Gout Medication: Complete Guide to Treatment & Prevention

What Is Gout and Why Does It Need Medication?

Gout is a form of inflammatory arthritis caused by the accumulation of uric acid crystals in joints, most commonly the big toe. It causes sudden, severe attacks of pain, swelling, redness, and tenderness. Medication is essential both to treat acute attacks and to lower uric acid levels to prevent future flare-ups and joint damage.

Gout develops when your body produces too much uric acid or doesn't eliminate enough of it through the kidneys. Uric acid is a normal waste product created when the body breaks down purines, substances found naturally in the body and in certain foods like red meat, organ meats, and some seafood. When uric acid levels become too high (a condition called hyperuricemia), needle-sharp crystals can form in and around joints, triggering the intense inflammation characteristic of a gout attack.

The typical gout attack strikes suddenly, often at night, with excruciating pain that reaches its peak within 12-24 hours. The affected joint—most commonly the base of the big toe, but also ankles, knees, wrists, fingers, and elbows—becomes so sensitive that even the weight of a bedsheet can be unbearable. Without treatment, attacks typically last one to three weeks before symptoms gradually subside. However, untreated gout tends to become more frequent and severe over time, eventually causing permanent joint damage and deformity.

Understanding why medication is necessary requires grasping the dual nature of gout management. First, acute attacks require immediate treatment to relieve the agonizing pain and inflammation—this is where NSAIDs, colchicine, and corticosteroids play their role. Second, preventing future attacks and long-term complications requires sustained reduction of uric acid levels below the threshold at which crystals form—this is the goal of urate-lowering therapies like allopurinol and febuxostat. Many patients need both types of medications at different times, and some require ongoing preventive treatment for life.

What Medications Treat Acute Gout Attacks?

Acute gout attacks are treated with NSAIDs (like naproxen or indomethacin), colchicine, or corticosteroids. These medications reduce inflammation and pain but don't lower uric acid levels. The choice depends on your other health conditions, other medications you take, and how quickly treatment begins after symptoms start.

When a gout attack strikes, the priority is rapid relief of the intense pain and inflammation. Three main classes of medications are used for acute attacks, and they work in different ways to interrupt the inflammatory cascade triggered by uric acid crystals. The key principle is to start treatment as early as possible—ideally within the first 24 hours of symptom onset—because earlier treatment leads to faster resolution and less total pain.

Your doctor will choose an acute treatment based on several factors: how long ago the attack started, whether you have kidney disease, heart disease, or diabetes, whether you're taking blood thinners or have a history of stomach ulcers, and your previous response to gout medications. In some cases, combining treatments (such as colchicine with NSAIDs) may be more effective than single-drug therapy, though this approach requires careful medical supervision due to increased side effect risks.

It's crucial to understand that acute gout medications treat the attack itself but don't address the underlying problem of high uric acid. Once the acute attack resolves, your healthcare provider will likely discuss long-term prevention strategies to reduce future attacks and protect your joints from ongoing damage.

NSAIDs (Nonsteroidal Anti-Inflammatory Drugs)

NSAIDs are often the first-line treatment for acute gout attacks because they provide relatively rapid pain relief and are widely available. These medications work by inhibiting cyclooxygenase (COX) enzymes, which reduces the production of prostaglandins—chemical messengers that cause pain and inflammation. When COX is blocked, both the inflammation and the pain it causes are diminished.

For gout, NSAIDs are typically taken at maximum doses for the first few days, then gradually reduced as symptoms improve. Pain relief usually begins within hours, but full anti-inflammatory effects may take one to three weeks. Common NSAIDs used for gout include naproxen, indomethacin, diclofenac, ibuprofen, and ketoprofen. Among these, indomethacin has traditionally been considered particularly effective for gout, though evidence suggests all NSAIDs work similarly well.

Several formulations are available, including standard tablets, extended-release tablets (useful for overnight coverage), capsules, and suppositories. Extended-release forms can be particularly helpful when taken at bedtime if morning stiffness is a problem. However, it's essential not to combine different NSAIDs or exceed recommended doses, as this significantly increases side effect risks without providing additional benefit.

Colchicine

Colchicine is an ancient medication derived from the autumn crocus plant, used for gout for over 2,000 years. It works through a different mechanism than NSAIDs—rather than blocking prostaglandin production, colchicine interferes with white blood cell function, preventing them from releasing inflammatory substances when they encounter uric acid crystals. This unique action makes colchicine particularly effective for gout, though exactly how it works is still being studied.

