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Gout in women

Gout

Gout is a potentially destructive inflammatory disease arising from hyperuricemia and the deposition of uric acid crystals. Although the pathology is genetically determined, it occurs 20 times less frequently in women than in men and typically manifests during the postmenopausal period.

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Urate poolNormally, the total serum urate pool in women is about 0.6 g, which is half of the male values.
Age of onsetIn women, the disease usually occurs in postmenopause, whereas in men, it develops in the 4th–6th decade of life.
Gold standardThe absolute confirmation of the diagnosis is the detection of monosodium urate crystals in tophi or synovial fluid.
Uric acid levelA normal serum uric acid level does not rule out an acute gout attack.
3 min readFor medical studentsUpdated 10.10.2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesPending instructor review

Pathogenesis and causes of inflammation

Gout belongs to the group of crystal arthropathies. The disease develops when the concentration of uric acid in the plasma increases (hyperuricemia). Crystals of monosodium urate are deposited in articular cartilage, the synovial membrane, and subcutaneous tissue.

The mechanism of development of an acute attack is mediated by neutrophils and macrophages:

  1. Leukocytes phagocytose urate crystals.
  2. Destruction of lysosomal membranes occurs.
  3. Lysosomal enzymes enter the cytosol, leading to cell destruction.
  4. Cellular catabolism products trigger a powerful inflammatory reaction.

Purine nucleotide metabolism disorders are often based on polymorphic variants of PRPP synthetase. Due to mutations in the gene, an anomalous response to regulatory factors occurs, the enzyme is superactivated, and purines are synthesized almost independently of the cell's actual needs.

Clinical Forms

The course of the disease can be divided into two main stages:

  • Acute intermittent gout. Characterized by severe pain, erythema (hyperemia), and swelling of the affected joint. In 50% of cases, the first metatarsophalangeal joint (1st MTP) becomes the first target. Joints of the midfoot, ankles, and knees are also frequently involved. In the periods between attacks, symptoms are completely absent.
  • Chronic tophaceous gout. Develops with a prolonged course. Pain-free intervals between attacks disappear, and chronic gouty arthritis forms. Chronic crystal deposition occurs, along with the formation of tophi (gouty nodules), effusion, synovitis, and bone erosions. The total urate pool in severe tophaceous form can reach 30 g (compared to the normal female value of 0.6 g).
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Diagnostic criteria

If synovial fluid analysis for crystals cannot be performed (lack of the "gold standard"), the diagnosis is made clinically (2015 ACR/EULAR criteria).

Main clinical and laboratory signs:

  • Asymmetric joint swelling.
  • Tenderness or swelling of the first metatarsophalangeal joint.
  • Hyperuricemia (uric acid level greater than 6 mg/dL).
  • Hyperemia over the joint.

A complete blood count may show leukocytosis and elevated inflammatory markers, which, combined with fever, requires differential diagnosis with infectious arthritis.

Instrumental imaging

Radiography and ultrasound are used to assess structural changes.

Radiography In the early stages, specific signs are often absent (only asymmetric soft tissue swelling is visible). In the chronic form, punched-out erosions—periarticular erosions with sclerotic overhanging margins—are detected. Tophi are also visualized.

Ultrasound (US) Ultrasound is highly informative in the early stages. In some patients, signs are visible even before the first attack of arthritis. Typical patterns:

  • "Double contour" sign on the cartilage surface.
  • "Blizzard" appearance in the synovial fluid.
  • Tophi (hyperechoic heterogeneous areas with an anechoic rim).

The inclusion of ultrasound in diagnostic criteria has significantly increased their sensitivity and specificity.

Class and exam questions

Does asymptomatic hyperuricemia mean that the patient will definitely develop gout?

No, asymptomatic hyperuricemia is common and does not always mean the presence of clinical gout. Only 1 in 8 patients with a urate level of 7–8 mg/dL will manifest the disease within 14 years.

Can an acute gout attack occur with a normal uric acid level?

Yes, a normal serum uric acid level at the time of testing does not rule out the development of an acute attack of gouty arthritis.

What conditions should an acute gout attack be differentiated from?

Primarily with infectious arthritis, as gout is frequently accompanied by joint hyperemia, fever, and blood leukocytosis.

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What else to study on this topic

  • Mechanisms of urate stone formation and gouty nephropathy
  • Other crystal arthropathies: calcium pyrophosphate dihydrate and hydroxyapatite
  • Seronegative arthritides: ankylosing spondylitis and psoriatic arthritis
  • Enteropathic arthritis and its connection with inflammatory bowel diseases

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