Gout is one of the most common and painful forms of inflammatory arthritis, affecting approximately 9.2 million Americans. Caused by the buildup of uric acid crystals in the joints, gout produces sudden, severe attacks of pain, swelling, and redness, most often in the big toe. The good news is that gout is one of the most treatable forms of arthritis when managed properly with the right combination of medication and lifestyle modifications.
Understanding Gout
Gout develops when uric acid, a natural waste product from the breakdown of purines in food and the body's cells, accumulates in the blood at higher-than-normal levels. This condition, called hyperuricemia, causes uric acid to form needle-like crystals that deposit in joints and surrounding tissues. When the immune system recognizes these crystals as foreign, it mounts an intense inflammatory response that produces the characteristic gout attack.
Gout is approximately three times more common in men than in women, and risk increases with age. Women's risk rises after menopause, when protective estrogen levels decline. Other risk factors include obesity, high blood pressure, kidney disease, diabetes, and a family history of gout. Certain medications, particularly diuretics, can also raise uric acid levels.
Without proper management, gout can progress from occasional acute attacks to chronic gout with persistent joint inflammation, the formation of tophi (uric acid crystal deposits under the skin), and permanent joint damage. Understanding the disease process and committing to long-term treatment are essential for preventing this progression.
Acute Gout Attacks
A gout attack typically strikes suddenly, often waking you in the middle of the night with intense pain in the affected joint. The big toe is the most commonly affected joint, involved in about half of all first gout attacks. The joint becomes swollen, red, warm, and exquisitely tender. Even the weight of a bedsheet can feel unbearable during a severe flare.
Gout attacks usually peak within 12 to 24 hours and, without treatment, gradually resolve over one to two weeks. However, prompt treatment can dramatically shorten this timeline. Medications used to treat acute attacks include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and corticosteroids. Starting treatment at the very first sign of an attack produces the best results.
After the first attack resolves, many patients experience a period of remission that can last months or even years. However, without treatment of the underlying hyperuricemia, attacks tend to become more frequent, last longer, and involve more joints over time. This is why transitioning from acute treatment to long-term management is so important.
Long-Term Urate-Lowering Therapy
Urate-lowering therapy (ULT) is the cornerstone of long-term gout management. The goal is to reduce serum uric acid levels to below 6 mg/dL, which allows existing uric acid crystals to gradually dissolve and prevents new crystals from forming. Despite its proven effectiveness, only about 40% of gout patients currently receive appropriate urate-lowering therapy.
Allopurinol is the most commonly prescribed urate-lowering medication and is effective for the majority of patients. It works by reducing the body's production of uric acid. Treatment is typically started at a low dose and gradually increased to reach the target uric acid level. Febuxostat is an alternative for patients who cannot tolerate allopurinol.
It is important to understand that starting urate-lowering therapy can temporarily increase the risk of gout flares as crystals begin to dissolve. For this reason, your rheumatologist will typically prescribe prophylactic anti-inflammatory medication during the first several months of ULT. Patience during this transition period is essential, as the long-term benefits of ULT are substantial in preventing future attacks and joint damage.
Diet Modifications for Gout
Dietary changes can play a meaningful supportive role in gout management, though they typically cannot replace medication in patients with established disease. High-purine foods that can raise uric acid levels include red meat, organ meats (liver, kidney, sweetbreads), and certain seafood such as sardines, anchovies, mussels, and scallops. Limiting these foods can help reduce uric acid production.
Sugar-sweetened beverages and foods high in fructose are increasingly recognized as significant contributors to hyperuricemia. Fructose is the only sugar that directly increases uric acid production in the body. Reducing or eliminating sugary sodas, fruit juices with added sugar, and high-fructose corn syrup can have a meaningful impact on uric acid levels.
Alcohol, particularly beer and spirits, raises uric acid levels and can trigger gout attacks. Beer is especially problematic because it contains purines in addition to alcohol. If you choose to drink, moderate wine consumption appears to carry a lower gout risk than beer or spirits. Staying well-hydrated by drinking plenty of water throughout the day helps the kidneys excrete uric acid more efficiently.
Medications Overview
Gout treatment involves two distinct categories of medications: those for managing acute attacks and those for long-term uric acid control. For acute attacks, your doctor may prescribe NSAIDs such as indomethacin or naproxen, colchicine (most effective when taken within the first 12 hours of an attack), or corticosteroids for patients who cannot take NSAIDs or colchicine.
