Gout - Free CE Continuing Education online pharmacy, pharmacists

Purdue University
School of Pharmacy
and Pharmaceutical
Sciences and
PharmCon Inc are accredited by
the Accreditation Council for
Pharmacy Education as a
provider of continuing pharmacy
education. The ACPE Universal
Program Number assigned to the
program by the accredited
providers is: 798-999-08-075-L01-P.
This activity is jointly sponsored
by PharmCon, Purdue
University School of Pharmacy
and Pharmaceutical Sciences,
and The Customer Link, Inc.
This activity is supported by an
educational grant from Takeda
Pharmaceuticals North America,
Inc.

Speaker : Dr. Randolph V. Fugit is an Internal Medicine Clinical Specialist at the Denver
Veterans Affairs Medical Center as well as Adjoint Assistant Professor in the Department of
Pharmacy Practice at the University of Colorado Health Sciences Center School of Pharmacy.
Dr. Fugit received his Doctor of Pharmacy degree from the University of New Mexico College
of Pharmacy. His areas of research include pharmacoeconomics and outcomes research
(including clinical pathway development) involved in the management of both acute and
chronic disease states in gastroenterology, rheumatology, infectious diseases, cardiology,
and pulmonology.
Speaker Disclosure:
Dr. Fugit reported that he is a consultant to Takeda Pharmaceuticals North America,
Inc. and Cubist Pharmaceuticals, Inc. He also reported that he is a speaker for Pfizer
Inc.; Boehringer Ingelheim Corporation; Cubist Pharmaceuticals, Inc.; Astellas
Pharma US, Inc.; and sanofi-aventis U.S. LLC.
Legal Disclaimer: The material presented here does not necessarily reflect the views of Pharmaceutical
Education Consultants (PharmCon) or the companies that support educational programming. A qualified
healthcare professional should always be consulted before using any therapeutic product discussed.
Participants should verify all information and data before treating patients or employing any therapies
described in this educational activity

This activity is supported by an
educational grant from Takeda
Pharmaceuticals North America,
Inc.
Accreditation:
Pharmacist –798-999-08-075-L01-P
Technicians- 798-999-08-075-L01-T
CE Credits:
1.0 Credit hour or 0.1 CEU for pharmacists/technicians
Target Audience: Pharmacists & Technicians
Program Overview: Gout is an enigma facing health care professionals today. Although it is an
ancient disease with centuries of clinical experience, gout’s incidence and prevalence continues
to rise owing to risk factors such as obesity from today’s more sedentary lifestyles. New
epidemiological issues such as the association between hyperuricemia and cardiovascular
disease also are now coming to the forefront in gout diagnosis and management.
Objectives:
• Recognize the general clinical presentations of gout, differentiating between acute attacks and
chronic underlying disease
• Advise patients about lifestyle interventions for the prevention and management of gout, focusing
on the importance of weight loss and dietary modifications
• Implement a patient education program for gout to improve knowledge about the disease state,
the importance of adherence to medications, and patient commitment to treatment
• Counsel patients about the appropriate medications to be used for acute and chronic gout, with a
special focus on comorbidities, medication contraindications, and drug interactions and advise
when a physician visit is necessary

Learning Objectives
• Recognize the general clinical presentations of gout,
differentiating between acute attacks and chronic underlying
disease
• Advise patients about lifestyle interventions for the prevention
and management of gout, focusing on the importance of weight
loss and dietary modifications
• Implement a patient education program for gout to improve
knowledge about the disease state, the importance of
adherence to medications, and patient commitment to
treatment
• Counsel patients about the appropriate medications to be used
for acute and chronic gout, with a special focus on
comorbidities, medication contraindications, and drug
interactions, and advise when a physician visit is necessary

Understanding
the Role of Uric Acid
and Hyperuricemia
for the Development of
Gout

How Prevalent Is Gout Compared
to Other Common Conditions?
Lupus
Rheumatoid arthritis
Prostate cancer
Breast cancer
Liver disease
Kidney disease
Fibromyalgia
Gout
Stroke
Gout affects
5 million adults in
the United States 1
0 1 2 3 4 5 6 7
Adults in the United States (millions) 1-6
• Gout is the most common inflammatory joint disease in men aged
> 40 years 7
• 3.9 million annual physician visits in the United States for gout; twothirds
at the primary care practitioner’s office 8
1
Kramer HM and Curhan G. Am J Kidney Dis. 2002;40:37-42. 2 Lethbridge-Cejku M, et al. Vital Health Stat. 2006;10(228).
3
Lawrence RC, et al. Arthritis Rheum. 2008;58:26-35. 4 Helmick CG, et al. Arthritis Rheum. 2008;58:15-25.
5
Rahman A and Isenberg DA. N Engl J Med. 2008;358:929-939. 6 American Heart Association Web site.
http://www.americanheart.org/downloadable/heart/1200078608862HS_Stats%202008.final.pdf. Accessed November 19,
2008. 7 Roubenoff R. Rheum Dis Clin North Am. 1990;16:539-550. 7 Krishnan E, et al. J Rheumatol. 2008;35:498-501.

Uric Acid, Hyperuricemia, and Gout
• Uric acid (urate) is the end product of purine
degradation in humans 1
• Hyperuricemia is a serum urate concentration in
excess of urate solubility (≥ 6.8 mg/dL) 2
– Results from underexcretion and/or overproduction of
uric acid 3
• Gout is the disease state resulting from deposition
of MSU crystals in tissues 4
1 Hahn PC, et al. In: Arthritis and Allied Conditions. 15th ed. 2005:2341-2355.
2
Schumacher HR Jr. Cleve Clin J Med. 2008;75(suppl 5):S2-S4.
3
Becker MA, et al. In: Arthritis and Allied Conditions. 15th ed. 2005:2303-2339.
4 Eggebeen AT. Am Fam Physician. 2007;76:801-808.

Uric Acid: End Product of Purine
Degradation in Humans
Purine
nucleotides
Purine
nucleosides
N
OH
N
Hypoxanthine
Solubility decreases
N
N
H
Xanthine
oxidase
OH
N
OH
N
Xanthine
N
N
H
Xanthine
oxidase
OH
N
OH
N
Uric acid
N
N
H
HO
Uricase
Uricase:
▪ Humans lost enzyme
during evolution
H 2 N
O
O
N
H
NH
N
H
O
Allantoin
Hahn PC, et al. In: Arthritis and Allied Conditions. 15th ed. 2005:2341-2355.

