GOUT

Gout is a disease that causes acute joint inflammation and pain

secondary to the deposition of monosodium urate (MSU) crystals
within the synovial fluid and lining. Clinically, acute gout presents as
monoarticular inflammation in 85% to 90% of patients with the first
metatarsophalangeal joint (great toe) typically affected; this is called
podagra. Patients presenting with acute gout may or may not have
hyperuricemia. OR
Gout is an inflammatory disease in which monosodium urate crystals
deposit into a joint, making it red, hot, tender, and swollen within
hours.
When this happens, it’s called a gouty attack.
The underlying cause is hyperuricemia—too much uric acid in the
blood, which results in the formation of sharp, needle-like crystals, in
areas with slow blood flow like the joints and the kidney tubules.
Over time, repeated gouty attacks can cause destruction of the joint
tissue which results in arthritis. OR
Gout is a syndrome characterized by: hyperuricemia and deposition of
urate crystals causing attacks of acute inflammatory arthritis; tophi
around the joints and possible joint destruction; renal glomerular,
tubular, and interstitial disease; and uric acid urolithiasis.
The disease most commonly affects the first toe (podagra), foot,
ankle, knee, fingers, wrist, and elbow; however, it can affect any joint.
Epidemiology: Gout is more prevalent in men than women, and
increases with age for both groups. Gout is rare in pre-menopausal
women.
Etiology: There is a causal relationship between hyperuricemia (high
urate level) and gout. Hyperuricaemia does not always lead to gout,
but the incidence of gout increases with urate level.
The annual incidence of gout in men is 0.4% for a urate level of 7 to
7.9 mg/dL, 0.8% for 8 to 8.9 mg/dL, 4.3% for 9 to 9.9 mg/dL, and 7%
for levels >10 mg/dL.
Uric acid has limited solubility in body fluids,
though. Hyperuricemia occurs when levels of uric acid exceed the rate
of its solubility, which is about 6.8mg/dL.
At a physiologic pH of about 7.4, uric acid loses a proton and
becomes a urate ion, which then binds sodium and forms
monosodium urate crystals.
These crystals can form as a result of increased consumption of
purines, like from consuming purine-rich foods like shellfish,
anchovies, red meat, or organ meat.
Also, though, they can result from increased production of purines,
for example, high-fructose corn syrup-containing beverages could
contribute to the formation of uric acid by increasing purine synthesis.
Another way crystals could form is from decreased clearance of uric
acid, which can result from dehydration from not drinking enough
water or from consumption of alcoholic beverages, both of allowing
uric acid to precipitate out.
Regularly eating these kinds of foods can also lead to obesity
and diabetes, both of which are risk-factors for gout.
Hyperuricemia can also develop as a result of chemotherapy or
radiation treatment, since cells die at a faster-than-normal rate.
Also, some individuals have a genetic predisposition to
overproduction of uric acid while others with chronic kidney
disease may be unable to excrete the uric acid.
Finally, there are some medications like thiazide
diuretics and aspirin which can also increase the levels of uric acid
and therefore the risk of
Hyperuricaemia - due to renal under-excretion of urate in 90% of
cases and to over-production in 10%, although there is often an
overlap of both.
Aspirin, ciclosporin, tacrolimus, or pyrazinamide- can raise serum
uric acid levels by increasing uric acid re-absorption.
Diuretics- can increase urate levels and are associated with an
increased risk of gout.
Risk factors for hyperuricaemia may eventually lead to gout, and
include dietary factors such as consumption of seafood, meat, and
alcohol, especially beer. Obesity, insulin resistance, and hypertension
have also been implicated.
High cell turnovers, such as from hematological cancer and
chemotherapy, and specific genetic enzymatic abnormalities,
constitute endogenous sources of purine and urate production.
Pathophysiology:
Purines, as well as pyrimidines, are key components of nucleic acids
like DNA and RNA, and when cells, along with the nucleic acids in
those cells, are broken down by the enzyme Xanthine oxidase
throughout the body, those purines are converted into uric acid—a
molecule that can be filtered out of the blood and excreted in the
urine.
Uric acid may be overproduced because of the increased breakdown
of tissue nucleic acids, as with myeloproliferative and
lymphoproliferative disorders.
Cytotoxic drugs can result in the overproduction of uric acid due to
lysis and the breakdown of cellular matter.
Dietary purines are insignificant in the generation of hyperuricemia
without some derangement in purine metabolism or elimination.
Two thirds of uric acid produced daily is excreted in urine. The
remainder is eliminated through the gastrointestinal (GI) tract after
degradation by colonic bacteria.
The decline in urinary excretion to a level below rate of production
leads to hyperuricemia and increased pool of sodium urate.
Drugs that decrease renal uric acid clearance include diuretics,
nicotinic acid, salicylates (>2g/day), ethanol, pyrazinamide, levodopa,
ethambutol, cyclosporine, and cytotoxic drugs.
