Stay informed for your
patients and practice.

Gout is a type of
arthritis associated with
high amounts of uric
acid, also known as
hyperuricemia.1,3
  • When uric acid builds up, it can turn into crystals that cause painful flares, tophi, and other symptoms of gout2
  • Uric acid crystals can deposit almost anywhere in the body, in organs like the kidney and heart and in the joints and bones1,2

Graphic showing how gout can affect the kidneys, heart, and spine

Graphic showing how gout can affect the kidneys, heart, and spine

KRYSTEXXA has not been studied to remove urate deposition in the kidney or heart.

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Uric acid crystal buildup isn't always visible from the
outside.

Up to 75% of the urate burden may not be detected upon physical examination7-9

Images courtesy of  Dr Jürgen Rech. Green areas indicate uric acid buildup. Individual patient presentations may vary.

Gout and elevated sUA
are associated with
increased risk of
mortality and
comorbidities10-12

Outlining the potential consequences of uncontrolled gout is critical to getting patients on the right treatment path.

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  • The risk of death tripled in patients with gout and visible tophi at diagnosis13*
  • All-cause mortality increased by 9% with every 1 mg/dL increase in sUA level14†
  • Gout has been shown to be an independent risk factor for heart failure, hypertension, CHD, PAD, PVD, and stroke12,15
  • ~2x greater risk of cardiovascular mortality in patients with high sUA compared to low sUA levels16‡
  • Studies show gout is an independent risk factor for development of type 2 diabetes and is associated with all components of metabolic syndrome12,17
  • As sUA levels increase, so does the prevalence of metabolic syndrome with an sUA level positively associated with the development of type 2 diabetes18
  • Uncontrolled gout is an independent risk factor for onset and progression of CKD12,19,20

KRYSTEXXA has not been studied to reverse damage to the heart, kidneys, or any organ.

* Among patients with gout for less than 10 years with tophi at baseline (based on a prospective 5-year observational study of 295 adults).

†Based on a meta-analysis of 14 studies involving 341,389 adults.

‡Cardiovascular mortality (RR 2.09; 95% CI: 1.45-3.02), all-cause mortality (RR 1.80; 95% CI: 1.39-2.34) after adjustment for potential confounders in a random effects model.

CI, confidence interval; CHD, congestive heart disease; CKD, chronic kidney disease; PAD, peripheral artery disease; PVD, peripheral vascular disease; RR, relative risk; sUA, serum uric acid.

Identifying uncontrolled gout in your patients21

Identifying patients with uncontrolled gout is the first step to getting them appropriate treatment.

While diet can help manage flares, it won’t treat the underlying
cause of gout22

Only one-third of uric acid crystal buildup in the body comes from what patients eat.22 For many patients, uric acid crystal buildup is primarily due to:

Gout genetics icon

Genetics

Some people are naturally prone to retaining higher levels of uric acid23

Gout and kidney damage icon Gout and kidney damage icon Gout and kidney damage icon

Renal issues

Chronic kidney disease can make it harder for the body to remove uric acid24

Even an improvement in diet can lower uric acid levels by only ~1 mg/dL.25

Pharmacologic
strategies to manage
gout

Oral gout treatments focus on either addressing acute symptoms or reducing uric acid levels but may not be sufficient for patients with uncontrolled gout.

Tophi icon Tophi icon Tophi icon

Acute26-28

Reduce symptoms of gout flare

  • Antigout anti-inflammatory agent
  • Non-steroidal anti-inflammatory drugs (NSAIDs)
  • Corticosteroids
Chronic gout icon Chronic gout icon Chronic gout icon

Chronic26-28

Lower uric acid levels

  • Xanthine oxidase inhibitors (XOIs)
  • Uricosurics
  • Uricase

Rendition of tophi the size of a marble

Rendition of tophi the size of a marble

Tophus resolution may require years of oral therapy29

Even with a uric acid level of 5.4 mg/dL, it would take 2 years to dissolve a lump of uric acid the size of a small marble.30§

§According to a long-term follow-up of 24 patients receiving a mean daily dosage of 320 mg of allopurinol.