Modern dosing of colchicine for acute gout attacks is much lower than historical regimens, which often caused severe diarrhea and other side effects. Current guidelines recommend taking 1.2 mg at the first sign of a gout attack, followed by 0.6 mg one hour later (a total of 1.8 mg in the first hour). Additional colchicine should not be taken for at least 12 hours after this loading dose. This lower-dose regimen is nearly as effective as older high-dose protocols but with far fewer gastrointestinal side effects.

Timing is critical with colchicine—it works best when taken within the first 12-24 hours of an attack. If treatment is delayed beyond 36 hours after symptom onset, colchicine becomes significantly less effective. Colchicine is available as tablets and capsules, and it's often prescribed as an alternative when NSAIDs are contraindicated due to kidney problems, heart disease, or risk of stomach bleeding.

Colchicine can also be used at low doses (0.6 mg once or twice daily) for preventing gout attacks during the initiation of urate-lowering therapy, when attacks are paradoxically more common. This prophylactic use typically continues for 3-6 months after reaching target uric acid levels.

Corticosteroids

Corticosteroids are powerful anti-inflammatory medications that mimic cortisol, a hormone naturally produced by your adrenal glands. In gout, corticosteroids rapidly suppress the inflammatory response triggered by uric acid crystals, providing effective pain relief when NSAIDs and colchicine aren't suitable options. They're particularly useful for patients with kidney disease, heart failure, or those taking blood thinners who cannot safely use NSAIDs.

Corticosteroids can be administered in several ways for acute gout. Oral corticosteroids like prednisone or prednisolone are commonly prescribed, typically starting with a higher dose that's tapered over 10-14 days. Injection directly into the affected joint (intra-articular injection) delivers high concentrations of medication exactly where it's needed, often providing rapid and dramatic relief—but requires a procedure and is limited to one or two affected joints. Intramuscular injection is another option for patients who cannot take oral medications.

While corticosteroids are highly effective for acute gout, they come with significant considerations for long-term use. Short courses for acute attacks are generally safe, but extended or repeated use can cause weight gain, elevated blood sugar, increased blood pressure, bone loss (osteoporosis), skin thinning, mood changes, and suppression of the body's natural cortisol production. The combination of NSAIDs and corticosteroids significantly increases the risk of gastrointestinal bleeding and should generally be avoided.

Interleukin-1 Inhibitors

For patients who cannot tolerate or have contraindications to all three first-line treatments (NSAIDs, colchicine, and corticosteroids), interleukin-1 (IL-1) inhibitors represent an alternative option. IL-1 is a key inflammatory messenger in the gout attack cascade—when uric acid crystals are engulfed by immune cells, IL-1 is released, triggering the intense inflammation characteristic of gout.

Anakinra and canakinumab are IL-1 inhibitors that can effectively treat acute gout attacks by blocking this inflammatory pathway. These medications are given by injection—anakinra daily for 3-5 days, canakinumab as a single dose. However, they're typically reserved for patients who have failed or cannot use other treatments due to their high cost and the requirement for injection administration.

What Medications Prevent Future Gout Attacks?

Preventive gout medications (urate-lowering therapies) include allopurinol, febuxostat, and probenecid. These medications work by either reducing uric acid production or increasing its elimination through the kidneys. The goal is to maintain serum uric acid below 6 mg/dL (or below 5 mg/dL for severe gout), which prevents crystal formation and allows existing deposits to dissolve.

While acute gout medications provide immediate relief, they don't address the underlying problem—elevated uric acid levels that allow crystals to form. Urate-lowering therapy (ULT) is the cornerstone of long-term gout management, aimed at reducing serum uric acid to levels where crystals cannot form and existing crystal deposits gradually dissolve. This process takes time; it typically requires 6-12 months of sustained low uric acid levels before the crystal burden diminishes enough to reduce attack frequency.

Not everyone with gout requires lifelong urate-lowering therapy. Current guidelines generally recommend starting ULT for patients who have two or more gout attacks per year, have tophi (visible uric acid deposits), have evidence of joint damage on X-rays, or have gout with chronic kidney disease or uric acid kidney stones. However, some patients with even a single severe attack may benefit from ULT, especially if they have very high uric acid levels or prefer to prevent future attacks.