For long-term management, urate-lowering medications are the primary therapy. Allopurinol and febuxostat reduce uric acid production, while probenecid works by increasing uric acid excretion through the kidneys. In severe, treatment-resistant cases, pegloticase, a biologic medication given by intravenous infusion, can rapidly lower uric acid levels by converting it to a more easily excreted compound.
Your rheumatologist will tailor your medication regimen to your specific needs, considering factors such as the frequency and severity of your attacks, your uric acid levels, kidney function, and other medical conditions. Adherence to long-term medication is critical for success, as stopping urate-lowering therapy allows uric acid to accumulate again and attacks to return.
Lifestyle Changes
Maintaining a healthy weight is one of the most impactful lifestyle changes for gout management. Obesity is strongly associated with higher uric acid levels and increased gout risk. Gradual weight loss through a balanced diet and regular exercise can lower uric acid levels and reduce the frequency of gout attacks. Avoid crash diets or fasting, as rapid weight loss can paradoxically trigger gout flares.
Regular physical activity supports gout management by promoting weight loss, improving cardiovascular health, and reducing insulin resistance, all of which can help lower uric acid levels. Choose low-impact exercises that are gentle on affected joints, such as walking, swimming, or cycling. During an active flare, rest the affected joint until the inflammation subsides.
Adequate hydration is essential for people with gout. Drinking at least eight glasses of water per day helps the kidneys filter and excrete uric acid. Dehydration concentrates uric acid in the blood and can trigger attacks. Be especially mindful of hydration during hot weather, exercise, and when traveling, as these situations increase your risk of dehydration.
Monitoring Your Uric Acid
Regular monitoring of serum uric acid levels is essential to ensure that your treatment is working effectively. The treatment target for most gout patients is a serum uric acid level below 6 mg/dL, though some patients with severe tophaceous gout may benefit from an even lower target of below 5 mg/dL. Your rheumatologist will check your levels periodically and adjust your medications accordingly.
During the initial phase of urate-lowering therapy, uric acid levels are typically checked every two to four weeks as doses are adjusted. Once a stable target level is achieved, monitoring may be reduced to every six to twelve months. Consistent monitoring helps your doctor optimize your treatment and detect any changes early.
Beyond uric acid levels, your doctor will also monitor kidney function, liver function, and blood counts during gout treatment. These tests help ensure that your medications are safe and well-tolerated. Keeping all follow-up appointments is an important part of successful gout management.
When to See a Specialist
While some cases of gout can be managed by primary care physicians, a rheumatologist should be consulted when the diagnosis is uncertain, attacks are frequent or difficult to control, uric acid remains elevated despite treatment, or tophi are present. Rheumatologists have specialized training in crystal arthritis and can provide advanced diagnostic and treatment strategies.
You should also seek specialist care if you have coexisting conditions that complicate gout management, such as kidney disease, heart disease, or diabetes. These conditions require careful medication selection and close monitoring to avoid adverse interactions. A rheumatologist can coordinate your gout care with your other healthcare providers.
At Arthritis Care of Los Angeles, we provide comprehensive gout management including crystal analysis for definitive diagnosis, personalized treatment plans, and long-term monitoring to help you achieve and maintain optimal uric acid levels. Our goal is to eliminate gout attacks and prevent long-term joint damage so you can maintain an active, pain-free lifestyle.
Key Statistics
9.2 Million
Americans affected by gout
Source: Arthritis & Rheumatology
3x
Gout is three times more common in men than women
Source: Centers for Disease Control and Prevention
Only 40%
Of gout patients receive appropriate urate-lowering therapy
Source: Journal of Rheumatology
References
- FitzGerald JD, Dalbeth N, Mikuls T, et al.. 2020 American College of Rheumatology Guideline for Management of Gout. Arthritis Care & Research. 2020. PMID: 27457514
- Chen-Xu M, Yokose C, Rai SK, et al.. Contemporary Prevalence of Gout and Hyperuricemia in the United States and Decadal Trends: The National Health and Nutrition Examination Survey, 2007-2016. Arthritis & Rheumatology. 2019. PMID: 30665232
- Dalbeth N, Merriman TR, Stamp LK. Gout. The Lancet. 2016. PMID: 28146099