Distribution of Serum Urate Values and
Hyperuricemia
40
Development of MSU
crystals associated with 1
• Decreased solubility of urate
(temperature)
• Low pH
• Trauma or tissue injury
• Supersaturation due to
reabsorption of water (lack of
joint activity during sleep)
Percent of distribution 2
35
30
25
20
15
10
Women
Men
Urate
crystallizes
at a level
of 6.8
mg/dL 3
5
0
0 1 2 3 4 5 6 7 8 9 10 11 12 13
Serum urate (mg/dL)*
* Serum urate levels in 1515 men
and 1670 women aged ≥ 30 years in
Taiwan; 1991-1992
1
Dalbeth N and Haskard DO. Rheumatology. 2005;44:1090-1096.
2 Lin K-C, et al. J Rheumatol. 2000;27:1045-1050.
3
Schumacher HR Jr. Cleve Clin J Med. 2008;75(suppl 5):S2-S4.

Medications Altering Urate Levels
Urate-Increasing Agent 1
Pyrazinamide
Nicotinate
Lactate, β-hydroxybutyrate,
acetoacetate
Salicylate (low dose)
Ethambutol
Diuretics
Cyclosporine
Tacrolimus
β-blockers
Urate-Decreasing Agent 1
Uricosurics:
Probenecid
Losartan
Salicylate (high dose)
Fenofibrate
Amlodipine
Xanthine oxidase inhibitor:
Allopurinol
Febuxostat
Uricase
Other components may also affect uric acid clearance 1-3
excessive alcohol intake, niacin, levodopa, cytotoxic drugs, and vitamin B 12
1 Choi HK, et al. Ann Intern Med. 2005;143:499-516.
2 Quiceno GA and Cush JJ. Rheum Dis Clin North Am. 2007;33:123-134. 3 Peronato G. Contrib Nephrol. 2005;147:1-21.

The Hyperuricemia Cascade
Dietary
purines
Tissue
nucleic acids
Endogenous
purine synthesis
Overproduction
5%-10% of all gout
patients
Urate
Hyperuricemia
Underexcretion
80%-90% of all gout
patients!
Most common
cause of
hyperuricemia
Silent
tissue
deposition
Gout
Renal
manifestations
Associated
cardiovascular
events
and mortality
Becker MA, et al. In: Arthritis and Allied Conditions. 15th ed. 2005:2303-2339.
Wortmann RL. In: Harrison’s Principles of Internal Medicine. 14th ed. 1998:2158-2165.
Hahn PC, et al. In: Arthritis and Allied Conditions. 15th ed. 2005:2341-2355.
Pittman JR and Bross MH. Am Fam Physician. 1999;59:1799-1806, 1810.

Understanding
Important Risk Factors
and Comorbidities
for Hyperuricemia
and Gout

Risk Factors
for the Development of Gout
• Male gender 1
• Drugs 2
• Postmenopausal women 2
– National Health and Nutrition
Examination Survey (NHANES) III
data show independent
association with higher serum uric
acid (SUA) levels 3
• Longevity/improved survival 2
• Diet:
– High alcohol intake:
• (Beer > hard liquor > wine) 2,4,5
– Red/organ meats and seafood 2,4,6
– Diuretics
– Cyclosporine
• Major organ transplantation 2
• End-stage renal disease
(ESRD) 2
• Genetic influences 4
1 Kramer HM and Curhan G. Am J Kidney Dis. 2002;40:37-42. 2 Bieber JD and Terkeltaub RA. Arthritis Rheum.
2004;50:2400-2414. 3 Hak AE and Choi HK. Arthritis Res Ther. 2008;10:R116. 4 Fam AG. J Rheumatol. 2005;
32:773-777. 5 Choi HK, et al. Lancet. 2004;363:1277-1281. 6 Choi HK, et al. N Engl J Med. 2004;350:1093-1103.
7 Nakagawa T, et al. Am J Physiol Renal Physiol. 2006;290:F625-F631.

Some Comorbidities Associated With
Hyperuricemia Warrant Consideration
• Obesity 1
• Hyperlipidemia 1
• Heart failure 3,4 • Cardiovascular disease 4,7
• Metabolic syndrome 2 • Hypertension 4-6
• Diabetes mellitus 1,8 • Chronic renal disease 4,7
No reliable predictor that gout will develop in a given
hyperuricemic patient 2
Currently, asymptomatic hyperuricemia is not treated
But, higher serum urate levels are more likely to lead to gout
1
Fam AG. J Rheumatol. 2005;32:773-777. 2 Mandell BF. Cleve Clin J Med. 2008;75(suppl 5):S5-S8.
3
Anker SD, et al. Circulation. 2003;107:1991-1997. 4 Baker JF, et al. Am J Med. 2005;118:816-826.
5 Feig DI and Johnson RJ. Hypertension. 2003;42:247-252. 6 Alper AB Jr, et al. Hypertension. 2005;45:34-38.
7
Zhou X, et al. Curr Hypertens Rep. 2006;8:120-124. 8 Choi HK, et al. Rheumatology. 2008;47:1567-1570.

Control of Metabolic Syndrome Components
Essential to Reduce Cardiovascular Disease Risk
in Patients With Hyperuricemia and Gout
Percent of patients with
metabolic syndrome
100
80
60
40
20
0
Higher prevalence of
metabolic syndrome associated
with gout across age groups* 1,2
* NHANES III (1988-1994)
Gout
No gout
20-39 40-59 ≥ 60
Age (years)
• High prevalence of the
metabolic syndrome in
hyperuricemic patients 1-3
• Patients with gout have an
approximately 30% elevated
cardiovascular disease (CVD)
risk 3,4
Hyperuricemia 3,4
Increases cardiovascular
mortality in patients at
high cardiovascular risk
1
Weaver AL. Cleve Clin J Med. 2008;75(suppl 5):S9-S12.
2 Choi HK, et al. Arthritis Rheum. 2007;57:109-115.
3 Puig JG and Martínez MA. Curr Opin Rheumatol. 2008;20:187-191.
4
Krishnan E, et al. Arch Intern Med. 2008;168:1104-1110.

Hyperuricemia and Incidence of Hypertension
Among Men Without Metabolic Syndrome
Multiple Risk Factor Intervention Trial
Proportion of men
without hypertension
1.00
0.75
0.50
0.25
Baseline hyperuricemia and risk
of subsequent hypertension
Adjusted for age
SUA ≤ 7 mg/dL (n = 2270)
SUA > 7 mg dL (n = 803)
• Hyperuricemia increases
the risk of developing
hypertension by
approximately 80%:
– Independent of baseline blood
pressure measurements, renal
function, serum lipid levels,
BMI, proteinuria, alcohol use,
and age
• Is it possible to
prevent/postpone the onset
of hypertension by reducing
SUA levels?
0.00
0 1 2 3 4 5 6 7 8
Follow-up in years
Log rank P < 0.001 for both survivor functions
Krishnan E, et al. Hypertension. 2007;49:298-303.

