Gouty Arthritis: Causes, Symptoms, Diet, and Treatment

What is Gouty Arthritis?

Gouty arthritis, commonly known simply as gout, is the most common form of inflammatory arthritis in adults, affecting approximately 1 to 2 percent of the population across most Western countries.

Despite how widespread this condition is, it has only been for a little over a decade that the diagnosis and treatment of gouty arthritis have genuinely improved, thanks to new scientific understanding of the disease’s underlying pathophysiology. For a very long time, gout was frequently misdiagnosed and poorly managed in clinical practice.

Today we know that gouty arthritis is a chronic, disabling rheumatic disease associated with elevated levels of uric acid in the blood, specifically above 7 mg/dl, a clinical condition known in medicine as hyperuricemia. Excess uric acid, in the form of precipitated urate crystals, tends to deposit within the joints, triggering a significant inflammatory process.

Beyond the joints themselves, uric acid can also deposit within the kidneys and the skin, contributing to a broader spectrum of disease manifestations.

Gout most commonly affects men, while among women, a notable increase in cases is observed following menopause, likely related to the loss of estrogen’s protective effect on uric acid excretion.

But what exactly is uric acid, and how does it form within the body? Let’s explain this in simple terms, examining some basic concepts of biochemistry related to purine metabolism.

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Uric Acid

Uric acid is a catabolite, meaning a substance that our body produces through the breakdown of other substances. In the case of uric acid, the substances being broken down are called purines.

Purines are organic compounds that form essential building blocks within all human cells, and our liver continuously produces them from amino acids. Two of these purines, called adenine and guanine, form the nitrogenous bases of the nucleic acids DNA and RNA. Beyond these two well-known purines, our body produces numerous other purine-based molecules that serve as cofactors and coenzymes in various metabolic processes, including ATP, GTP, NADH, and coenzyme A, among others.

A portion of the purines present in our body, however, comes directly from the food we eat, since many foods naturally contain varying amounts of these substances.

Uric acid forms through the breakdown of purines, a process catalyzed by an enzyme called xanthine oxidase. Once formed, uric acid enters the bloodstream and travels to the renal tubules and the intestine, where it is eliminated primarily through urine, with a smaller portion excreted through stool.

Uric acid is therefore fundamentally a waste product that the body needs to eliminate efficiently.

In certain individuals, due to genetic predisposition, plasma levels of uric acid can become elevated. In these cases, the excess uric acid undergoes a process of crystallization and deposits within the joints, where it triggers activation of the immune system. The immune system then attacks these uric acid crystals as if they were foreign invaders, producing significant local inflammation, pain, and swelling, the hallmark features of an acute gout attack.

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Causes and Risk Factors

Gouty arthritis was historically referred to as “the disease of kings” or “the rich man’s disease”, because it was long believed to be directly linked to the habit of consuming abundant, rich meals and drinking large quantities of alcohol, indulgences that were once available almost exclusively to the wealthier social classes.

Indeed, many historical figures and popes are believed to have suffered from gouty arthritis during their lifetimes, including:

• Charlemagne,
• Catherine of Aragon,
• Henry VIII of England,
• Piero di Cosimo de’ Medici,
• Isaac Newton,
• Charles Darwin,
• Leonardo da Vinci,
• Benjamin Franklin,

just to name a few notable examples.

Without question, poor dietary habits can interfere with the proper functioning of our overall metabolism, and purine metabolism in particular. However, in reality, research has demonstrated that it is actually quite rare for gouty arthritis to develop solely as a result of dietary excess.

A far more decisive factor underlying the origin of the disease is genetic predisposition. It is now understood that many individuals with gouty arthritis inherit a genetic defect affecting one or more enzymes involved in purine metabolism, causing them to either:

• produce excessive amounts of uric acid (in approximately 10% of cases),
• or eliminate uric acid inefficiently through the kidneys (in approximately 90% of cases).