Deposition of urate crystals in synovial fluid results in inflammation,
vasodilation, increased vascular permeability, complement activation,
and chemotactic activity for polymorphonuclear leukocytes.
Phagocytosis of urate crystals by leukocytes results in rapid lysis of
cells and discharge of proteolytic enzymes into the cytoplasm. The
ensuing inflammatory reaction causes intense joint pain, erythema,
warmth, and swelling.
Urate crystals in the joint interact with undifferentiated phagocytes
and trigger an acute inflammatory response by inducing tumor
necrosis factor (TNF)-alpha and activating signal pathways and
endothelial cells.
TNF-alpha, interleukin (IL)-8, and other chemokines lead to
neutrophil adhesion to endothelium, influx, and amplification,
resulting in neutrophilic synovitis.
In addition, there is evidence that urate crystals activate NALP3
inflammasome (a key regulator of IL-1beta secretion), which plays a
role in the gout inflammatory reaction.
Urate crystals can induce chondrocytes to produce metalloproteinase
and nitric oxide, and chronic inflammation, leading to synovitis,
cartilage loss, bone damage by inhibiting osteoblasts, and bone
erosions.
Colchicine works by intercepting the neutrophil-endothelial
interaction. IL-8 accounts for 90% of the chemotactic activity of
neutrophils in response to uric acid crystals; hence, inhibiting IL-8
may have therapeutic implications.
Clinical presentation: Acute gout attacks are characterized by rapid
onset of excruciating pain, swelling, and inflammation.
The pain is most severe in the hours immediately following the attack
and then generally lessens over time, but that discomfort and swelling
can last for days or weeks.
The attack is typically monoarticular, most often affecting the first
metatarsophalangeal joint (podagra)- a person will wake up from
sleep feeling like their big toe is on fire; even the weight of the sheets
can be painful.
And then, in order of frequency, the insteps, ankles, heels, knees,
wrists, fingers, and elbows.
Attacks commonly begin at night, with the patient awakening with
excruciating pain.
Affected joints are erythematous, warm, and swollen. Fever and
leucocytosis are common. Untreated attacks last from 3 to 14 days
before spontaneous recovery.
Acute attacks may occur without provocation or be precipitated by
stress, trauma, alcohol ingestion, infection, surgery, rapid lowering of
serum uric acid by uric acid– lowering agents, and ingestion of drugs
known to elevate serum uric acid concentrations.
Clinical manifestations:
1. Recurrent flares of inflammatory arthritis (gout flare)
2. A chronic arthropathy
3. Accumulation of urate crystals in the form of tophaceous deposits
4. Uric acid nephrolithiasis
Diagnosis:
Gout is clinically suspected in patients with typical history and
examination findings. A clinical diagnosis can be made with a good
degree of certainty in patients with a reliable history of recurrent acute
monoarthritis of the first metatarsophalangeal joint (podagra).
Rapid onset of severe pain, redness or swelling of joints other than the
first metatarsophalangeal (e.g., midfoot, ankle, knee, hand, wrist,
elbow) may also indicate a diagnosis of gout.
Diagnosis is confirmed by arthrocentesis showing monosodium urate
crystals.
History: more common in men and rare in pre-menopausal. A history
of previous attacks that are self-limiting (7-14 days) supports the
diagnosis. Medications, dietary habits, and family history should be
assessed.
Most common presentation is acute monoarticular arthritis
characterised by sudden-onset severe pain and swelling.
The disease may be oligoarticular (<4 joints involved) or, to a lesser
degree, polyarticular (e.g., in older people, where it may be associated
with marked oedema and swelling of the hands and feet).
Physical examination: Involved joints are warm, red, and
swollen. Usually, there is considerable tenderness and limited range of
movement due to pain.
Hard subcutaneous nodules (tophi) over the extensor surface of the
joint, especially over the elbows, knees, and Achilles tendons, may be
present.
Tophi may also be evident over the dorsal aspects of hands and feet,
and in the helix of the ears.
Investigations:
1. Arthrocentesis with synovial fluid analysis
WBC> 2.0 x 10⁹/L (2000/mm³ or 2000/microlitre), and the cells are
mostly polymorphonuclear neutrophils type. Monosodium urate
crystals (intracellular and/or extracellular needle-shaped crystals
strongly negative for birefringence under polarised light) confirm the
diagnosis
2. Serum uric acid level
May be low, normal, or high during an acute gout attack. This test
becomes more reliable when done at least 2 weeks after the attack
resolves (>6.8mg/dL).
3. Ultrasound
Ultrasound is more sensitive than x-rays in detecting erosions, tophi,
and the gout-specific double contour sign (linear urate deposits over
hyaline cartilage). Ultrasound findings, including tophi and erosion
beside a double contour sign, have a sensitivity of 65% and specificity
approaching 90%.
4. Dual energy computed tomography (DECT)
Could be helpful in the diagnosis of gout when it is in question, or for
patients with contraindications for, or who refuse to have joint
aspiration.
5. Radiography