Hyperuricemia Increases Risk
of Renal Manifestations
Relative risk of renal failure
10
8
6
4
2
0
Increased risk of renal failure
with hyperuricemia*
Low
(0.3-4.9)
†
P < 0.01 vs moderate
SUA level
Moderate
(5.0-6.4)
Slightly
high
(6.5-8.4)
SUA level (mg/dL)
†
High
(> 8.5)
Cumulative incidence of
ESRD per 1000 screenees
10
8
6
4
2
0
SUA (mg/dL) < 7.0
Screenees (n) 15,617
ESRD cases (n) 19
Hyperuricemia
predicts ESRD ‡
Men
≥ 7.0
7332
34
< 6.0
21,795
19
≥ 6.0
3433
31
Women
* Prospective cohort study of 49,413 Japanese men
‡
Screened cohort of Japanese men and women
Edwards NL. Cleve Clin J Med. 2008;75(suppl 5):S13-S16.
Tomita M, et al. J Epidemiol. 2000;10:403-409.
Iseki K, et al. Am J Kidney Dis. 2004;44:642-650.

Differentiating
the Varying Stages of
Gout and Deciding on a
Confirmed Versus
Presumptive Diagnosis

Clinical Stages of Gout
• Elevated serum urate with no
clinical manifestations of gout
• Crystal deposition may be
starting
1
Asymptomatic
Hyperuricemia
• Acute inflammation in the joint
caused by urate crystallization
and crystal phagocytosis
2
• Intervals between acute flares
• Crystals persist in joints 3
• Long-term complications of
uncontrolled hyperuricemia
• Chronic arthritis and tophi
4
Acute Gouty
Arthritis
Intercritical
Periods
Advanced
Gout
Uncontrolled
Hyperuricemia:
Flares are
longer lasting
and more severe
Intercritical
periods diminish
Chronic pain and
polyarticular gout
Becker MA, et al. In: Arthritis and Allied Conditions. 15th ed. 2005:2303-2339.

Features of Acute Gouty Attacks
• Lower extremities most often involved 1
• First metatarsophalangeal joint (podagra) is the most common
initial site (approximately 90%) 1
– 80% of first attacks are monoarticular
• Pain and inflammation 1-4
– Dramatic inflammatory response
• Fever in some patients 1,4
• Can occur in bursae, tendons, and joints 1
– Rarely affects shoulders, sternoclavicular joints, hips, spine, and
sacroiliac joints
• Untreated, an initial acute gout attack resolves completely
within 3 to 14 days 4
– The majority of patients experience second acute flare within 1 year of
first gout flare 5 1
Becker MA, et al. In: Arthritis and Allied Conditions. 15th ed. 2005:2303-2339.
2 Schumacher HR Jr. Cleve Clin J Med. 2008;75(suppl 5):S2-S4. 3 Terkeltaub R. Bull NYU Hosp Jt Dis. 2006;64:82-86.
4
Mandell BF. Cleve Clin J Med. 2008;75(suppl 5):S5-S8. 5 Yu TF and Gutman AB. Ann Intern Med. 1961;55:179-192.

Typical Clinical Features of Gout
Differ With Age of Onset
Feature Typical Gout Elderly Onset Gout
Age of
Onset
Sex
Distribution
Presentation
Peak in mid-40s Over 65
Men > women
Acute monoarthritis
Lower extremity (podagra 60%)
Men = women
More often:
Polyarticular onset
Upper extremity affected
Tophi
Associated
Features
After years of attacks
Elbows > fingers
Obesity
Hyperlipidemia
Hypertension
Alcohol use, heavy
Courtesy of the Clinical Slide Collection on the Rheumatic Diseases,
American College of Rheumatology, 1996; with permission.
May occur early or
without history of prior attacks
Possibly more often over fingers
Renal insufficiency
Diuretic use, especially in women
Alcohol use less common
Wise CM. Rheum Dis Clin North Am. 2007;33:33-55.
Images courtesy of Charles Goldberg, MD.

Diagnosing Gout: Why Aspirate the Joint?
Separate Septic Arthritis From Gout
• Gout defined: deposition of
MSU crystals in joints and
other connective tissues 1
– Consequentially, the gold
standard for diagnosis is correct
identification of these crystals
• Does the patient have gout?
• Are current inflammatory
symptoms due to gout?
Inflammatory Joint Fluids 2
(> 2000 white blood cells [WBCs] per
mm 3 )
Septic arthritis
Crystal-induced monoarthritis
(eg, gout, pseudogout)
Other potential causes:
Rheumatoid arthritis
Spondyloarthropathy
Systemic lupus erythematosus
Juvenile rheumatoid arthritis, Lyme
disease, and other crystalline
arthritides
1
Eggebeen AT. Am Fam Physician. 2007;76:801-808.
2 Adapted from Siva C, et al. Am Fam Physician. 2003;68:83-90.

Diagnosing Gout: Aspirate the Joint
The Gold Standard
• Synovial fluid analysis 1-4
– Examine for MSU crystals
– Culture and gram stain
analysis (differential for septic
arthritis)
– Perform WBC count:
• 5000 to 50,000/μL
This superolateral approach may be
best when there is a large effusion 5
• Normal synovial fluid 4
– Viscous, straw-colored substance
found in small amounts in joints,
bursae, and tendon sheaths
• All studies can be performed
with only 1-2 mL of fluid 3
1
Rott KT and Agudelo CA. JAMA. 2003;289:2857-2860. 2 Schlesinger N. Drugs. 2004;64:2399-2416.
3 Wheeless' Textbook of Orthopaedics. http://www.wheelessonline.com/ortho/synovial_fluid.
Accessed November 20, 2008. 4 MedlinePlus Web site. http://www.nlm.nih.gov/MEDLINEPLUS/ency/article/003629.htm.
Accessed November 20, 2008. 5 Zuber TJ. Am Fam Physician. 2002;66:1497-1500, 1503-1504, 1507.