Help patients
understand the impact
of reducing their uric
acid levels

To reduce uric acid crystal buildup, a patient’s sUA must be low enough for crystals to dissolve.
Graphic showing uric acid levels above 6 mg/dL are associated with increased risk of future flares and joint damage, while uric acid levels below 6 mg/dL are associated with decreased risk of future flares and joint damage Graphic showing uric acid levels above 6 mg/dL are associated with increased risk of future flares and joint damage, while uric acid levels below 6 mg/dL are associated with decreased risk of future flares and joint damage Graphic showing uric acid levels above 6 mg/dL are associated with increased risk of future flares and joint damage, while uric acid levels below 6 mg/dL are associated with decreased risk of future flares and joint damage
  • Treat-to-target guidelines recommend lowering the sUA level to a minimum of <6 mg/dL21
  • Lowering the sUA level to <5 mg/dL may be needed to more rapidly dissolve crystals and reduce flare frequency31

Lower sUA levels have been shown to increase the speed of tophus resolution and reduce the frequency of flares, suggesting that a lower sUA target may be preferred for patients with more severe gout21

The lower the sUA level, the faster crystal buildup will dissolve21

IMPORTANT SAFETY INFORMATION

WARNING: ANAPHYLAXIS AND INFUSION REACTIONS, G6PD DEFICIENCY ASSOCIATED HEMOLYSIS AND METHEMOGLOBINEMIA

  • Anaphylaxis and infusion reactions have been reported to occur during and after administration of KRYSTEXXA.
  • Anaphylaxis may occur with any infusion, including a first infusion, and generally manifests within 2 hours of the infusion. Delayed hypersensitivity reactions have also been reported.
  • KRYSTEXXA should be administered in healthcare settings and by healthcare providers prepared to manage anaphylaxis and infusion reactions.
  • Premedicate with antihistamines and corticosteroids and closely monitor for anaphylaxis for an appropriate period after administration of KRYSTEXXA.
  • Monitor serum uric acid levels prior to each infusion and discontinue treatment if levels increase to above 6 mg/dL, particularly when 2 consecutive levels above 6 mg/dL are observed.
  • Screen patients at risk for glucose-6-phosphate dehydrogenase (G6PD) deficiency prior to starting KRYSTEXXA. Hemolysis and methemoglobinemia have been reported with KRYSTEXXA in patients with G6PD deficiency. KRYSTEXXA is contraindicated in patients with G6PD deficiency.

CONTRAINDICATIONS:

  • In patients with G6PD deficiency.
  • In patients with history of serious hypersensitivity reactions, including anaphylaxis, to KRYSTEXXA or any of its components.

WARNINGS AND PRECAUTIONS

Gout Flares: An increase in gout flares is frequently observed upon initiation of anti-hyperuricemic therapy, including KRYSTEXXA. Gout flare prophylaxis with a non-steroidal anti-inflammatory drug (NSAID) or colchicine is recommended starting at least 1 week before initiation of KRYSTEXXA therapy and lasting at least 6 months, unless medically contraindicated or not tolerated.

Congestive Heart Failure: KRYSTEXXA has not been formally studied in patients with congestive heart failure, but some patients in the pre-marketing placebo-controlled clinical trials experienced exacerbation. Exercise caution in patients who have congestive heart failure and monitor patients closely following infusion.

ADVERSE REACTIONS

The most commonly reported adverse reactions (≥5%) are:

KRYSTEXXA co-administration with methotrexate trial:

KRYSTEXXA with methotrexate: gout flares, arthralgia, COVID-19, nausea, and fatigue; KRYSTEXXA alone: gout flares, arthralgia, COVID-19, nausea, fatigue, infusion reaction, pain in extremity, hypertension, and vomiting.