Radiographs are of limited diagnostic utility.[52] In late/severe gout,

radiographic changes may help to differentiate between chronic gout
and other joint conditions.

Differentials:

1. Pseudogout (Calcium pyrophosphate deposition disease)

Pseudogout is more likely to affect wrist and knee joints.

Investigated by synovial fluid examination and ultrasound.
2. Septic arthritis

Occurs in both sexes and at any age. Risk factors for infection,
such as intravenous drug use and immunocompromise, may be
present. Synovial fluid microscopy and culture may be Gram
positive and show growth.

3. Trauma

A positive history is present. Usually, there are fewer inflammatory

signs, such as erythema or warmth, on joint examination than with
gout.

4. Rheumatoid arthritis

Chronic tophaceous and polyarticular gout may present like RA, and
tophi can be misdiagnosed as rheumatoid nodules. History of
intermittent, acute, self-limiting attacks of arthritis and podagra
suggests gout.

Associated with positive rheumatoid factor (RF) in 70% to 78% of

cases; however, 30% of patients with gout have a positive RF. Anti-
cyclic citrullinated peptide (anti-CCP) has high specificity, but low
sensitivity, for RA. It may be useful in the early detection of patients
who will have severe RA.

5. Reactive arthritis

Recent infection with appropriate organism. Oligoarthritis present.

Commonly affects weight-bearing joints.

May have tendon insertion inflammation and dactylitis (whole digit

inflammation). X-rays may show soft-tissue swelling.

6. Psoriatic arthritis

Patients usually have a history of psoriasis. Asymmetrical joint

distribution. Commonly affects the distal interphalangeal joints.
Presence of dactylitis.
Typical radiographic findings include joint erosions, joint space
narrowing, bony proliferation including periarticular and shaft
periostitis, osteolysis including 'pencil in cup' deformity and acro-
osteolysis, ankylosis, spur formation, and spondylitis

American College of Rheumatology/European League Against

Rheumatism (ACR-EULAR) gout classification criteria

 The sensitivity of the 2015 classification criteria is 92%, and the

specificity is 89%.
 The criteria include clinical, imaging, and laboratory-based
features.
 The maximum possible score in the final criteria is 23 and a
threshold score of 8 classifies an individual as having gout.
 A unique aspect of these classification criteria is that there are 2
categories that elicit negative scores. Specifically, if the synovial
fluid is negative for monosodium urate, 2 points are subtracted
from the total score. Similarly, if the serum urate level is <240
micromol/L (<4 mg/dL), 4 points are subtracted from the total
score.
 Associated Web-based calculators are available.

TREATMEMT/MANAGEMENT

Goals of Treatment:

1. Terminate the acute attack

2. Prevent recurrent attacks

3. Prevent complications associated with chronic deposition of

urate crystals in tissues.

4. The short-term treatment goal for acute gout is rapid resolution

of pain and preservation of function.

5. Long-term goals are to prevent recurrent attacks and chronic

joint destruction
Nonpharmacologic Therapy Local ice application is the most
effective adjunctive treatment. Dietary supplements (eg, flaxseed and
celery root) are not recommended.

Pharmacological therapy:

Short-term management

Non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or

colchicine are recommended first-line treatments for patients
experiencing a gout flare. The treatment course is generally 7 to 14
days. However, NSAIDs should be given for the shortest period
possible, at the lowest effective dose.

The choice between treatments should be guided by patient

preference, and potential risks and contraindications (e.g., renal
impairment in the case of NSAIDs).