Differential Diagnosis:
MSU (Gout) or CPPD (“Pseudogout”) Crystals?
• Serum urate crystals are
negatively birefringent:
– Usually needle shaped under
• Calcium pyrophosphate dihydrate (CPPD)
crystals are weakly positively
birefringent 1,4,5
– Rhomboid, rods, squares, or irregular under
compensated polarized light; crystals
frequently missed
– Consider the possibility of septic arthritis 5
MSU crystals 3
CPPD crystals 6
Direction of
polarized light
1
Schumacher HR and Reginato AJ. Atlas of Synovial Fluid Analysis and Crystal Identification.
Philadelphia, PA: Lea & Febiger; 1991. 2 Dore RK. Cleve Clin J Med. 2008;75(suppl 5):S17-S21. 3 Reprinted with permission
from ‘Gout and Hyperuricemia,’ February 151999, American Family Physician. Copyright © 1999 American Academy of
Family Physicians. All Rights Reserved. 4 Siva C, et al. Am Fam Physician. 2003;68:83-90. 5 Pascual E and Jovaní V. Best
Pract Res Clin Rheumatol. 2005;19:371-386. 6 Image reprinted with permission from eMedicine.com, 2008. Available at:
http://www.emedicine.com//med/topic1938.htm. Accessed November 20, 2008.

Advanced Gout: Principal Sites of Tophi
• Risk factors include 1
– Long duration of
hyperuricemia
– High serum urate levels
– Long periods of active,
untreated gout
• Subcutaneous gouty tophi
occur frequently at sites of
friction or trauma 1
Be careful:
• Chronic gout can mimic
rheumatoid or psoriatic arthritis! 2
Helix of the ear
Olecranon bursa
Extensor surface
of the forearm
Wrists
Finger pads
Knee
Achilles tendon
1
Becker MA, et al. In: Arthritis and Allied Conditions. 15th ed. 2005:2303-2339.
2 Mandell BF. Cleve Clin J Med. 2008;75(suppl 5):S5-S8.
Reproduced with permission from The Hand Center Web site. http://www.handcenter.org. Accessed November 20, 2008.

Long-term Consequences
of Chronic MSU-induced Inflammation
Low-grade synovitis
in involved joints
can persist after acute
attacks
Chronic synovitis
Bone erosion
Cartilage loss
Factors involved in in acute
attacks also contribute to to
chronic inflammation:
Cytokines
Chemokines
Proteases
Oxidants
Tophi on on cartilage surface
may contribute to to chondrolysis,
which can can occur despite
adequate treatment
Choi HK, et al. Ann Intern Med. 2005;143:499-516.

Diagnosing Gout
Common Challenges and Pitfalls
History and
Physical
Examination
Serum
Urate Level
Some Patients
Refuse
Tapping the
Joint
• Acute versus chronic state, atypical joint
involvement (eg, Heberden’s nodes) 1
• Elderly onset gout, (postmenopausal) women 1,2
• Not a definitive test; normal SUA levels common
during acute attacks 1
– Clinically significant hyperuricemia includes SUA levels
that fall within the population-defined “normal” range of
many clinical laboratories 2
• Alternative: presumptive clinical diagnosis 3
– History and physical examination for characteristic
features 4
– Clinical diagnosis wrong in about 20% of the cases 5
• Danger of joint destruction with sepsis 6,7
– Within 24-48 hours
1
Rott KT and Agudelo CA. JAMA. 2003;289:2857-2860. 2 Mandell BF. Cleve Clin J Med. 2008;75(suppl 5):S5-S8.
3 Harrold LR, et al. Arthritis Rheum. 2007;57:103-108. 4 Dore RK. Cleve Clin J Med. 2008;75(suppl 5):S17-S21.
5
Chen LX and Schumacher HR. J Clin Rheumatol. 2008;14(5 suppl):S55-S62.
6
Siva C, et al. Am Fam Physician. 2003;68:83-90. 7 Zhang W, et al. Ann Rheum Dis. 2006;65:1301-1311.

Question to Ask the Patient
Presumptive Diagnosis of Gout
• When did the symptoms start? Was the onset
sudden?
• Was this the first time you experienced pain/swelling
at this joint? If not, which other joints have been
affected and how long ago has this been?
• Are you running a fever?
• Do you have relatives with similar complaints?
• Are you taking any medications, and which?
• What have you been eating and/or drinking?
Anything like red meat, shellfish, or beer?

What Is the Evidence for Gout Diagnosis?
Ten Recommendations From EULAR Modified to US
Standards
1
In acute attacks, rapid development of severe pain, swelling, and
tenderness, reaching peak within 6-12 hours is highly suggestive of
crystal inflammation, though not specific for gout
2
For typical gout presentations (eg, recurrent podagra), a clinical
diagnosis of gout is reasonably accurate but not definitive unless
crystal confirmed
3
4
5
Demonstration of MSU crystals in synovial fluid or tophus aspirates
permits a definitive gout diagnosis
A routine search for MSU crystals is recommended in all synovial
fluid aspirates from inflamed joints
Identification of MSU crystals from asymptomatic joints may allow
gout diagnosis between attacks
Adapted from Becker MA and Chohan S. Curr Opin Rheumatol. 2008;20:167-172.
Adapted from Zhang W, et al. Ann Rheum Dis. 2006;65:1301-1311.

What Is the Evidence for Gout Diagnosis?
Ten Recommendations From EULAR Modified to US
Standards (Cont.)
6
7
8
9
Gout and sepsis may coexist; if sepsis is suspected, Gram stain and
culture of synovial fluid should be carried out even if MSU crystals
are identified
Although the most important risk factor for gout, serum urate levels
do not confirm or exclude gout
Renal uric acid excretion should be determined in selected gout
patients (family history of young onset gout, onset of gout under age
25, or with renal calculi); hyperuricemia as a marker in acute gout
Radiographs may be useful for differential diagnosis and may show
typical features in chronic gout; they are not useful in confirming a
diagnosis of early or acute gout
10
Risk factors for gout and associated comorbidity should be
assessed, including features of metabolic syndrome
Adapted from Becker MA and Chohan S. Curr Opin Rheumatol. 2008;20:167-172.
Adapted from Zhang W, et al. Ann Rheum Dis. 2006;65:1301-1311.

Clinical Picture and Radiographic Evidence
Polyarticular, tophaceous gout in
a patient originally treated for
rheumatoid arthritis for 8 years 1
Advanced gout: joint destruction
from large erosions with
“overhanging” edges 2
Metacarpal-
phalangeal joints
of the hand with
calcification of the
tophus on the
ulnar side 2
1 Image courtesy of N. Lawrence Edwards, MD.
2
Images reprinted with permission from Ferguson M.
http://uwmsk.org/residentprojects/gout.html. Accessed November 20, 2008.