KRYSTEXXA pre-marketing placebo-controlled trials:

gout flares, infusion reactions, nausea, contusion or ecchymosis, nasopharyngitis, constipation, chest pain, anaphylaxis, and vomiting.

INDICATION

KRYSTEXXA® (pegloticase) is indicated for the treatment of chronic gout in adult patients who have failed to normalize serum uric acid and whose signs and symptoms are inadequately controlled with xanthine oxidase inhibitors at the maximum medically appropriate dose or for whom these drugs are contraindicated.

Limitations of Use: KRYSTEXXA is not recommended for the treatment of asymptomatic hyperuricemia.

Please see Full Prescribing Information, including Boxed Warning.

IMPORTANT SAFETY INFORMATION

WARNING: ANAPHYLAXIS AND INFUSION REACTIONS, G6PD DEFICIENCY ASSOCIATED HEMOLYSIS AND METHEMOGLOBINEMIA

  • Anaphylaxis and infusion reactions have been reported to occur during and after administration of KRYSTEXXA.
  • Anaphylaxis may occur with any infusion, including a first infusion, and generally manifests within 2 hours of the infusion. Delayed hypersensitivity reactions have also been reported.
  • KRYSTEXXA should be administered in healthcare settings and by healthcare providers prepared to manage anaphylaxis and infusion reactions.
  • Premedicate with antihistamines and corticosteroids and closely monitor for anaphylaxis for an appropriate period after administration of KRYSTEXXA.
  • Monitor serum uric acid levels prior to each infusion and discontinue treatment if levels increase to above 6 mg/dL, particularly when 2 consecutive levels above 6 mg/dL are observed.
  • Screen patients at risk for glucose-6-phosphate dehydrogenase (G6PD) deficiency prior to starting KRYSTEXXA. Hemolysis and methemoglobinemia have been reported with KRYSTEXXA in patients with G6PD deficiency. KRYSTEXXA is contraindicated in patients with G6PD deficiency.

CONTRAINDICATIONS:

  • In patients with G6PD deficiency.
  • In patients with history of serious hypersensitivity reactions, including anaphylaxis, to KRYSTEXXA or any of its components.

WARNINGS AND PRECAUTIONS

Gout Flares: An increase in gout flares is frequently observed upon initiation of anti-hyperuricemic therapy, including KRYSTEXXA. Gout flare prophylaxis with a non-steroidal anti-inflammatory drug (NSAID) or colchicine is recommended starting at least 1 week before initiation of KRYSTEXXA therapy and lasting at least 6 months, unless medically contraindicated or not tolerated.

Congestive Heart Failure: KRYSTEXXA has not been formally studied in patients with congestive heart failure, but some patients in the pre-marketing placebo-controlled clinical trials experienced exacerbation. Exercise caution in patients who have congestive heart failure and monitor patients closely following infusion.

ADVERSE REACTIONS

The most commonly reported adverse reactions (≥5%) are:

KRYSTEXXA co-administration with methotrexate trial:

KRYSTEXXA with methotrexate: gout flares, arthralgia, COVID-19, nausea, and fatigue; KRYSTEXXA alone: gout flares, arthralgia, COVID-19, nausea, fatigue, infusion reaction, pain in extremity, hypertension, and vomiting.

KRYSTEXXA pre-marketing placebo-controlled trials:

gout flares, infusion reactions, nausea, contusion or ecchymosis, nasopharyngitis, constipation, chest pain, anaphylaxis, and vomiting.

INDICATION

KRYSTEXXA® (pegloticase) is indicated for the treatment of chronic gout in adult patients who have failed to normalize serum uric acid and whose signs and symptoms are inadequately controlled with xanthine oxidase inhibitors at the maximum medically appropriate dose or for whom these drugs are contraindicated.

Limitations of Use: KRYSTEXXA is not recommended for the treatment of asymptomatic hyperuricemia.

Please see Full Prescribing Information, including Boxed Warning.

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