Starting urate-lowering therapy requires careful timing and patient education. Paradoxically, initiating ULT can trigger gout attacks, likely because changes in uric acid levels destabilize existing crystal deposits. For this reason, ULT should not be started during an acute attack—wait until the attack has fully resolved, typically 2-4 weeks. Additionally, prophylactic low-dose colchicine or NSAIDs are usually given for the first 3-6 months of ULT to prevent mobilization flares.

Allopurinol

Allopurinol is the first-line urate-lowering medication for most patients with gout, recommended by both American and European rheumatology guidelines. It works by inhibiting xanthine oxidase, the enzyme responsible for the final steps of uric acid production. By blocking this enzyme, allopurinol reduces the amount of uric acid your body makes, allowing existing crystal deposits to gradually dissolve over months to years.

Treatment with allopurinol typically begins at a low dose (100 mg daily, or 50 mg for patients with kidney disease) and is gradually increased every 2-4 weeks until the target uric acid level is achieved. This "start low, go slow" approach minimizes the risk of triggering gout attacks during treatment initiation. Most patients eventually require 300-400 mg daily, though some may need up to 800 mg daily to reach target levels.

It's critical to understand that allopurinol is a long-term medication—it doesn't work during acute attacks and shouldn't be started when you're having a flare. However, if you're already taking allopurinol when an attack occurs, continue taking it at the same dose. Stopping allopurinol during an attack can actually prolong or worsen the flare. Regular blood tests are needed to monitor uric acid levels and adjust the dose accordingly, as well as to check kidney and liver function.

Febuxostat

Febuxostat (brand name Uloric) is another xanthine oxidase inhibitor that works similarly to allopurinol but has a different chemical structure. It's typically prescribed as an alternative for patients who cannot tolerate allopurinol or don't respond adequately to it. Because febuxostat is metabolized primarily by the liver rather than the kidneys, it may be preferred for patients with significant kidney impairment who cannot take adequate doses of allopurinol.

Febuxostat is started at 40 mg daily and can be increased to 80 mg if target uric acid levels aren't achieved after 2-4 weeks. Like allopurinol, it shouldn't be started during an acute attack, and prophylactic anti-inflammatory treatment is recommended for the first several months. Regular monitoring of uric acid levels and liver function tests is necessary during treatment.

An important consideration with febuxostat is cardiovascular safety. A large clinical trial (CARES trial) found a higher rate of cardiovascular death in patients taking febuxostat compared to allopurinol, though overall death rates were similar. As a result, febuxostat now carries a boxed warning about increased cardiovascular death risk, and it's generally reserved for patients who cannot take allopurinol. Patients with a history of heart disease or stroke should discuss the risks and benefits carefully with their healthcare provider.

Probenecid

Probenecid takes a different approach to lowering uric acid—instead of reducing production, it increases elimination through the kidneys. By blocking uric acid reabsorption in the kidney tubules, probenecid causes more uric acid to be excreted in the urine. This mechanism is called "uricosuric" and represents an alternative pathway for patients who under-excrete uric acid or cannot take xanthine oxidase inhibitors.

Probenecid is typically used as a second-line option or in combination with allopurinol when single-drug therapy doesn't achieve target uric acid levels. However, it has significant limitations. It's less effective in patients with kidney disease (creatinine clearance below 50 mL/min) and is contraindicated in those with a history of uric acid kidney stones, as the increased uric acid excretion can promote stone formation. Patients taking probenecid must drink plenty of fluids to reduce kidney stone risk, and some may need sodium bicarbonate tablets to alkalinize the urine.

It's essential to take probenecid consistently and not to interrupt treatment, as stopping can trigger gout attacks. The medication can also interact with many other drugs, including aspirin, which blocks its uricosuric effect. Regular uric acid monitoring and kidney function tests are necessary during treatment.

What Are the Side Effects of Gout Medications?

Side effects vary by medication class. NSAIDs commonly cause stomach upset and can lead to ulcers, kidney problems, and cardiovascular issues. Colchicine causes diarrhea at higher doses. Corticosteroids can affect blood sugar, mood, and bones with prolonged use. Allopurinol may cause rash (rarely severe) and liver problems. Understanding these risks helps you recognize problems early and take appropriate precautions.