Case Presentation
Matthew, 66 Years Old
• Matthew comes to the pharmacist for an
over-the-counter (OTC) pain reliever:
– He limps on the left foot using a cane
• Questioning the patient reveals:
– Swelling and erythema of first metatarsophalangeal joint on left
foot
– Started last night; patient runs a light fever
– Patient cannot bear any weight on the painful toe
No other symptoms,
no recent injury:
Patient remembers similar
pain a few months ago on
his elbow that subsided
after a few days
Matthew’s medication profile:
Hydrochlorothiazide 50 mg/day
Glipizide 10 mg/day
Enalapril 20 mg/day
Aspirin 81 mg/day
Matthew adheres to medication
schedule for hypertension,
diabetes, and cardiovascular
protection
His BMI is 33 kg/m 2 ; he
admits having
difficulties with
changing his diet:
He enjoys meat,
alcohol, and
caffeinated nondiet
sodas

Polling
Case: Matthew, 66 Years Old
Polling Question 1
• What is the likely cause of Matthew’s
symptoms?
1. No answer
2. Unspecific joint inflammation
3. Acute gout
4. Rheumatoid arthritis

Polling
Case: Matthew, 66 Years Old
Polling Question 2
• What is your next step?
1. No answer
2. Provide OTC pain reliever
3. Suggest physician review of symptoms and current
medications
4. 2 and 3

Treatment Options
for Gout

Considerations for the Treatment of Acute
Gout
Agent
NSAIDs 1
Indomethacin 50 mg TID for
10 days
Naproxen 500 mg BID for
4-10 days
Sulindac 200 mg BID for
4-10 days
Colchicine (oral) 1,2
Acute attacks:
0.6 mg once every hour for
up to 3 hours (maximum,
3 pills = 1.8 mg total)
Prophylaxis:
0.6 mg BID, TID
If creatinine clearance
≥ 50 mL/min: BID
< 10 mL/min: avoid
Considerations and Cautions
• All NSAIDs can be effective 1-4
• Use with caution in older patients, patients with renal
insufficiency, heart failure, peptic ulcer disease, and/or
liver disease, and those on anticoagulant therapy 2,4
• Interacts with warfarin 5
• Can be effective with early use 1,4
• Gastrointestinal adverse events, particularly diarrhea,
can limit use 1,3,4
• Avoid in patients with severe renal or hepatic impairment:
risk of bone marrow suppression and neuromyopathy 1-3
• Interacts with cyclosporine, statins, and macrolides 5
• Low-dose approach may have similar efficacy without
gastrointestinal concerns 6
1 Eggebeen AT. Am Fam Physician. 2007;76:801-808. 2 Terkeltaub RA. N Engl J Med. 2003;349:1647-1655.
3
Wortmann RL. Curr Rheumatol Rep. 2004;6:235-239. 4 Schlesinger N. Drugs. 2004;64:2399-2416.
5
Schumacher HR, et al. Cleve Clin J Med. 2008;75(suppl 5):S22-S25.
6 Terkeltaub R, et al. ACR Meeting 2008. Presentation 1944.

Considerations for the Treatment of Acute
Gout
Agent
Considerations and Cautions
Corticosteroids 1
Prednisone 20-40 mg daily 2-3
days, taper over 10-14 days
Intra-articular methylprednisolone
20-40 mg once
Intramuscular methylprednisolone
80-120 mg once
• Oral, intra-articular, and intramuscular
administration 2
• Useful when renal and/or gastrointestinal
contraindications to other therapies 3
• Avoid in patients with joint sepsis and use
cautiously in patients with diabetes 1,4
Adrenocorticotropic
Hormone 3
No dosing guidelines;
common IM regimen:
40 IU every 8 hours, followed by
40 IU every 12 hours, then 40 IU
daily (total 14 days)
• Limited availability 4
• Very expensive
• Rarely used in primary care
• Concomitant use with colchicine 3
1
Eggebeen AT. Am Fam Physician. 2007;76:801-808. 2 Wortmann RL. Curr Rheumatol Rep. 2004;6:235-239.
3 Schlesinger N. Drugs. 2008;68:407-415. 4 Terkeltaub RA. N Engl J Med. 2003;349:1647-1655.

Anti-inflammatory Prophylaxis Prior to
Urate-lowering Therapy
Reduce pain
and
inflammation
Avoid
hyperuricemia
treatment
during the
acute attack
• Prophylactic agents 1-3
– NSAIDs, low-dose, oral colchicine
– Useful for decreasing the frequency and severity of
acute flares
– Will not stop silent tissue deposition of crystals
• Initiate prophylaxis prior to starting uratelowering
therapy and continue for 6-12 months 2,3
– Crystals often persist during intercritical periods 3
– Risk for continued flares, low-grade persistent
inflammation, and progressive disease 3,4
Importance of patient dialogue and consistent follow-up
1
Borstad GC, et al. J Rheumatol. 2004;31:2429-2432. 2 Schlesinger N. Drugs. 2004;64:2399-2416.
3 Schumacher HR, et al. Cleve Clin J Med. 2008;75(suppl 5):S22-S25. 4 Choi HK, et al. Ann Intern Med. 2005;143:499-516.

Urate-lowering Therapy to Prevent Disease
Progression
Achieve and maintain
SUA level < 6 mg/dL
to allow depletion of
serum urate pool and
deposited crystals 1-4
Reduce frequency
of acute attacks
during urate-lowering
therapy 1-4
Maintain and improve
quality of life (QOL) 1-4
• Urate-lowering therapy 2-4
– Often started at week 2-4 with continuous
prophylaxis, but no evidence from studies
– Incidence of flares and SUA levels decline over
time with treatment
• Urate-lowering therapy should be lifelong 3
– If attack occurs when therapy is initiated, do not
discontinue (will only cause another flux in urate
levels) 2
– Agents: uricosurics and xanthine oxidase
inhibitors 1,2
• Carefully weigh potential drug interactions
and side effects
Importance of patient dialogue and consistent follow-up
1 Terkeltaub RA. N Engl J Med. 2003;349:1647-1655. 2 Schlesinger N. Drugs. 2004;64:2399-2416.
3
Schumacher HR Jr and Chen LX. Cleve Clin J Med. 2008;75(suppl 5):S22-S25.
4
Becker MA, et al. Nucleosides Nucleotides Nucleic Acids. 2008;27:585-591.

