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Table 97.1

Epidemiology of Gout and Pseudogout

GoutPseudogout (calcium pyrophosphate dihydrate deposition (CPPD) disease)
AgePredominantly 30–60 years, risk increases with advancing age>60 years, risk increases in the elderly
SexMale predominance, post-menopausal women, very rare in premenopausal womenMale: female ratio 50:50
Risk factors

Conditions which promote hyperuricaemia, due to overproduction or under-excretion of urate

Overproduction of urate

Genetic diseases:

  • Hypoxanthine-guanine phosphoribosyltransferase deficiency (Lesch-Nyhan syndrome)
  • Superactivity of phosphoribosyl pyrophosphate synthetase (PRPP)
High cell turnover:
  • Cell lysis from chemotherapy for malignancies
  • Lympho- and myelo-proliferative diseases

Under-excretion of urate:

  • Chronic alcohol abuse (beer and hard liquor)
  • Renal insufficiency (also below)
  • Dehydration

Conditions that promote altered concentrations of calcium, inorganic pyrophosphate (PPi) and the solubility products of these ions

Genetic diseases:

  • Mutations in the ANKH gene, leading to altered PPi metabolism (familial CPPD deposition disease)

Metabolic conditions causing CPPD deposition:

  • Hyperparathyroidism
  • Haemochromatosis
  • Hypomagnesaemia
  • Hypophosphataemia
  • Familial hypocalciuric hypercalcaemia (The 5 Hs of CPPD disease)
Related comorbid conditions

Hypertension

Diabetes mellitus

Renal insufficiency

Hypertriglyceridaemia

Hypercholesterolaemia

Obesity

Anaemia

Hyperparathyroidism

Haemochromatosis

Hypomagnesaemia (Chapter 88)

Hypophosphataemia (Chapter 89)

Familial hypocalciuric hypercalcaemia

Dietary factorsFoods rich in purines such as red meat and sea foodNo clear dietary causes