In both scenarios, a condition known as hyperuricemia develops, meaning an excess of uric acid within the body. This condition can:

• remain entirely asymptomatic in milder forms,
• or manifest clinically in more severe cases, producing the characteristic symptoms of an acute gout attack.

It has also been observed that the presence of certain risk factors is associated with a significantly higher prevalence of gout. In particular, the individuals at greatest risk of developing gouty arthritis include:

• males over the age of 30, or women over the age of 50,
• smokers,
• individuals who are obese or overweight,
• individuals suffering from:
  • high blood pressure (hypertension),
  • hypothyroidism,
  • elevated cholesterol and/or triglyceride levels in the blood,
  • diabetes mellitus or insulin resistance,
  • metabolic syndrome,
  • polycythemia,
  • chronic kidney disease,
  • hemolytic anemia,
  • psoriasis,
  • inherited enzyme deficiencies,
  • certain cancers,
• organ transplant recipients,
• individuals with chronic exposure to lead,
• patients undergoing long-term treatment with certain medications, including:
  • diuretics,
  • levodopa,
  • immunosuppressants,
  • acetylsalicylic acid (aspirin).

Gout also appears to be more common among individuals of African American, Chinese, and Polynesian descent, suggesting an important genetic and ethnic component to disease susceptibility.

The scientific literature indicates that gout attacks occur more commonly following physical trauma or surgical procedures, and during seasons characterized by lower temperatures, likely related to changes in peripheral circulation and joint temperature that favor crystal formation.

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Symptoms

Acute gout attacks develop as a result of severe joint inflammation, producing sudden, localized symptoms within the affected joint, including:

• pain,
• redness,
• swelling,
• warmth to the touch.

Joint pain typically manifests at night or in the early morning hours, coinciding with the natural physiological drop in body temperature that occurs during nighttime rest, combined with increased venous stasis favored by prolonged immobility while lying in bed.

The pain is often described as excruciating and unbearable, sometimes accompanied by:

• fever,
• increased skin sensitivity in the affected area, to the point where even the light weight of a bedsheet resting on the affected joint can become extremely uncomfortable.

Symptoms generally last for up to a maximum of 10 days if left untreated, though appropriate treatment can significantly shorten this duration and reduce the intensity of discomfort.

The joint most frequently affected, accounting for more than half of all cases, is the metatarsophalangeal joint of the big toe, a condition sometimes specifically referred to as podagra.

Other joints that may be affected include:

• the knee,
• the wrist,
• the elbow,
• the fingers,
• the ankles,
• the heel.

During the chronic phase of the disease, patients typically report a dull, persistent joint tenderness and stiffness, accompanied by noticeable limitation in range of motion.

Beyond the joints themselves, persistently elevated uric acid levels over time can also lead to deposits within:

• the kidneys,
• the skin,

contributing to a characteristic pattern of debilitating, long-term gout-related complications.

• In the kidneys, uric acid deposits can cause significant renal dysfunction, potentially leading to the formation of kidney stones, and in more advanced cases, progressing to a clinical picture of chronic kidney failure.

• In the skin, particularly around the ears, the fingers and/or toes, the elbows, and generally in the cartilaginous portions of affected joints, gout can cause the development of characteristic, hard, painful subcutaneous swellings known as tophi. These tophi can occasionally ulcerate and become infected, releasing a milky white discharge containing visible uric acid crystals that can be identified under microscopic examination.

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Comorbidities and Complications

Many patients with gouty arthritis also suffer from underlying heart disease or exhibit other significant comorbidities. In some cases, these conditions are already present in the patient’s medical history at the time gout is diagnosed, while in other cases, they develop subsequently, sometimes as a direct consequence of chronic hyperuricemia.

Among the principal comorbidities associated with gout, we can identify:

• kidney failure,
• ischemic heart disease,
• heart failure,
• stroke,
• peripheral artery disease,
• obesity,
• hyperlipidemia,
• hypertension,
• diabetes mellitus.