What Is the Evidence for Gout Management?
Twelve Recommendations From EULAR Modified to US Standards (1)
1
2
3
4
5
6
7
Utilize both nonpharmacologic and pharmacologic modalities; tailor
to risk factors and clinical phase
Stress patient education and lifestyle changes (eg, weight loss and
alcohol reduction)
Address comorbidities like hyperlipidemia, hypertension,
hyperglycemia, obesity, and smoking
Oral colchicine and/or NSAIDs are first-line agents for systemic
treatment of acute attacks
Side effects with high doses of colchicine; low doses (eg, 0.6 mg TID)
may be sufficient for some patients with acute gout
Intra-articular aspiration and injection of long-acting steroid is
effective and safe for an acute attack
Urate-lowering therapy: patients with recurrent acute attacks,
arthropathy, tophi, or radiographic changes
Adapted from Becker MA and Chohan S. Curr Opin Rheumatol. 2008;20:167-172.
Adapted from Zhang W, et al. Ann Rheum Dis. 2006;65:1312-1324.

What Is the Evidence for Gout Management?
Twelve Recommendations From EULAR Modified to US Standards (2)
8
9
Therapeutic goal of urate-lowering therapy: promote crystal dissolution and
prevent crystal formation by maintaining the SUA level below the saturation
point for MSU (6.8 mg/dL), target for SUA level < 6.0 mg/dL
Allopurinol: appropriate long-term urate-lowering drug; start at a low dose (eg,
100 mg daily) and increase by 100 mg every 2-4 weeks, if required; adjust
dose in patients with renal impairment; options with allopurinol toxicity: other
xanthine oxidase inhibitors, uricosuric agent, allopurinol desensitization
(cases of mild rash)
10
11
12
Uricosuric agents (probenecid): alternative to allopurinol (with normal renal
function); relatively contraindicated in patients with urolithiasis
Prophylaxis against acute attacks during the first months of urate-lowering
therapy: colchicine (0.6-1.2 mg daily) and/or an NSAID (with gastro-protection,
if indicated)
Gout associated with diuretic therapy: stop diuretic, if possible; hypertension
and hyperlipidemia: consider use of losartan and fenofibrate, respectively
(both have modest uricosuric effects)
Adapted from Becker MA and Chohan S. Curr Opin Rheumatol. 2008;20:167-172.
Adapted from Zhang W, et al. Ann Rheum Dis. 2006;65:1312-1324.

Adjunctive Therapy for Gout
and Associated Comorbidities:
Increasing Evidence for Dietary and Lifestyle Recommendations
• Control weight with daily exercise 1,2
• Limit red meat consumption 1,2
• Replace fish consumption with omega-3 fatty acids 1
– Or supplements of docosahexaenoic acid and eicosapentaenoic acid
• Refrain from high-fructose–containing foods/drinks 2,3
• Consume 1-2 servings of dairy or calcium supplement daily 1,2
• Consume nuts and vegetables daily 1,2
• Supplementation with vitamin C 500 mg/day 2,4
• Some evidence for beneficial effect of coffee consumption 2
• Counsel on benefits of dietary and lifestyle changes 1
– Implementation creates health benefits that may extend beyond gout, but
preventive strategies alone in patients with existing disorders may not be
sufficient 5
– Impact on the SUA level limited: 1-2 mg/dL
– Less than 20% of patients make sustained lifestyle changes 5
1 Choi HK. Curr Rheum Rep. 2005;7:220-226. 2 Hak AE and Choi HK. Curr Opin Rheumatol. 2008;20:179-186.
3
Nakagawa T, et al. Am J Physiol Renal Physiol. 2006;290:F625-F631.
4 Huang H-Y, et al. Arthritis Rheum. 2005;52:1843-1847. 5 Levinson W, et al. Ann Intern Med. 2001;135:386-391.

Urate-lowering Agents
Uricosurics
• Uricosurics correct renal urate
underexcretion by inhibiting
postsecretory SUA reabsorption 1
During Treatment 2
Alkalinize
urine
Increase
fluid
consumption
Steps
• Probenecid 1,2
• Mild uricosurics as adjunctive approach:
– Diflunisal*, losartan*, and fenofibrate* 2,3
• Possible benefit with hypertension
treatment and lipid reduction 2
– 20%-40% reduction in SUA levels reported 3
• Lose effectiveness as renal function
deteriorates 4
• Other agents with uricosuric properties:
– Atorvastatin 5
– Amlodipine (increased renal urate excretion) 6
– Vitamin C (400-500 mg/day) 6,7
Multiple
medication doses
required
Emphasize compliance
* Off-label
1
Terkeltaub RA. N Engl J Med. 2003;349:1647-1655. 2 Daskalopoulou SS, et al. Curr Pharm Des.
2005;11:4161-4175. 3 Bardin T. Ann Rheum Dis. 2003;62:497-498. 4 Gaffo AL and Saag KG. Am J Kidney Dis.
2008;5:994-1009. 5 Lee SJ, et al. Curr Rheumatol Rep. 2006;8:224-230. 6 Choi HK, et al. Ann Intern Med.
2005;143:499-516. 7 Gao X, et al. J Rheumatol. 2008;35:1853-1858.

Urate-lowering Agents
Mechanism of Action of Xanthine Oxidase Inhibitors
Solubility decreases
N
OH
N
Xanthine
oxidase
N
OH
N
Xanthine
oxidase
N
OH
N
OH
N
N
H
Hypoxanthine
HO
N
Xanthine
N
H
HO
N
Uric acid
N
H
Xanthine oxidase inhibitors
block the conversion of
hypoxanthine to xanthine to
uric acid
H 2 N
O
O
N
H
Uricase
NH
N
H
O
Allantoin
Hahn PC, et al. In: Arthritis and Allied Conditions. 15th ed. 2005:2341-2355.

Xanthine Oxidase Inhibitor
Advantages
• Effective in overproducers and underexcretors
• Not dependent on renal function
• Maximal dose 800 mg/day
Limitations
• Numerous drug interactions
• Rare but life-threatening hypersensitivity reaction possible
• Dose adjustments required for concomitant azathioprine (AZA) and 6-
mercaptopurine (6-MP)
• Guidelines suggest to base allopurinol dosing on creatinine clearance
or glomerular filtration rate (GFR), particularly in patients with chronic
kidney disease (CKD)
N
O
N
Allopurinol
N
H
NH
Hahn PC, et al. In: Arthritis and Allied Conditions. 15th ed. 2005:2341-2355.
Perez-Ruiz F, et al. J Clin Rheumatol. 2005;11:129-133.

