Can ticagrelor cause gout? The Link Between an Antiplatelet Drug and Uric Acid

October 10, 2025 •

4 min read

In a major clinical trial, patients taking ticagrelor saw their serum uric acid levels increase by approximately 0.6 mg/dL from baseline [1.2.5]. This has led to questions about a potential side effect: can ticagrelor cause gout?

Quick Summary

Ticagrelor is associated with an increased risk of elevated uric acid levels (hyperuricemia) and subsequent gout attacks compared to other antiplatelet agents like clopidogrel [1.2.3, 1.6.8].

Key Points

Direct Link: Ticagrelor is associated with increased serum uric acid (hyperuricemia) and can cause gout [1.2.4].
Higher Incidence: The incidence of in-hospital gout is significantly higher with ticagrelor (9.8%) compared to clopidogrel (1.9%) [1.2.3].
Dual Mechanism: Ticagrelor likely raises uric acid by both increasing its production (via adenosine) and decreasing its excretion by the kidneys [1.4.5].
Reversible Effect: The increase in uric acid is typically modest and reversible, returning to baseline within a month of stopping the drug [1.2.5].
Key Risk Factors: Patients with a history of gout, high baseline uric acid, alcohol use, and high cholesterol are at greater risk [1.2.3].
Clopidogrel Alternative: Clopidogrel does not significantly raise uric acid and may be an alternative for at-risk patients, as determined by a physician [1.6.2, 1.6.8].
Management is Key: Management involves monitoring uric acid levels, treating acute flares, and potentially switching medications under a doctor's care [1.4.9].

What is Ticagrelor?

Ticagrelor, often known by its brand name Brilinta, is a potent antiplatelet medication prescribed to patients with acute coronary syndrome (ACS) [1.2.6]. It belongs to a class of drugs known as P2Y12 inhibitors. These drugs work by preventing platelets in the blood from clumping together and forming dangerous clots, which can lead to heart attacks or strokes [1.2.6]. Unlike some other antiplatelet medications such as clopidogrel, ticagrelor is a reversible inhibitor and does not require metabolic activation to be effective, allowing for a faster onset of action [1.2.6]. It is widely recommended in treatment guidelines for ACS due to its clinical benefits in reducing cardiovascular events [1.2.6].

The Connection: Can Ticagrelor Cause Gout and Hyperuricemia?

Yes, evidence confirms that ticagrelor can lead to elevated levels of uric acid in the blood, a condition known as hyperuricemia, which is a direct precursor to gout [1.2.4, 1.4.5]. One major study found the incidence of in-hospital gout was significantly higher in patients treated with ticagrelor (9.8%) compared to those on clopidogrel (1.9%) [1.2.3]. Another large trial, the PLATO study, observed that serum uric acid levels increased by about 14% after one to two months of ticagrelor administration and that gout occurred in 0.6% of patients on the drug [1.2.5, 1.2.6].

This increase is generally considered modest and is reversible, with uric acid levels typically returning to normal within 30 days of stopping the medication [1.2.4, 1.2.5]. However, for susceptible individuals, this elevation can be enough to trigger a painful gout attack [1.2.7].

How Does Ticagrelor Increase Uric Acid?

The exact mechanism is complex, but research points to two primary pathways through which ticagrelor elevates uric acid:

Altered Kidney Function: Ticagrelor and its metabolites may interfere with how the kidneys handle uric acid. It is believed to inhibit transporters in the renal tubules, such as OAT1 and OAT3, which are responsible for secreting uric acid from the blood into the urine [1.4.1, 1.4.5]. By impairing this secretion process, more uric acid is retained in the bloodstream [1.4.6].
Increased Adenosine Levels: Ticagrelor works by inhibiting the reuptake of adenosine, a natural chemical in the body [1.4.5]. This leads to higher concentrations of adenosine. Uric acid is the final breakdown product (metabolite) of adenosine [1.4.5]. Therefore, by increasing the amount of available adenosine, ticagrelor may indirectly boost the production of uric acid [1.4.5, 1.4.3].

Risk Factors for Developing Gout on Ticagrelor

While ticagrelor increases uric acid in many patients, not everyone will develop gout. Certain factors increase the risk of a gouty flare-up while taking the medication. A recent study identified several key independent risk factors [1.2.3]:

High Baseline Uric Acid: Patients who already have hyperuricemia before starting the drug are more susceptible.
Alcohol Consumption: Alcohol is a known trigger for gout and can exacerbate the effects of the medication.
High Total Cholesterol: Elevated cholesterol levels were also linked to a higher risk of gout attacks in patients on ticagrelor.

Comparison of Antiplatelet Drugs and Gout Risk

Patients and clinicians often have a choice between different P2Y12 inhibitors. When it comes to uric acid levels, there are clear differences.


