Bone & joints


Gout and gouty arthritis

Topic Completed: 1 May 2013

Minor changes: 17 January 2022

Copyright: 2002-2022,, Inc.

PubMed Search: Gouty arthritis [title] loattrfree full text[sb]

Vijay Shankar, M.D.
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Cite this page: Shankar V. Gout and gouty arthritis. website. Accessed January 19th, 2022.
Definition / general
  • Transient attacks of acute arthritis initiated by crystallization of urates and neutrophils followed by chronic gouty arthritis with tophi in joints and urate nephropathy
  • Causes 2 - 5% of chronic joint disease
  • 50% have initial attack in first metatarsophalangeal joint; also ankles, heels, knees, wrists, fingers, elbows
  • Gout is due to hyperuricemia (present in 10% of population, although only half develop gout) and deposition of monosodium urate crystals in joints and viscera and uric acid kidney stones
  • Need serum urate > 7 mg/dl for deposition (saturation threshold for urate at 98.6 F)
  • Uric acid / urate is product of metabolic breakdown of purine nucleotides
  • Two pathways for purine synthesis: de novo (creates purines) and salvage pathway (HGPRT)
  • HGPRT deficiency causes increased synthesis via de novo pathway, leading to hyperuricemia (The Medical Biochemistry Page)
  • Primary gout (90%): idiopathic (85%) with overproduction of uric acid (may have normal excretion) or known enzyme defects (partial hypoxanthine-guanine phosphoribosyl transferase deficiency [HGPRT])
  • Secondary gout (10%): increased nucleic acid turnover due to leukemia/lymphoma, chronic renal disease, HGPRT deficiency
  • Lesch-Nyhan syndrome: rare; men with HGPRT deficiency causing hyperuricemia, severe neurologic deficits with developmental disabilities, self mutilation, gouty arthritis (OMIM: Lesch-Nyhan Syndrome; LNS)
  • Arthritis: synovial fluid is poorer solvent for sodium urate than plasma, so with hyperuricemia, urates in joint fluid crystallize, particularly in ankle due to lower temperature; crystals develop in synovial lining cells, stimulate formation of antibodies, which accelerates formation of new crystals; release of crystals attracts neutrophils and complement, generates C3a, C5a, attracts more neutrophils, releases free radicals, releases lysosomal enzymes which eventually causes acute arthritis that last days to weeks without treatment; repeated attacks of acute arthritis cause chronic arthritis and formation of tophi in synovial membranes and periarticular tissue, which eventually damages joints
Clinical features
  • Males more commonly affected
  • Onset in women occurs at very late age (Clin Rheumatol 2010;29:575)
  • Risk factors for gout with hyperuricemia are age > 30 years, familial history of gout, alcohol use, obesity, thiazide administration, lead
  • Aspirate: grossly white gray and granular; strongly negative birefringent needle shaped crystals under polarized light; foreign body giant cells
Case reports
Clinical images

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Gross description
  • Chalky white appearance of gouty deposits
Microscopic (histologic) description
  • Early: edematous synovium with acute and chronic inflammatory infiltrate
  • Late: tophi (large aggregates of urate crystals, granulomatous inflammation, hyperplastic fibrotic synovium); gout crystals are long, slender, needle shaped but difficult to visualize with routine staining because they are dissolved during formalin processing (crystals are water soluble); easier to identify on scrape or with alcohol fixation
  • With chronic disease, urate deposits may be present in soft tissue, ligaments, skin
  • Gouty deposits may be surrounded by fibrous tissue and be rimmed by histiocytes and giant cells
Microscopic (histologic) images

Contributed by Eman Abdelzaher, M.D., Ph.D.
Big toe Big toe

Big toe

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Uric acid crystals

Needle shaped monosodium crystals

Differential diagnosis
  • Crystal deposition: deposition of calcium pyrophosphate, calcium phosphate, talc, methyl methacrylate (prosthetic joints)
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