Initiation of treatment with urate-lowering drugs (e.g., xanthine

oxidase inhibitors such as allopurinol and febuxostat; uricosuric
agents such as probenecid, or pegloticase) is not typically
recommended in patients experiencing their first gout flare.

Long-term management: dietary modifications

The long-term management of gout includes dietary modifications

and weight loss (if indicated). Limiting the intake of alcohol, purine,
and high-fructose corn syrup, in conjunction with weight loss, are
conditionally recommended lifestyle changes for people with gout.
Treatment of acute gout:

1. Choice of NSAID should be guided by patient preference.

In patients at high risk of gastrointestinal complications, a proton-

pump inhibitor or misoprostol should be co-prescribed.

Proton-pump inhibitors should be considered for all patients who are

taking an NSAID.

COX-2 inhibitors may be safer than traditional NSAIDs in patients

with a history of gastrointestinal bleeding or comorbidities.

Treatment course is generally 7 to 14 days. However, NSAIDs should

be given for the shortest period possible, at the lowest effective dose.

Start therapy within 24 hours of attack onset and continue until

complete resolution (usually 5–8 days).

The most common adverse effects involve the GI tract (gastritis,

bleeding, and perforation),

kidneys (renal papillary necrosis and reduced creatinine

clearance [CLcr]),
cardiovascular system (increased blood pressure, sodium and
fluid retention),

and central nervous system (impaired cognitive function,

headache, and dizziness).

Selective cyclooxygenase-2 inhibitors (eg, celecoxib) may be an

option for patients unable to take nonselective NSAIDs, but the risk-
to-benefit ratio in acute gout is unclear, and cardiovascular risk must
be considered.
 2. Corticosteroid

Efficacy is equivalent to NSAIDs; they can be used systemically or by

intra-articular (IA) injection. Systemic therapy is necessary if an
attack is polyarticular.
Primary options

prednisolone: 1 mg/kg orally given as a single dose. This regimen

may be adequate if started within 24 hours of attack. OR

prednisolone: 20-40 mg orally once daily initially, decrease by 5-10

mg/day decrements every 3 days until discontinuation; or 30 mg
orally once daily for 5 days. OR

methylprednisolone acetate: small joint: 4-10 mg intra-articularly as a

single dose; medium joint: 10-40 mg intra-articularly as a single dose;
large joint: 20-80 mg intra-articularly as a single dose; consult
specialist for guidance on parenteral dose. OR

triamcinolone acetonide: small joint: 2.5 to 10 mg intra-articularly as

a single dose; larger joint: 5-40 mg intra-articularly as a single dose.

Short-term corticosteroid use is generally well tolerated. Use with

caution in patients with diabetes, GI problems, bleeding disorders,
cardiovascular disease, and psychiatric disorders. Avoid long-term
use because of risk for osteoporosis, hypothalamic–pituitary–adrenal
axis suppression, cataracts, and muscle deconditioning.

Adrenocorticotropic hormone (ACTH) gel 40 to 80 USP units may

be given IM every 6 to 8 hours for 2 or 3 days and then discontinued.
Limit use for patients with contraindications to first-line therapies (eg,
heart failure, chronic renal failure, and history of GI bleeding) or
patients unable to take oral medications.

3. Colchicine:

Colchicine is highly effective in relieving acute gout attacks; when it

is started within the first 24 hours of onset, about two thirds of
patients respond within hours. Use only within 36 hours of attack
onset because the likelihood of success decreases substantially if
treatment is delayed.

Colchicine causes dose-dependent GI adverse effects (nausea,

vomiting, and diarrhea).
Non-GI effects include neutropenia and axonal neuromyopathy,
which may be worsened in patients taking other myopathic drugs (eg,
statins) or in renal insufficiency.

Do not use concurrently with P-glycoprotein or strong CYP450 3A4

18 inhibitors (eg, clarithromycin) because reduced biliary excretion
may lead to increased plasma colchicine levels and toxicity. Use with
caution in renal or hepatic insufficiency.

colchicine: 1.2 mg orally initially, followed by 0.6 mg orally after

1 hour, maximum 1.8 mg total dose

4. interleukin (IL) -1 inhibitor- 2nd line agent

Anakinra and canakinumab are second-line therapies. They are

conditionally recommended over no therapy (beyond
supportive/analgesic treatment) for patients experiencing a gout flare
who are refractory to, are intolerant of, or have contraindications to
other anti-inflammatory therapies.