Feature	Ticagrelor	Clopidogrel	Prasugrel
Effect on Uric Acid	Significant Increase [1.6.8]	No significant change or slight decrease [1.6.8]	Less data available, but not strongly associated with hyperuricemia like ticagrelor [1.5.4].
Incidence of Gout	Higher incidence compared to clopidogrel (e.g., 9.8% vs 1.9% in one study) [1.2.3]	Lower incidence [1.2.3]	Not a commonly reported side effect [1.5.4].
Mechanism	Reversible P2Y12 inhibitor; increases adenosine [1.2.6]	Irreversible P2Y12 inhibitor; requires metabolic activation [1.2.6]	Irreversible P2Y12 inhibitor; requires metabolic activation [1.5.4].

Studies consistently show that patients switched from clopidogrel to ticagrelor experience an increase in their uric acid levels, while those taking clopidogrel do not see a similar effect [1.3.2, 1.6.8]. This makes clopidogrel a potential alternative for patients with a history of gout or those who develop hyperuricemia on ticagrelor, after consultation with their cardiologist [1.6.2].

Managing Ticagrelor-Associated Gout

If a patient develops symptoms of gout (sudden joint pain, swelling, and redness, often in the big toe) while taking ticagrelor, it is crucial to consult a healthcare provider immediately [1.2.4]. Management strategies may include:

Confirmation and Monitoring: The doctor will confirm the diagnosis and regularly monitor serum uric acid levels [1.4.9].
Acute Flare Treatment: The acute gout attack itself can be treated with medications like NSAIDs, colchicine, or corticosteroids [1.6.1].
Urate-Lowering Therapy: For patients who must remain on ticagrelor, a doctor might prescribe urate-lowering drugs like allopurinol to manage hyperuricemia prophylactically [1.4.5, 1.6.2].
Switching Medication: In some cases, the cardiologist may decide to switch the patient from ticagrelor to an alternative antiplatelet agent like clopidogrel, which does not have the same effect on uric acid [1.6.2].
Lifestyle Adjustments: Patients may be advised to avoid foods and drinks known to increase uric acid, such as red meat, seafood, alcohol, and sugary beverages [1.4.9].

Conclusion

The evidence is clear that there is a direct link between ticagrelor treatment and an increase in serum uric acid levels, which can cause gout in susceptible individuals [1.2.3, 1.2.4]. This side effect, while often reversible, is considered an important and potentially underestimated complication of long-term ticagrelor therapy [1.4.9]. Compared to clopidogrel, ticagrelor presents a significantly higher risk for hyperuricemia and in-hospital gout attacks [1.2.3]. Clinicians are encouraged to monitor uric acid levels in patients on ticagrelor, especially those with pre-existing risk factors like a history of gout, high baseline uric acid, or alcohol use [1.4.9]. For patients who experience this adverse effect, management options including lifestyle changes, urate-lowering therapy, or switching to an alternative antiplatelet drug are available under medical supervision.

For further reading on the mechanisms of drug-induced hyperuricemia, consider this resource from Oxford Academic: Drug-induced hyperuricaemia and gout

Frequently Asked Questions

Yes, clinical studies show that ticagrelor (Brilinta) is associated with a modest but significant increase in serum uric acid levels, a condition known as hyperuricemia [1.3.1, 1.2.5].

The incidence varies. One large study (PLATO) reported gout in 0.6% of patients taking ticagrelor [1.2.5]. A more recent study focusing on hospitalized patients found a much higher incidence of 9.8% in the ticagrelor group versus 1.9% in the clopidogrel group [1.2.3].

No, the effect is typically reversible. Studies have shown that serum uric acid levels usually return to their normal baseline within 30 days of discontinuing ticagrelor [1.2.4, 1.2.5].

Clopidogrel is associated with a much lower risk of causing high uric acid and gout compared to ticagrelor [1.2.3, 1.6.8]. For a patient with a history of gout, a doctor might prefer clopidogrel, but the decision depends on balancing cardiac risk and side effect profile [1.6.2].

You should contact your healthcare provider immediately. Do not stop taking ticagrelor without medical advice. Your doctor can prescribe medication to treat the gout flare and will determine the best long-term strategy, which may involve monitoring, adding a uric-acid-lowering drug, or changing your antiplatelet therapy [1.2.4, 1.4.9].

Ticagrelor is believed to cause gout by raising uric acid levels in two main ways: by increasing the body's production of uric acid as a byproduct of adenosine, and by reducing the kidneys' ability to excrete uric acid into the urine [1.4.5].

While not always preventable, you can reduce your risk by avoiding alcohol, red meat, seafood, and sugary drinks [1.4.9]. If you have a history of gout, your doctor may prophylactically prescribe urate-lowering therapy when starting ticagrelor [1.4.5].