These well-documented associations have allowed researchers to draw several important conclusions:

• the risk factors for gout are likely not fundamentally different from those already well-established for cardiovascular disease,
• hyperuricemia and/or gout appear to represent independent risk factors for the development of coronary artery disease, heart failure, stroke, peripheral artery disease, and diabetes. These conditions are also associated with an increased risk of death from cardiovascular causes specifically,
• chronic kidney disease appears to be an important risk factor for the development of gout, while at the same time, gout itself can directly contribute to the development of renal dysfunction, creating something of a bidirectional relationship between these two conditions.

For these reasons, every patient diagnosed with gout should ideally undergo comprehensive screening to identify the presence or absence of one or more of these associated comorbidities. When present, these conditions require appropriate, coordinated treatment as an integral part of the overall management strategy for gout.

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Diagnosis

A family physician or rheumatologist can often establish a diagnosis of gouty arthritis based simply on the patient’s clinical history. During an acute gout attack, patients typically describe intense joint pain, accompanied by visible redness and swelling of the affected joint, a presentation that is often quite distinctive and recognizable.

A simple blood test allows doctors to measure the amount of uric acid present in the body. In this regard, it is worth noting an interesting clinical nuance:

conventionally, the maximum blood uric acid concentration considered normal is generally set at 7 mg/dl, but in practice, there is no single, absolute threshold value that definitively separates health from disease, since some individuals with levels above this threshold never develop symptoms, while others with levels closer to normal can experience clinical gout.

Common markers of inflammation may also be elevated during an active flare, providing additional supportive evidence for the diagnosis.

In cases involving easily accessible joints and diagnostic uncertainty, a doctor may sometimes request an arthrocentesis, a procedure involving the withdrawal of a small amount of joint fluid using a thin needle under local anesthesia, for subsequent microscopic analysis. Under the microscope, uric acid crystals characteristically appear as small, needle-shaped structures with pointed ends, a finding that is essentially diagnostic when identified.

An X-ray and/or ultrasound can help reveal the presence of uric acid crystal deposits, as well as any joint and bone damage associated with the disease process over time.

Magnetic resonance imaging (MRI) may be indicated in certain specific cases, such as in complicated forms of gout where more detailed soft tissue imaging is required.

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Remedies and Treatment

An acute gout attack should be treated as soon as the very first warning signs appear, since early intervention is generally associated with faster and more complete symptom relief.

Several supportive measures can prove helpful during an acute flare:

• drinking plenty of water to help dilute the concentration of uric acid crystals in the blood and facilitate their easier elimination through the urine,
• applying ice packs to the affected joint to help reduce inflammation and provide symptomatic relief,
• resting the affected joint and avoiding unnecessary weight-bearing or movement.

The medications available to physicians for treating an acute attack include:

• NSAIDs (nonsteroidal anti-inflammatory drugs),
• colchicine,
• corticosteroids (either oral or injectable).

NSAIDs are generally the first-line medications used, provided the patient does not have chronic kidney disease, gastritis, gastric ulcers, or a known allergy to this class of drugs. Indomethacin is traditionally considered the NSAID of first choice, though a wide variety of alternative NSAIDs can be effectively used depending on individual patient factors. Paracetamol (acetaminophen) can also be useful as an additional pain-relieving medication, particularly when NSAIDs are contraindicated or need to be used cautiously.

Colchicine is generally prescribed in cases where NSAIDs are contraindicated. According to the AGREE study, colchicine proves most effective when taken within 12 hours of symptom onset. Patients should be properly educated on how to use this medication at low doses as a form of self-administered treatment at the very first sign of acute gout symptoms, as well as informed about the important contraindications that limit its safe use. Specifically, colchicine should NOT be taken:

• by patients who are currently taking statins, ketoconazole, cyclosporine, clarithromycin, verapamil, or other strong inhibitors of P-glycoprotein and/or CYP3A4, due to potentially dangerous drug interactions,
• by patients with chronic kidney disease,

since these situations could significantly increase the risk of exposure to serious side effects.