Optimizing Allopurinol Dosing
• Practice recommendation for
allopurinol dose increase:
– Prevent flare risk in all gout
patients with gradual
introduction 1
– Monitor titration in patients with
CKD, emphasize target SUA
level of ≤ 6 mg/dL 1-3
• Inform patients of the risks
and benefits trade off:
– Potential allopurinol toxicity
versus gout progression 1
Creatinine
Clearance
(mL⁄ minute)
0
10
20
40
60
80
100
120
140
Dosing Guidelines for Allopurinol
Dosing 1,4
Maintenance Dose
Allopurinol
100 mg every 3 days
100 mg every 2 days
100
150
200
mg⁄day
250
300
350
400
1
Dalbeth N and Stamp L. Semin Dial. 2007;20:391-395.
2 Fels E and Sundy JS. Curr Opin Rheumatol. 2008;20:198-202.
3 Perez-Ruiz F, et al. J Clin Rheumatol. 2005;11:129-133. 4 Hande KR, et al. Am J Med. 1984;76:47-56.

Allopurinol Hypersensitivity Reaction
Extremely rare, occurs in < 1% of patients on allopurinol
Can present as
mild erythema
and progress to
fatal reactions
with continued
therapy
Usually appears
within first
5 weeks of
treatment
• Mild reactions usually subside with discontinuation
of allopurinol
• Progression to Stevens-Johnson syndrome or toxic
epidermal necrolysis well reported:
– Hepatomegaly, jaundice, and renal and hepatic dysfunction
can accompany severe reactions
– Risk factors include: renal dysfunction, hepatic disease,
thiazide diuretics, and chronic alcohol abuse
• However, reactions delayed by > 2 years have been
reported:
– Unknown mechanism for this reaction
Rechallenge with allopurinol should not be performed
Fels E and Sundy JS. Curr Opin Rheumatol. 2008;20:198-202.
Bohan KH, et al. In: Applied Therapeutics: The Clinical Use of Drugs. 9th ed.
Philadelphia, PA: Lippincott Williams and Wilkins; 2008:42.1-42.14.

Target Serum Urate Levels Are Often Not
Achieved
Percent of
patients reaching
target SUA 1
(n = 5942)
50
40
30
20
10
0
Median SUA level with allopurinol treatment
decreased from 8.7 to 7.1 mg/dL (P < 0.001) 1,2
Patients on pharmacotherapy with nontarget levels were 59%
(allopurinol: 75%) more likely to flare than those at target level
32
17
24
< 200 mg/day ≥ 200 to < 300
mg/day
≥ 300 to < 400
mg/day
In this observational study of a managed care organization, the majority of
gout patients on varying doses of allopurinol therapy did not reach target
SUA level of < 6.0 mg/dL 1
• In a prospective clinical study of allopurinol (n = 49) in male patients
with gout, 53% achieved SUA < 6.0 mg/dL on 300 mg allopurinol daily 3
– Patients with poor results on 300 mg were titrated to 450-600 mg daily
1
Yang W, et al. ACR Meeting 2005. Poster 362.
2 Sarawate CA, et al. J Clin Rheumatol. 2006;12:61-65.
3
Perez-Ruiz F, et al. Ann Rheum Dis. 1998;57:545-549.

Typical Prescribing Errors With Available
Xanthine Oxidase Inhibitor
Percent of patients receiving
incorrect prescription
60
50
40
30
20
10
0
Data from United Kingdom
General Practice research
database
25.9 25.0
Incorrect dosing
of allopurinol in
renal failure
Inadequate dose
adjustment with
concomitant allopurinol
+ AZA or 6-MP*
56.7
48/185 13/52 267/471
Treatment of
asymptomatic
hyperuricemia
• Allopurinol is frequently prescribed inappropriately; more
common with advancing age, male gender, and presence of
polypharmacy
* Allopurinol enhances effects of AZA and 6-MP
Adapted from Mikuls TR, et al. Rheumatology. 2005;44:1038-1042.

Potential Drug Interactions With Allopurinol
Interacting Drug
AZA/6-MP
Warfarin
Angiotensin-converting
enzyme inhibitors
Cyclophosphamide
Ampicillin/amoxicillin
Antacids/aluminum salts
Chlorpropamide
Cyclosporine
Probenecid
Phenytoin
Theophylline
Potential Effect
Increased 6-MP serum concentration with
increased risk of bone marrow suppression;
reduce AZA dose by one-quarter
Anecdotal reports of increased potential for bleeding
Increased risk of allopurinol hypersensitivity
Increased risk of bone marrow suppression
Increased risk of rash
Decreased absorption of allopurinol
Increased hypoglycemic effect
Increased cyclosporine concentrations
with potential for toxicity
Increased renal elimination of oxypurinol;
inhibition of probenecid metabolism
Inhibited metabolism of phenytoin resulting
in increased serum concentrations
Increase in theophylline AUC, t ½
,
and reduction in clearance
Tatro DS. 2008 Drug Interaction Facts. St Louis, MO: Lippincott Williams & Wilkins; 2008.

Xanthine Oxidase Inhibitor
• Febuxostat*: a nonpurine, selective inhibitor of xanthine oxidase in
phase III studies for the treatment of hyperuricemia associated with
gout 1-3
CH 3
H 3 C
O
NC
N
CH 3
Febuxostat
S
CO 2 H
• Current data support:
– Potent inhibition with significant urate reduction 1
– Ability to administer in renal insufficiency and mild or moderate
hepatic insufficiency with no dosage adjustments 1,2
– Safe, effective, and well tolerated in allopurinol-intolerant patients 3
* Investigational
1
Khosravan R, et al. J Clin Pharmacol. 2006;46:88-102.
2
Swan S, et al. Arthritis Rheum. 2003;48:S529. Abstract 1348.
3 Becker MA, et al. ACR Meeting 2004. Poster 183.

Comparison of Xanthine Oxidase Inhibitors
(Efficacy and Safety)
Phase III, Randomized, Controlled, Multicenter, Double-blind Trial
100
Patients achieving SUA levels < 6.0 mg/dL at final visit at 6 months
(mean baseline SUA: 9.6 mg/dL; mean gout duration: 11.6 years)
Percent of patients
80
60
40
20
All patients
72*
CKD subgroup
67*
50* †
45
*
* P < 0.001 for all comparisons
†
P < 0.021 vs allopurinol
42
*
42
*
0
40 mg 80 mg 300 mg
Febuxostat ‡ Allopurinol §
• Comorbidities: mild/moderate CKD (65%; n = 1483), obesity (64%),
hyperlipidemia (42%), hypertension (53%)
• Comparable rates of all adverse events, including cardiovascular events,
across study groups or by renal function
(n = 2269)
‡
Investigational
§
145 subjects with moderate CKD in allopurinol group received 200 mg
Becker M, et al. ACR Meeting 2008.
Presentation L11.

