthesis and decreased clearance of uric
acid
can be used in mild-moderate renal
impairment
rarely associated with bone marrow
suppression and hepatotoxicity
Pegloticase

Uricase is an enzyme that converts poorly

soluable urate (uric acid) to the more soluable
allantoin (excreted in the urine). Uricase is
present in most mammals, and these mammals
with uricase do not develop gout. However,
humans and some primates lack uricase
(because of evoluationary gene inactivation) and
lack the ability to make uric acid more soluable
and hence, have gout. Pegloticase is a porcine
uricase which was approved by the FDA in
September 2010 for the treatment of gout in
patients who have failed conventional therapy.

Pegloticase is administered by intravenous

infusion every 2 weeks. Patients should be
treated prophylactically for allergic reations to
the infusion with steroids and anti-histamines
and monitored closely for the development of an
infusion reaction. Caution should be used in
prescribing this treatment in patients with a
known cardiac history.

pegylated porcine uricase

useful in both patients with increased
synthesis and decreased clearance of uric
acid
 increases solubility of uric acid
patients should be pre-medicated prior to
infusions and monitored for allergic
reactions
caution should be used in patients with
known cardiac history

Treatment: Lifestyle
Nutrition / Body Composition

Avoidance of purine rich foods and alcohol may

help lower uric acid levels and prevent
significant fluctuations in serum uric acid that
may precipitate acute attacks. Obesity and
increased fat distribution are risk factors for
gout.

Eating a healthy balanced diet of low-fat

proteins, low-fat dairy and vegetables will help
maintain a healthy weight which is beneficial for
the prevention of gout attacks as well.

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Updated: March 16, 2017

 About Rebecca Manno,
MD, MHS

Assistant Professor of Medicine

Johns Hopkins University

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