Allopurinol is by far the most popular medication for gout. Nearly 80% of people on prescription gout treatment take it, making it the dominant choice over every other option. The American College of Rheumatology recommends it as the first-line therapy for all patients who need long-term uric acid management.
That said, gout treatment involves two distinct goals: preventing future attacks by lowering uric acid over time, and stopping the pain of an acute flare. Different medications handle each job, and most people with recurring gout end up using both.
Why Allopurinol Is the Go-To for Prevention
Gout happens when uric acid builds up in the blood and forms sharp crystals in your joints. Allopurinol works by blocking the enzyme that produces uric acid in the first place. Your body normally converts certain compounds (called purines) into uric acid through a step-by-step process. Allopurinol interrupts that process partway through, so less uric acid gets made and less ends up in your bloodstream.
Once you break it down, your body converts allopurinol into an active form that keeps working for a long time in your tissues, which is why a single daily pill is enough for most people. It’s been on the market for decades, it’s inexpensive, and it has a long track record. Those practical advantages, combined with strong clinical evidence, explain why it accounts for such a large share of gout prescriptions.
The goal of treatment is to get your uric acid level below 6 mg/dL. At that threshold, existing crystals gradually dissolve and new ones stop forming. If you have visible lumps of uric acid deposits (called tophi) or keep getting frequent flares even after hitting 6 mg/dL, your doctor may aim for a stricter target of 5 mg/dL to speed things up.
How Allopurinol Is Started
Most people begin at a low dose of 100 mg per day, sometimes even lower if you have kidney problems. The dose gets increased gradually over weeks or months until your uric acid level drops to the target range. The maximum dose can go as high as 800 mg daily, though most people land somewhere in between. This slow approach matters because ramping up too quickly can actually trigger gout flares.
One important safety note: a small percentage of people carry a genetic marker (HLA-B*5801) that puts them at risk for a rare but serious allergic skin reaction to allopurinol. This marker is found in about 7% of people with Southeast Asian ancestry and 4% of people with African American ancestry. The American College of Rheumatology recommends genetic testing for these groups before starting the medication. A negative test doesn’t eliminate all risk, but it significantly lowers the concern.
Febuxostat: The Main Alternative
Febuxostat works through the same mechanism as allopurinol, blocking uric acid production. It was approved in 2009 and has been gaining market share steadily since then. In the U.S., it’s typically reserved for people who can’t tolerate allopurinol or don’t reach their uric acid target on it.
Febuxostat carries a more cautious safety profile. The FDA added its strongest warning label (a black box warning) to the drug in 2019 due to a potential increase in heart-related deaths compared with allopurinol. That warning is a major reason it remains a second-line option in U.S. guidelines, even though some countries, including China, consider it equally acceptable as a first choice.
Medications for Acute Flares
When a gout attack strikes, you need something different from allopurinol. Allopurinol prevents future attacks but does nothing for the one happening right now. That’s where anti-inflammatory medications come in. The two most common options are over-the-counter NSAIDs (like naproxen or ibuprofen) and colchicine.
Colchicine is the second most widely used prescription gout medication overall, taken by about 30% of people with gout prescriptions. It works by dampening the inflammatory response your body mounts against uric acid crystals. A randomized trial of nearly 400 participants found that low-dose colchicine and naproxen performed equally well at reducing pain within seven days. The main tradeoff: colchicine is more likely to cause diarrhea and headaches, while NSAIDs tend to cause fewer side effects in short courses. NSAIDs also have the advantage of being available without a prescription, so many people can start treating a flare immediately at home.
For people who can’t take either NSAIDs or colchicine, corticosteroids (like prednisone) are another effective option for calming an acute flare.
Why Flares Can Happen When You Start Treatment
One of the most frustrating things about starting allopurinol is that it can temporarily make flares worse. As uric acid levels drop, existing crystal deposits start to shift and dissolve, which can trigger inflammation. This doesn’t mean the medication isn’t working. It’s actually a sign that things are changing in the joint.
To get through this transition period, doctors typically prescribe a low dose of colchicine or an NSAID alongside allopurinol for the first several months. This prophylactic anti-inflammatory coverage helps prevent flares while your body adjusts to lower uric acid levels. Over time, as crystal deposits shrink, the risk of flares drops and the preventive anti-inflammatory can be stopped.
Long-Term Expectations
Allopurinol is a lifelong medication for most people. Stopping it allows uric acid to climb back up, crystals to reform, and flares to return. The good news is that once your uric acid stays consistently below target for a year or two, flares typically become rare or stop entirely. Tophi, if present, can take longer to fully dissolve, sometimes two to three years or more depending on their size.
Regular blood tests to check uric acid levels are a normal part of ongoing management, especially during the dose adjustment phase. Once you’re stable at the right dose, monitoring becomes less frequent but still periodic to make sure levels haven’t drifted.