Regarding corticosteroids, oral prednisolone is generally recommended. However, in patients with involvement limited to a single, easily accessible joint, direct injection of corticosteroids into the affected joint itself may be indicated. That said, this particular approach tends to be less practical from a clinical standpoint, since it cannot be self-administered by the patient at home and requires a healthcare visit.

In cases where all of these standard medications are contraindicated, and only in such cases, treatment with interleukin-1 inhibitors (such as canakinumab or subcutaneous anakinra) may be considered.

The disadvantages of this particular therapeutic approach include significantly higher treatment costs and an increased risk of serious infections, which limits its use to carefully selected patients who have exhausted other treatment options.

What to Do After a First Acute Gout Attack?

Contrary to previous recommendations, current clinical guidelines now suggest initiating urate-lowering therapy with allopurinol already after the very first gout attack, rather than waiting until the second or third acute episode of the disease as was traditionally recommended in the past. This updated approach aims to:

• reduce the body’s own production of uric acid and thereby prevent future acute gout attacks,
• maintain plasma uric acid concentration below 6 mg/dl in cases of mild to moderate gout, and below 5 mg/dl in cases of severe gout,

while also avoiding exposing the patient to prolonged chronic hyperuricemia, which itself increases the risk of serious complications, particularly cardiovascular and renal complications, over the long term.

Allopurinol, available in tablet or sachet form, should be taken daily, starting at a low dose (typically 100 mg per day) and gradually increasing until an optimal level of blood uric acid is achieved. In patients with kidney impairment, the maximum allopurinol dosage must be carefully adjusted based on residual kidney function, typically assessed through creatinine clearance measurement.

This medication is considered essential for patients with:

• recurrent gout attacks (occurring more than twice per year),
• visible tophi,
• urate-related joint damage and/or kidney stones,
• young patients with uric acid levels at or above 8 mg/dl,
• the presence of significant comorbidities.

Possible side effects of this medication include:

• nausea and vomiting,
• abdominal cramping,
• general malaise, drowsiness, and fatigue,
• liver toxicity,
• increased blood pressure,
• hypersensitivity reactions (including fever, skin rash, and vasculitis),
• severe adverse cutaneous reactions (SCARs), particularly in patients with underlying kidney disease.

Allopurinol should generally be discontinued during an active acute gout attack, given the risk that it could potentially worsen the episode. Additionally, this medication should not be taken during pregnancy or breastfeeding.

What to Do in Cases of Frequent Acute Gout Attacks Poorly Controlled by Standard Urate-Lowering Therapy?

For patients whose gout remains poorly controlled despite standard treatment, several pharmacological alternatives are available, including:

• febuxostat,
• a combination of a xanthine oxidase inhibitor together with a uricosuric medication,
• pegloticase.

These alternative treatment options are generally reserved for more complex or treatment-resistant cases and require careful specialist supervision.

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Diet and Lifestyle

Patients with gout should be educated about practical lifestyle recommendations and behavioral guidelines designed to adopt an overall lifestyle that supports general health while also helping to prevent or reduce the frequency of acute gout attacks.

Medical recommendations generally focus on the following key areas:

• weight loss for patients who are overweight or clinically obese,
• limiting alcohol consumption, particularly beer, which appears to carry a particularly strong association with increased gout risk,
• avoiding overeating at meals, and specifically limiting the consumption of protein-rich foods that are also high in purines,
• avoiding the use of aspirin as a pain reliever or anti-inflammatory medication, preferring paracetamol (acetaminophen) instead,
• avoiding foods and beverages that are high in fructose,
• drinking plenty of water, along with diuretic herbal infusions and teas, to help promote the elimination of uric acid through the urine,
• engaging regularly in physical exercise.

