Gout is a chronic inflammatory form of arthritis caused by elevated levels of uric acid in the blood (hyperuricemia). This condition is classified as a metabolic disorder in which excessive uric acid accumulates in the body, forming crystals that deposit in joints and other tissues, triggering a strong inflammatory response.
Uric acid is a breakdown product of purines—organic compounds found in certain foods and naturally present in the body’s cells. In a healthy individual, uric acid is excreted by the kidneys through urine. However, when uric acid production exceeds the body’s ability to eliminate it, or when kidney function is impaired, gout can develop.
Gout is one of the oldest known inflammatory joint diseases and is directly linked to the accumulation of uric acid crystals in the joints. It belongs to the arthritis group and is characterized by recurrent, extremely painful inflammatory attacks, most commonly affecting small joints—especially the joint at the base of the big toe.
The development of gout is influenced by a combination of factors:
Genetic factors – inherited predisposition can increase the risk of gout
Diet – purine-rich foods (red meat, seafood) and alcohol, especially beer, promote uric acid accumulation
Overweight and obesity – increase uric acid production and impair its elimination
Comorbid conditions – hypertension, diabetes, metabolic syndrome, kidney disease
Medications – certain diuretics, beta-blockers, and low-dose aspirin may raise uric acid levels
When uric acid crystals deposit in the joints, they activate an intense inflammatory process, leading to the hallmark symptoms of gout: pain, swelling, redness, and localized heat.
Gout progresses through distinct stages and, if left untreated, can cause permanent joint damage.
Elevated uric acid levels in the blood are often asymptomatic but form the basis for disease development.
A sudden onset of severe joint pain—often occurring at night—accompanied by swelling, redness, and warmth. Attacks may last from several days to several weeks.
A symptom-free interval between attacks during which the underlying pathological process continues.
Persistent joint damage develops over time, with the formation of tophi—hard nodules of uric acid crystals that can deform joints and restrict movement.
Uncontrolled gout may lead to joint erosion, kidney stone formation, and impaired kidney function.
Gout is frequently associated with other metabolic disorders, and symptom severity may vary:
Sudden, intense joint pain
Swelling, redness, and warmth
Extreme sensitivity to touch
Limited joint mobility
Recurrent acute attacks
Formation of tophi
General malaise or fever during acute episodes
Improper diet and alcohol consumption
Excess body weight and lack of physical activity
Inadequate fluid intake
Kidney disease and certain medications
Managing gout involves both controlling acute attacks and regulating long-term uric acid levels.
Acute attacks are treated with nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, or corticosteroids
Long-term treatment focuses on reducing uric acid production or improving its excretion
Lifestyle modifications include a balanced diet, weight management, and adequate hydration
Although gout is a chronic condition, proper management can significantly reduce symptoms, protect joints, and maintain a good quality of life.
Gout differs from other types of arthritis in its specific origin—it is caused by a disorder of uric acid metabolism rather than autoimmune processes. Therefore, treatment strategies focus on restoring metabolic balance rather than solely suppressing inflammation, as is often the case with other forms of arthritis.
American College of Rheumatology
Arthritis Foundation
The New England Journal of Medicine
Journal of Rheumatology
