Treatment Guideline Chart
Gout is a condition that resulted from deposition of monosodium urate crystals in various tissues (eg joints, connective tissue, kidney).
The patient experiences acute and chronic arthritis, soft tissue inflammation, tophus formation, gouty nephropathy and nephrolithiasis.
Primary hyperuricemia occurs when uric acid saturation arises without coexisting diseases or drugs that alter uric acid production or excretion, while secondary hyperuricemia is a condition where excessive uric acid production or diminished renal clearance occurs as a result of a disease, drug, dietary product or toxin. 

Gout Signs and Symptoms


  • Gout is a condition wherein there is increased urate in the body, also called hyperuricemia, that leads to deposition of monosodium urate monohydrate crystals in various tissues (eg joints, connective tissue, kidney)


  • It is the most common inflammatory arthritis in men
  • In US and Europe, the estimated prevalence of gout is 3% of the adult population
  • Prevalence of gout in the Asia-Pacific region varies
    • Ethnic groups in China and Malaysia (eg Malays, Tamils) were found to have higher uric levels as compared to the Japanese and Thai
    • Taiwan is one of the countries in the world with the highest prevalence of gout


  • Hyperuricemia is a necessary precondition for the development of monosodium urate monohydrate crystal deposition but this has to be distinguished from gout, the clinical syndrome
  • Results in acute and chronic inflammation associated with changes in articular and periarticular structures

Causes of Hyperuricemia

  • Excessive uric acid production
    • Inherited enzyme defects (eg hypoxanthine-guanine phosphoribosyl transferase deficiency, phosphoribosyl pyrophosphate synthetase overactivity, glycogen storage diseases, fructose-1-phosphate aldolase deficiency, myoadenylate deaminase deficiency, carnitine palmitoyltransferase II deficiency)
    • Clinical disorders (eg myeloproliferative and lymphoproliferative disorders, malignancies, psoriasis, Down syndrome)
    • Induced by diet, drugs, or toxins (eg Ethanol, excessive purine in diet, fructose, vitamin B12 deficiency, Nicotinic acid, cytotoxic drugs, Warfarin)
  • Decreased renal clearance
    • Genetic disorders such as medullary cystic kidney disease, familial juvenile hyperuricemic nephropathy and uric acid transportasome mutations
    • Chronic renal insufficiency, volume depletion (eg heart failure, volume loss), obesity, diabetic or starvation ketoacidosis, lactic acidosis, hyperparathyroidism, hypothyroidism, sarcoidosis
    • Induced by diet or drugs (eg Aspirin, diuretics, Ciclosporin, Tacrolimus, Ethambutol, Pyrazinamide, Ethanol, Levodopa)
    • Saturnine gout is a rare form of gout due to chronic lead exposure
      • Commonly seen in plumbers and those exposed to lead-based paints

Clinical Phases of Gout

Acute Gout

  • Usually manifests as an acute, self-limiting, monoarticular inflammatory arthritis in majority of patients
    • Symptoms of a gout flare include severe pain, redness, swelling, warmth and disability
  • Lower extremity joints are affected more often than upper extremity joints
    • Joints most commonly affected include the 1st metatarsophalangeal joint (podagra), forefoot, ankle, knee
  • Extra-articular sites (eg olecranon bursa and Achilles tendon) may also be involved
  • Attacks may occur and last from a few days to 2-3 weeks, with resolution of all inflammatory signs
    • Early attack: <12 hours after onset of attack
    • Well-established attack: 12-36 hours after onset of attack
    • Late attack: >36 hours after attack onset

Intercritical Gout

  • Periods in between attacks when patient is free of symptoms
  • Asymptomatic joints may still have crystals detected in the synovial fluid

Chronic Gout

  • If hyperuricemia is not treated properly, intermittent acute gouty attack can develop into chronic gouty arthritis
  • There is persistent inflammation in the joints and connective tissues associated with bony erosions and deformities
  • Chronic tophaceous gout:
    • Marked by polyarticular arthritis and the formation of tophi which are chalky deposits of monosodium urate
    • Tophi are usually painless, appearing as firm, nodular or fusiform masses located subcutaneously
    • Risk factors include polyarticular presentation, serum urate level 9 mg/dL (>0.54 mmol/L)
  • Presence of urate nephropathy or urate renal calculi

Risk Factors

  • Risk factors for gout and associated comorbidity should be assessed

Risk Factors Associated with Gout

  • Hyperuricemia
    • Single most important risk factor for developing gout
  • Male sex
  • Menopausal women
  • Age
  • Purine-rich diet (eg meat, seafood)
  • Alcohol intake
  • Drug use (eg diuretics, low-dose Aspirin, Ciclosporin)
  • Lead exposure
  • Obesity
  • Renal insufficiency

Metabolic Abnormalities/Comorbidities Associated with Gout

  • Hypertension
  • Obesity
  • Dyslipidemia
  • Hyperglycemia and insulin resistance
  • Coronary artery disease
  • Type 2 diabetes mellitus
  • Renal insufficiency
  • Metabolic syndrome
  • Kidney stone
Editor's Recommendations
Special Reports