Several scientific studies have confirmed that weight loss, whether achieved through carefully controlled diets or, in appropriate cases, bariatric surgery, effectively reduces blood uric acid levels. Regular physical activity, meanwhile, has been shown to lower the overall mortality risk associated with chronic hyperuricemia.

Additionally, acute gout attacks appear to occur more frequently in patients who consume excessive quantities of meat and alcohol simultaneously, suggesting a potentially synergistic negative effect when these two dietary factors are combined.

Permitted Foods

• Skimmed milk,
• low-fat yogurt,
• cheeses,
• eggs,
• pasta and cereals,
• vegetables (excluding those specifically listed among foods to avoid below),
• cherries,
• coffee.

These foods are generally believed to have a potentially protective, anti-inflammatory effect against acute gout attacks and disease flares, making them reasonable choices for regular inclusion in the diet of individuals managing gout.

Foods to Limit or Avoid

• Sardines,
• herring,
• mackerel,
• mussels,
• oysters,
• shrimp,
• crab,
• shellfish in general,
• sweetbreads,
• organ meats (liver, kidney, brain, sweetbreads),
• meat extracts,
• game meat,
• poultry,
• fish in general,
• cured meats and sausages,
• dried peas,
• beans,
• lentils,
• asparagus,
• spinach,
• cauliflower,
• mushrooms,
• peanuts,
• whole grain flours,
• sugary beverages, sweets, and refined sugar.

These foods should be consumed only in moderation by individuals with gout, and should be avoided entirely during acute gout attacks, due to their high or moderate purine content. For a more detailed exploration of these dietary considerations, readers are encouraged to consult our dedicated article on gout and diet.

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Frequently Asked Questions

Can gout be completely cured?

While there is no permanent cure that reverses the underlying genetic predisposition to gout, the condition can be very effectively managed and controlled with appropriate long-term urate-lowering medication combined with dietary and lifestyle modifications. Many patients achieve excellent long-term control with few or no further acute attacks when treatment is properly maintained.

How quickly does an acute gout attack develop?

Acute gout attacks are notoriously sudden, often developing literally overnight, with patients frequently waking in the middle of the night or early morning with severe, excruciating pain in the affected joint that reaches peak intensity within just a few hours.

Is gout only caused by diet?

No. While dietary factors, particularly excessive alcohol and purine-rich food consumption, can certainly contribute to and trigger gout attacks, research has shown that genetic predisposition affecting how the body produces or eliminates uric acid plays a far more significant role in most cases than diet alone.

Can women get gout?

Yes, although gout is considerably more common in men. Women’s risk of developing gout increases notably after menopause, likely due to the loss of estrogen’s protective effect on kidney uric acid excretion.

Should I stop taking allopurinol during a gout attack?

Generally, if you are already established on allopurinol therapy before the attack begins, most current guidelines recommend continuing the medication at the same dose during an acute flare, rather than stopping it, since discontinuation can sometimes destabilize uric acid levels further. However, allopurinol should not be newly started during an active acute attack. Always follow your physician’s specific guidance regarding your individual treatment plan.

Are tophi dangerous?

Tophi themselves are generally not immediately dangerous, but they indicate long-standing, poorly controlled hyperuricemia and can cause joint damage, deformity, and occasionally ulceration with secondary infection if left untreated. Their presence typically indicates a clear need for more aggressive urate-lowering therapy.

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Sources and Bibliography

• Richette P, et al. “2016 updated EULAR evidence-based recommendations for the management of gout”. Annals of the Rheumatic Diseases, 2016
• Terkeltaub RA, et al. “High versus low dosing of oral colchicine for early acute gout flare: Twenty-four-hour outcome of the first multicenter, randomized, double-blind, placebo-controlled, parallel-group, dose-comparison colchicine study”. Arthritis & Rheumatism, 2010