In patients for whom a non-steroidal anti-inflammatory drug (NSAID)

and colchicine was ineffective or contraindicated, treatment with
either anakinra or the corticosteroid triamcinolone reduced patient-
assessed gout flare pain to a similar extent within 72 hours.

Canakinumab is an IL-1-beta inhibitor monoclonal antibody- rapid

and effective pain relief compared with patients receiving
triamcinolone.

Anakinra

Canakinumab

Long term management/ Recurrent gout/ Hyperuricemia in gout:

After the first attack of acute gout, prophylactic pharmacotherapy is
recommended if patients have two or more attacks per year, even if
serum uric acid is normal or only minimally elevated.

Other indications include presence of tophi, chronic kidney disease, or

history of urolithiasis.

Urate-lowering therapy can be started during an acute attack if anti-

inflammatory prophylaxis has been initiated.

The goal of urate-lowering therapy is to achieve and maintain serum

uric acid less than 6 mg/dL (357 μmol/L), and preferably less than 5
mg/dL (297 μmol/L) if signs and symptoms of gout persist.
Urate lowering should be prescribed for long-term use. Serum urate
can be reduced by decreasing synthesis of uric acid (xanthine oxidase
inhibitors) or by increasing renal excretion of uric acid (uricosurics).

Xanthine oxidase inhibitors- reduce uric acid by impairing

conversion of hypoxanthine to xanthine and xanthine to uric acid.
Because they are effective in both overproducers and underexcretors
of uric acid, they are the most widely prescribed agents for long-term
prevention of recurrent gout attacks.

Allopurinol lowers uric acid levels in a dose-dependent manner.

ACR guidelines recommend a starting dose no greater than 100 mg

daily in patients with normal renal function and no more than 50
mg/day in patients with chronic kidney disease (stage 4 or worse) to
avoid allopurinol hypersensitivity syndrome and prevent acute gout
attacks common during initiation of urate-lowering therapy. The dose
should be titrated gradually every 2 to 5 weeks up to a maximum dose
of 800 mg/day until the serum urate target is achieved.

Mild adverse effects of allopurinol include skin rash, leukopenia, GI

problems, headache, and urticaria. More severe adverse reactions
include severe rash (toxic epidermal necrolysis, erythema multiforme,
or exfoliative dermatitis) and allopurinol hypersensitivity syndrome
characterized by fever, eosinophilia, dermatitis, vasculitis, and renal
and hepatic dysfunction that occurs rarely but is associated with a
20% mortality rate.

Febuxostat (Uloric) also lowers serum uric acid in a dose-dependent

manner. The recommended starting dose is 40 mg once daily.
Increase the dose to 80 mg once daily for patients who do not achieve
target serum uric acid concentrations after 2 weeks of therapy.

Febuxostat is well tolerated, with adverse events of nausea,

arthralgias, and minor hepatic transaminase elevations. Febuxostat
does not require dose adjustment in mild to moderate hepatic or renal
dysfunction. Due to rapid mobilization of urate deposits during
initiation, give concomitant therapy with colchicine or an NSAID for
at least the first 8 weeks of therapy to prevent acute gout flares.
URICOSURICS

Probenecid increases renal clearance of uric acid by inhibiting the

post secretory renal proximal tubular reabsorption of uric acid.
Patients with a history of urolithiasis should not receive uricosurics.
Start therapy with uricosurics at a low dose to avoid marked
uricosuria and possible stone formation.

Maintaining adequate urine flow and alkalinization of the urine during

the first several days of therapy may also decrease likelihood of uric
acid stone formation. Initial probenecid dose is 250 mg twice daily for
1 to 2 weeks, then 500 mg twice daily for 2 weeks. Increase the daily
dose thereafter by 500-mg increments every 1 to 2 weeks until
satisfactory control is achieved or a maximum dose of 2 g/day is
reached.

Major side effects of probenecid include GI irritation, rash and

hypersensitivity, precipitation of acute gouty arthritis, and stone
formation. Contraindications include impaired renal function
(CLcr<50mg/dL), and overproduction of uric acid.

Lesinurad (Zurampic) is a selective uric acid reabsorption inhibitor

that inhibits urate transporter 1, a transporter in proximal renal
tubules, thereby increasing uric 21 acid excretion.

It is approved as combination therapy with a xanthine oxidase

inhibitor for treatment of hyperuricemia associated with gout in
patients who have not achieved target serum uric acid levels with
xanthine oxidase inhibitor monotherapy.