SUA Reduction May Benefit Estimated
Long-term GFR in Hyperuricemic Patients
Mean changes in expected GFR after 5 years of treatment
with febuxostat 40, 80, and 120 mg/day (baseline mean SUA: 9.7 mg/dL)
Mean changes in
expected GFR (mL/min)
5
0
-5
-10
-15
-10.8
-2.0 -1.5
0.6 0.5
Greater benefit on GFR with
increased SUA reduction from baseline
≤ 3 > 3 to ≤ 4 > 4 to ≤ 5 < 5 to ≤ 6 > 6
Average SUA decrease from baseline (mg/dL)
• Significant relationship between GFR improvement and SUA reduction:
– 1.0 mL/min GFR improvement for each 1.0 mg/dL reduction in SUA (P = 0.02)
– Normal expected annual reduction in GFR: 0.8 mL/min in healthy adults
aged 30-80 years
n = 116; 91% male
Comorbidities: 52% hypertension and 23% CVD
Whelton A, et al. ACR Meeting 2008. Poster L7.

Investigational Recombinant
Uricase Enzymes
HO
N
OH
N
Uricase
H 2 N
O
Uric acid
O
N
H
Allantoin
N
N
H
NH
N
H
(Kidney excretion)
OH
O
Solubility increases
• Rapid and effective
reduction in SUA levels and
tophus burden 1-5
• Issues requiring further
investigation 1-3
– Short- and long-term effects?
– Role of immunogenicity
– Hemolysis risk
• Phase II clinical trials of
polyethylene glycol (PEG)-
uricases complete; phase III
studies in published in
abstracts* 3-5
* Investigational
1 Bieber JD and Terkeltaub RA. Arthritis Rheum. 2004;50:2400-2414.
2
Bomalaski JS and Clark MA. Curr Rheumatol Rep. 2004;6:240-247. 3 Sundy JS, et al. Arthritis Rheum. 2008;58:2882-2891.
4
Sundy JS, et al. ACR Meeting 2008. Presentation 635. 5 Baraf HS, et al. ACR Meeting 2008. Presentation 22.

Intravenous Uricase Enzyme: Treatment Response
in Patients With TFG GOUT1 and GOUT2 Phase III Randomized,
Double-blind Efficacy and Safety Trials
Percent of
patients
100
80
60
40
20
0
Patients with plasma urate < 6.0 mg/dL after 6 months of
intravenous pegloticase* 1
Every 2 weeks Every 4 weeks Placebo
42.5
†
34.5
Every 2 weeks Every 4 weeks Placebo
0
• Reduced tophus burden in 40% 2
– Complete resolution (of ≥ 1 tophus without increase in size in any other
tophus or appearance of new tophi) in 20% of the patients receiving treatment
every 2 weeks within 13 weeks of treatment 2
– QOL improvement: pain, physical functioning, and disability 3
* Investigational
†
P value was significant versus placebo (mean values from GOUT1 and GOUT2 depicted)
Treatment failure gout (TFG) was defined as: ≥ 3 flares in the previous 18 months, or ≥ 1 tophus,
or gouty arthropathy; serum urate > 8.0 mg/dL; and prior failure of maximum medically
appropriate dose of allopurinol or contraindication to allopurinol
•*
1
Sundy JS, et al. ACR Meeting 2008. Presentation 635.
2 Baraf HS, et al. ACR Meeting 2008. Presentation 22. 3 Edwards NL, et al. ACR Meeting 2008. Presentation 27.

Immunoreactivity and Clinical Response to
Intravenous Uricase Enzyme
Pooled Data From GOUT1 and GOUT2
Percent of patients on
pegloticase 8 mg IV*
100
80
60
40
20
0
Injection reactions and high antipegloticase titers are
increased with every 4 weeks in treatment group 1
Every 2 weeks
24
38
Injection reactions
Every 4 weeks
• Main adverse events were gout flares and infusion reactions 2
• Injection reactions associated with anti-PEG and high
antipegloticase titers 1
– Negative correlation with responder status in both groups (1% of
responders, 60% of nonresponders; P < 0.001)
* Investigational
Response: plasma urate < 6 mg/dL for ≥ 80% of the time in months 3 and 6
1
Becker MA, et al. ACR Meeting 2008. Presentation 1945. 2 Sundy JS, et al. ACR Meeting 2008. Presentation 635.
52
67
High antipegloticase and injection
reactions

Managing Inflammatory
Manifestations of Gout
• Relative contraindications to symptomatic therapies
frequent in refractory gout patients 1,2
– eg, NSAIDs or corticosteroids
• Potential benefit of biologic therapies 1
– Pain assessment, reduction of tender and swollen joint and c-
reactive protein levels
• Use not established in large trials 1
• Small uncontrolled trials
– Interleukin-1 inhibition (anakinra, rilonacept) 1-4
– Tumor necrosis factor-α inhibition (etanercept, infliximab, and
adalimumab) 1,5,6 1 Fels E and Sundy JS. Curr Opin Rheumatol. 2008;20:198-202.
2 Pillinger MH, et al. Bull NYU Hosp Joint Dis. 2007;65:215-221.
3
So A, et al. Arthritis Res Ther. 2007;9:R28.
4 Terkeltaub R, et al. ACR meeting 2007. Poster 518.
5 Fiehn C and Zeier M. Rheumatol Int. 2006;26:274-276.
6
Tausche AK, et al. Ann Rheum Dis. 2004;63:1351-1352.

Case Discussion
Matthew, 66 Years Old
• An acute gout attack has
been confirmed by
MSU crystal analysis:
– The patient returns to the
pharmacist with new prescriptions
Previous medications:
Hydrochlorothiazide 50 mg/day
Glipizide 10 mg/day
Enalapril 20 mg/day
Aspirin 81 mg/day
Discussion Question:
• Should this patient be started on urate-lowering
therapy at this point?

Conclusions
• Remember the 4 stages of gout:
– Asymptomatic hyperuricemia, acute flares, intercritical segments, and
advanced gout
• Hyperuricemia is defined as an SUA level > 6.8 mg/dL
• SUA levels can be normal, especially during the attack:
– The target goal of uric acid treatment is < 6.0 mg/dL
• Encourage lifestyle modifications to benefit overall treatment
• Reinforce the importance of proper timing, dosing, and
adherence to pharmacotherapy:
– Use of anti-inflammatory treatment and when to initiate urate-lowering
therapy
– Counsel on potential adverse events with therapy
– Ensure that contributory comorbidities are addressed
• New therapies are on the horizon

Questions and
Answers