Every medication carries potential side effects, and gout medications are no exception. Understanding what to watch for allows you to recognize problems early and work with your healthcare provider to manage them effectively. Most side effects are dose-related, meaning they're more likely at higher doses and with longer treatment duration. For many patients, the benefits of properly treating gout far outweigh the risks of medication side effects, but this balance should be evaluated individually.

NSAID Side Effects

NSAIDs affect multiple body systems, leading to a range of potential side effects. Gastrointestinal problems are the most common—stomach upset, nausea, and heartburn affect many users, while stomach ulcers and bleeding are less common but potentially serious complications. The risk increases with age, higher doses, longer use, and in those with a history of ulcers or who take blood thinners.

NSAIDs can also affect the kidneys by reducing blood flow, potentially worsening kidney function or causing fluid retention. This is particularly concerning for patients with pre-existing kidney disease, heart failure, or those who are dehydrated. Cardiovascular risks include elevated blood pressure and increased risk of heart attack and stroke, especially with long-term use or in patients with existing heart disease.

Colchicine Side Effects

The most common side effects of colchicine involve the gastrointestinal tract—diarrhea, nausea, vomiting, and abdominal cramping. These effects were very common with older high-dose regimens but are much less frequent with modern lower-dose protocols. If diarrhea develops, it usually indicates the maximum tolerated dose has been exceeded.

At very high doses or in patients with kidney or liver disease who accumulate the drug, colchicine can cause bone marrow suppression, muscle weakness (myopathy), and nerve damage (neuropathy). These serious effects are rare with appropriate dosing but underscore the importance of following prescribed doses and adjusting for kidney function.

Corticosteroid Side Effects

Short courses of corticosteroids for acute gout attacks rarely cause significant side effects beyond temporary blood sugar elevation (important for diabetics to monitor) and potential mood changes (euphoria or irritability). However, repeated or prolonged use leads to cumulative effects including weight gain, particularly around the face and trunk, thinning skin and easy bruising, elevated blood pressure, osteoporosis with increased fracture risk, cataracts, and suppression of the body's natural cortisol production.

Allopurinol Side Effects

Most patients tolerate allopurinol well, with minor side effects like headache, nausea, or diarrhea occurring occasionally. Skin rash occurs in 2-10% of patients and usually requires stopping the medication. The most serious concern is allopurinol hypersensitivity syndrome, a rare but potentially fatal reaction involving severe skin reactions (including Stevens-Johnson syndrome and toxic epidermal necrolysis), fever, and organ damage. Risk is highest in the first few months and in certain ethnic groups.

Febuxostat Side Effects

Febuxostat side effects are similar to allopurinol—liver function abnormalities, nausea, joint pain, and rash. The cardiovascular safety concern mentioned earlier means patients should be monitored for heart-related symptoms. Unlike allopurinol, febuxostat has not been associated with the same severe hypersensitivity syndrome, making it an alternative for some patients who developed rash on allopurinol.

When Should You Seek Medical Care?

Seek immediate medical care if you develop fever with joint pain (possible infection), severe skin rash while taking gout medications (especially allopurinol), difficulty breathing, or if a gout attack doesn't improve after 3-5 days of treatment. Regular follow-up is important to monitor uric acid levels and adjust medications.

While most gout attacks can be managed with appropriate medication at home, certain situations require prompt medical attention. Learning to distinguish between expected symptoms and warning signs ensures you get help when it's truly needed.

One of the most important distinctions is between gout and joint infection (septic arthritis). Both cause sudden, severe joint pain with swelling and redness, but infection is a medical emergency requiring immediate treatment. Fever accompanying joint inflammation should raise concern for infection—while low-grade fever can occasionally occur with severe gout attacks, significant fever (above 101°F/38.3°C) warrants urgent evaluation. Infection is more likely in joints with previous damage, in immunocompromised patients, and when pain developed very rapidly (hours rather than gradually overnight).

Any new rash while taking allopurinol or febuxostat should be evaluated promptly, especially if accompanied by fever, mouth sores, or feeling generally unwell. While most rashes are minor and resolve after stopping the medication, early recognition of severe hypersensitivity reactions can be lifesaving. Don't wait to see if the rash gets worse—contact your healthcare provider immediately.

How Do Lifestyle Changes Complement Medication?

Lifestyle modifications including dietary changes, weight management, limiting alcohol, and staying hydrated can help reduce uric acid levels and gout attack frequency. However, lifestyle changes alone rarely achieve adequate uric acid reduction for patients with established gout—they work best as a complement to medication rather than a replacement.