The only approved dose of lesinurad dose is 200 mg once daily in the
morning with food and water in combination with a xanthine oxidase
inhibitor. The drug should not be used in patients with creatinine
clearance below 45 mL/min.

Adverse effects of lesinurad include urticaria and elevated levels of

serum creatinine, lipase, and creatine kinase. It carries a black box
warning about increased risk of acute renal failure when used in the
absence of xanthine oxidase inhibitor therapy.
PEGLOTICASE

Pegloticase (Krystexxa) is a pegylated recombinant uricase that

reduces serum uric acid by converting uric acid to allantoin, which is
water soluble. Pegloticase is indicated for antihyperuricemic therapy
in adults refractory to conventional therapy.

The dose is 8 mg by IV infusion over at least 2 hours every 2 weeks.

Because of potential infusion-related allergic reactions, patients must
be pretreated with antihistamines and corticosteroids.

Pegloticase is substantially more expensive than first-line urate-

lowering therapies. The ideal duration of pegloticase therapy is
unknown. Development of pegloticase antibodies resulting in loss of
efficacy may limit the duration of effective therapy. Because of its
limitations, reserve pegloticase for patients with refractory gout who
are unable to take or have failed all other urate-lowering therapies.

ANTI-INFLAMMATORY PROPHYLAXIS DURING

INITIATION

Initiation of urate-lowering therapy can precipitate an acute gout

attack due to remodeling of urate crystal deposits in joints after rapid
lowering of urate concentrations.

Prophylactic anti-inflammatory therapy is often used to prevent such

gout attacks. The ACR guidelines recommend low-dose oral
colchicine (0.6 mg twice daily) and low-dose NSAIDs (eg, naproxen
250 mg twice daily) as first-line prophylactic therapies, with stronger
evidence supporting use of colchicine.

For patients on long-term NSAID prophylaxis, a proton pump

inhibitor or other acid-suppressing therapy is indicated to protect from
NSAID-induced gastric problems.

Low-dose corticosteroid therapy (eg, prednisone ≤10 mg/day) is an

alternative for patients with intolerance, contraindication, or lack of
response to first-line therapy.
The potential severe adverse effects of prolonged corticosteroid
therapy preclude their use as first-line therapy.

Continue prophylaxis for at least 6 months or 3 months after

achieving target serum uric acid, whichever is longer.

For patients with one or more tophi, continue prophylactic therapy for
6 months after achieving the serum urate target

EVALUATION OF THERAPEUTIC OUTCOMES

1. Check the serum uric acid level in patients suspected of having an

acute gout attack, particularly if it is not the first attack.

2. Monitor patients with acute gout for symptomatic relief of joint

pain as well as potential adverse effects and drug interactions
related to drug therapy.

3. For patients receiving urate-lowering therapy, obtain baseline

assessment of renal function, hepatic enzymes, complete blood
count, and electrolytes. Recheck the tests every 6 to 12 months in
patients receiving long-term treatment.

4. During titration of urate-lowering therapy, monitor serum uric acid

every 2 to 5 weeks; after the urate target is achieved, monitor uric
acid every 6 months.

5. Because of the high rates of comorbidities associated with gout

(diabetes, chronic kidney disease, hypertension, obesity,
myocardial infarction, heart failure, and stroke), elevated serum
uric acid levels or gout should prompt evaluation for
cardiovascular disease and the need for appropriate risk reduction
measures.

6. When initiating allopurinol, patients should be closely monitored

for drug-induced hypersensitivity syndrome (fever, eosinophilia,
widespread rash, facial oedema, and multi-system failure).[140]
7. Long-term colchicine use may be associated with neuromyopathy.
Probenecid may increase the risk of nephrolithiasis.
Patient Counselling:

Patients should be made aware of the signs, symptoms and causes

of gout. They should also be advised of any risk factors they have
for gout, for example:

 Genetics
 Excess body weight or obesity
 Medicine they may be taking
 Comorbidities such as kidney disease or hypertension.

Patients should understand that gout is a lifelong condition, and

that disease progression will occur without long term urate
lowering treatment to eliminate urate crystals and prevent flares,
shrink tophi and prevent long term joint damage.

Patients should be advised that foods with a high purine content

(i.e., alcohol, seafood, and offal) are associated with higher risk for
elevated uric acid and gout.

Reducing intake of alcohol, especially beer, lowers the risk of gout.

Reducing seafood and meat intake helps to a lesser degree.

Reducing fructose and concentrated sweets might help to reduce

uric acid and the risk for gout attacks.

Dairy products reduce the risk of gout.