Aspirin-Containing Antiplatelet Therapy and In-Hospital Gout Flares in Acute Ischemic Stroke Patients with Gout and Hyperuricemia: A Retrospective New-User Cohort Study

Every year, millions of people worldwide suffer an acute ischemic stroke, a sudden blockage of blood flow to the brain. To prevent a second, potentially more devastating stroke, doctors often prescribe antiplatelet medications. These drugs work by thinning the blood just enough to stop clots from forming, acting as a shield against future blockages. For many patients, the standard approach involves a combination of two such drugs, often including aspirin, especially in the critical days immediately following the event. However, a significant number of stroke survivors also live with gout, a painful form of arthritis caused by high levels of uric acid in the blood. Uric acid is a natural waste product that, when it builds up, can form sharp crystals in the joints, triggering sudden and severe attacks of inflammation. The medical dilemma arises because aspirin, while excellent for preventing strokes, can sometimes interfere with how the body clears uric acid, potentially raising its levels and triggering a gout attack. For a patient already hospitalized for a stroke, a sudden gout flare is more than just a new pain; it can prolong their stay, complicate their recovery, and force doctors to make difficult choices about their life-saving stroke medication.

Researchers at Tianjin Huanhu Hospital in China set out to understand exactly how often this conflict occurs and what happens when it does. They looked back at the medical records of nearly 106,000 patients admitted with acute ischemic stroke between 2019 and 2025. From this massive pool, they identified 457 adults who had a known history of gout and high uric acid levels and who were starting antiplatelet therapy for the first time during their hospital stay. The team split these patients into two groups based on the medication they received: one group took aspirin, either alone or combined with another drug called clopidogrel, while the other group took only clopidogrel. The goal was to see which group was more likely to experience a gout flare while still in the hospital.

The study found that patients who started on an aspirin-containing regimen were significantly more likely to suffer a gout flare than those who took clopidogrel alone. Out of the 457 patients, nearly 41 percent experienced a flare during their hospitalization. When the researchers compared the two groups, they determined that the patients taking aspirin had a roughly 57 percent higher chance of having a flare compared to those who did not. This risk held true even after the team carefully adjusted for other factors that could influence the outcome, such as the patient's age, kidney function, and the severity of their stroke. The data also revealed that patients with higher levels of uric acid in their blood before treatment and those who had more severe strokes requiring significant assistance were at a higher risk of flaring, regardless of which medication they took. However, the study showed that the type of antiplatelet drug was the key differentiator for the aspirin group.

Perhaps the most telling part of the story was what happened after a flare occurred. When a patient on the combined therapy of aspirin and clopidogrel developed a gout attack, doctors frequently chose to stop the aspirin to relieve the pain, leaving the patient on the single drug, clopidogrel, for the rest of their hospital stay. This happened in more than half of the cases where a flare occurred. In contrast, patients who did not have a flare were much less likely to have their aspirin stopped. The researchers observed that this pattern of stopping aspirin persisted over the years of the study, even as medical practices evolved. This creates a difficult situation for patients who are supposed to be on dual therapy to prevent another stroke; the very medication meant to protect them from a second stroke is often the one removed when a gout attack strikes, potentially leaving them less protected during a vulnerable time.

The study did not find that the patient's baseline uric acid levels or the use of other medications to lower uric acid changed the likelihood of the aspirin causing a flare. This suggests that the risk is a direct effect of the aspirin itself, rather than just a result of how high the uric acid levels were to begin with. The researchers also considered whether the pain might have been caused by a different condition that mimics gout, but their analysis indicated that the link between aspirin and the flare remained strong even when accounting for the severity of the stroke. While the study was limited to a single hospital and relied on medical records rather than a controlled experiment, the consistency of the findings across different statistical checks suggests a real and important connection.

Ultimately, this research highlights a complex trade-off in modern stroke care. While aspirin-containing therapies are a standard and effective way to prevent recurrent strokes, they carry a tangible risk of triggering painful gout attacks in susceptible patients. When these attacks happen, the immediate response is often to remove the aspirin, which may inadvertently undermine the stroke prevention strategy. The findings suggest that doctors need to be particularly careful when prescribing aspirin to stroke patients with a history of gout, weighing the benefits of stroke prevention against the high probability of a painful flare that could disrupt the entire treatment plan. The study concludes that identifying patients at high risk for these flares before starting treatment could help avoid unnecessary interruptions in the life-saving therapy they need.