While medication is the cornerstone of gout management, lifestyle modifications can reduce uric acid levels by 1-2 mg/dL and decrease attack frequency. For patients with mild hyperuricemia who haven't yet developed gout, lifestyle changes may prevent the disease from developing. For those already diagnosed with gout, these modifications enhance the effectiveness of medication but typically cannot replace it.

Dietary modification focuses on reducing purine intake and limiting foods that increase uric acid production. High-purine foods to limit include organ meats (liver, kidney, sweetbreads), certain seafood (anchovies, sardines, herring, mussels, scallops), red meat, and meat extracts and gravies. Moderate-purine foods like chicken, other fish, and legumes can be consumed in moderation. Contrary to older beliefs, moderate consumption of purine-rich vegetables (spinach, asparagus, mushrooms) doesn't appear to significantly increase gout risk.

Alcohol reduction is particularly important—beer raises uric acid levels most significantly due to its purine content, followed by spirits. Wine appears to have less effect on uric acid and may be acceptable in moderation for some patients. Sugar-sweetened beverages containing high-fructose corn syrup should also be limited, as fructose increases uric acid production.

Weight management benefits gout in multiple ways: obesity is associated with higher uric acid production, increased insulin resistance (which impairs uric acid excretion), and greater mechanical stress on weight-bearing joints. Gradual weight loss of 1-2 pounds per week is recommended—rapid weight loss or fasting can actually trigger gout attacks by temporarily raising uric acid levels.

Hydration helps dilute uric acid in the blood and promotes its excretion through the kidneys. Aim for at least 8 glasses of water daily, more in hot weather or during physical activity. For patients on uricosuric medications like probenecid, adequate hydration is especially critical to prevent kidney stone formation.

What About Special Situations?

Gout management requires special consideration in patients with kidney disease, heart disease, diabetes, or during pregnancy. Drug interactions with blood thinners, aspirin, and other medications must be carefully managed. Your healthcare provider will adjust medication choices and doses based on your individual situation.

Gout with Kidney Disease

Chronic kidney disease (CKD) both increases gout risk and complicates its treatment. Many gout medications require dose adjustment or caution in patients with reduced kidney function. NSAIDs should generally be avoided in CKD due to the risk of further kidney damage. Colchicine doses must be reduced, and it's contraindicated in severe CKD. Allopurinol can be used but requires starting at lower doses (50 mg daily or less) with careful titration. Febuxostat may be preferred because it's less affected by kidney function. Probenecid is ineffective when kidney function is significantly reduced.

Gout with Heart Disease

Cardiovascular disease is common in gout patients due to shared risk factors. NSAIDs increase cardiovascular risk and should be used cautiously, if at all, in patients with heart failure or coronary artery disease. Febuxostat carries a cardiovascular warning and is generally avoided in patients with serious heart disease. Colchicine at low doses may actually have cardiovascular benefits and is often preferred for acute attacks in this population.

Gout with Diabetes

Corticosteroids can significantly raise blood sugar, requiring careful monitoring and potentially insulin adjustment in diabetic patients during treatment. Metformin, a common diabetes medication, can actually have mild uricosuric effects. The diabetes medication SGLT2 inhibitors (like empagliflozin, dapagliflozin) also lower uric acid and may benefit patients with both conditions.

Pregnancy and Breastfeeding

Gout is uncommon in premenopausal women due to estrogen's uricosuric effect, but when it occurs during pregnancy, treatment options are limited. Colchicine should be avoided. NSAIDs are contraindicated, especially in the third trimester. Corticosteroids may be used cautiously for acute attacks. Allopurinol and febuxostat are not recommended during pregnancy. Women planning pregnancy should discuss medication management with their healthcare provider in advance.

Drug Interactions

Several important drug interactions affect gout medication choices. Aspirin (even low-dose) blocks the uricosuric effect of probenecid and should not be combined. Warfarin and other blood thinners interact with NSAIDs, increasing bleeding risk. Certain antibiotics (clarithromycin, erythromycin) and antifungals increase colchicine levels and can cause toxicity. Azathioprine and 6-mercaptopurine interact dangerously with allopurinol, requiring significant dose reduction or alternative therapy. Always inform your healthcare provider of all medications you're taking.