Which lipid-lowering agent causes hyperuricemia (gout)?

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From the Guidelines

Fenofibrate is the lipid-lowering agent most clearly associated with an increase in serum uric acid levels, which can precipitate gout attacks in susceptible individuals. According to the study published in the Annals of the Rheumatic Diseases 1, fenofibrate has been shown to increase serum uric acid levels, although it may also have protective effects against gout flares through other mechanisms. The mechanism involves competition for renal excretion, as fenofibrate and uric acid use similar transport pathways in the kidneys.

Some key points to consider when prescribing lipid-lowering agents to patients with a history of gout or elevated uric acid levels include:

  • Monitoring patients for signs of gout when starting fenofibrate, especially at higher doses
  • Considering alternative lipid-lowering agents that do not increase serum uric acid levels
  • Adding uric acid-lowering therapy such as allopurinol if fenofibrate is necessary for cardiovascular risk reduction
  • Being aware of the potential for fenofibrate to increase serum uric acid levels, although the clinical significance of this effect is still unclear

It's also important to note that the 2012 American College of Rheumatology guidelines for management of gout 1 do not specifically address the use of lipid-lowering agents in patients with gout, but they do emphasize the importance of considering the potential effects of all medications on serum uric acid levels in patients with gout.

In terms of specific lipid-lowering agents, fenofibrate is the one that has been most clearly associated with an increase in serum uric acid levels, although other agents such as statins may also have this effect to a lesser extent. The decision to use a particular lipid-lowering agent in a patient with gout should be based on a careful consideration of the potential benefits and risks, as well as the patient's individual circumstances and medical history.

From the FDA Drug Label

Elevated uric acid levels have occurred with nicotinic acid therapy, therefore use with caution in patients predisposed to gout. The lipid lowering agent that may cause gout is nicotinic acid 2.

  • Key points:
    • Nicotinic acid may increase uric acid levels
    • Use with caution in patients predisposed to gout

From the Research

Lipid Lowering Agents and Gout

  • Nicotinic acid (niacin) is a lipid lowering agent that has been associated with hyperuricemia, a condition that can increase the risk of gout 3.
  • The mechanism of action of niacin involves the inhibition of hepatocyte diacylglycerol acyltransferase-2, a key enzyme for triglyceride synthesis, which can lead to increased uric acid levels 4.
  • Gout is caused by monosodium urate crystal deposition in joints and tissues, and risk factors include male sex, obesity, hypertension, and certain dietary factors 5.
  • Nicotinic acid (niacin) is the lipid lowering agent that has been specifically linked to an increased risk of gout due to its effects on uric acid levels 3, 6.

Key Findings

  • Nicotinic acid (niacin) can increase uric acid levels, which can increase the risk of gout 3, 4.
  • The incidence of hyperuricemia, a condition that can increase the risk of gout, is a known side effect of nicotinic acid (niacin) therapy 3, 6.

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

Nicotinic acid: clinical considerations.

Expert opinion on drug safety, 2012

Research

Mechanism of action of niacin.

The American journal of cardiology, 2008

Research

Gout: Rapid Evidence Review.

American family physician, 2020

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Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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