[Durgical](https://durgical.com/en/) › [DurgiPedia](https://durgical.com/en/durgipedia/) › [General pathology](https://durgical.com/en/general-pathology/) › [Bones, joints and soft tissue](https://durgical.com/en/general-pathology/areas/bone-soft/) › Gout

# Gout

- Lesion

Too much uric acid crystallizes in and around joints; neutrophils attack the crystals and the big toe swells, red and very painful.

Updated Nov 12, 2026

## Key points

- Crystals: needle-shaped, negatively birefringent (yellow when parallel to the compensator axis).
- Classic first attack: first metatarsophalangeal joint (podagra), often at night, after alcohol, a heavy meal, diuretics or surgery.
- Primary gout mostly underexcretion; secondary from leukaemia or lymphoma treatment (tumour lysis), CKD, diuretics, low-dose aspirin, lead.
- Lesch-Nyhan syndrome (HGPRT deficiency) and PRPP synthetase overactivity cause overproduction.
- Tophus: urate crystal mass surrounded by foreign-body giant cells and macrophages; ear helix, olecranon, Achilles, fingers.
- Kidney: urate nephropathy, uric acid stones and acute urate nephropathy after tumour lysis.

## What it is

Gout is caused by deposition of monosodium urate crystals in joints and soft tissue in people with long-standing hyperuricaemia. Most patients underexcrete urate through the kidney; a minority overproduce it, as with inherited enzyme defects or high cell turnover. Crystals shed into the joint are taken up by macrophages, which activate the NLRP3 inflammasome and release IL-1β, bringing an intense neutrophilic attack. Repeated attacks lead to chronic arthritis and tophi, and urate also harms the kidney.

## Structure

- Acute arthritis: dense neutrophilic synovitis; crystals inside neutrophils in the fluid.
- Tophus: chalky white deposit; under the microscope, amorphous or feathery urate masses (dissolved by aqueous fixatives, kept by alcohol) ringed by foreign-body giant cells.
- Chronic tophaceous gout: synovial hyperplasia, fibrosis and punched-out erosions with overhanging edges.
- Kidney: tophi in the medulla and intratubular urate crystals.

## Step by step

- Uric acid, the end product of purine breakdown, rises from underexcretion or overproduction.
- Above its solubility limit, especially in cool distal joints, it crystallizes as monosodium urate.
- Crystals shed into the joint are phagocytosed by macrophages and activate the NLRP3 inflammasome.
- IL-1β and chemokines recruit neutrophils that release enzymes and form NETs; the joint becomes red, hot and swollen.
- Attacks subside, but persistent hyperuricaemia lets tophi grow and erode bone.

## Stages of gout

| Stage | What happens |
| --- | --- |
| Asymptomatic hyperuricaemia | High urate for years; most people never develop gout |
| Acute gouty arthritis | Sudden, very painful monoarthritis that resolves in days to weeks |
| Intercritical gout | Symptom-free intervals that shorten over time |
| Chronic tophaceous gout | Tophi, erosions and persistent arthritis after years of attacks |

## Clinical notes

- Diagnosis by aspiration: needle-shaped negatively birefringent crystals in neutrophils; serum urate can be normal during an attack.
- Acute attacks are treated with anti-inflammatory drugs, colchicine or glucocorticoids; long term, urate-lowering drugs such as xanthine oxidase inhibitors.
- Gout is linked to obesity, metabolic syndrome, hypertension and kidney disease.

## Memory aid

Gout: needles, negative, neutrophils at night in the big toe.

## Test yourself

Think of the answer, then tap the question to see it.

## How do gout crystals look under polarized light?

Needle-shaped and negatively birefringent.

## Which innate immune complex is activated by urate crystals?

The NLRP3 inflammasome, leading to IL-1β release.

## What is a tophus?

A deposit of urate crystals surrounded by foreign-body giant cells and macrophages.

## Is serum urate always high during an acute attack?

No, it can be normal; joint fluid crystals make the diagnosis.

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[More Pathology questions →](https://durgical.com/en/practice/?f=pathology)

## Elsewhere in DurgiPedia

- [Uric acid](https://durgical.com/en/biochemistry/molecules/uric-acid/)
- [Hypoxanthine-guanine phosphoribosyltransferase (HGPRT)](https://durgical.com/en/biochemistry/enzymes/hypoxanthine-guanine-phosphoribosyltransferase/)
- [Interleukin-1](https://durgical.com/en/immunology/interleukin-1/)
- [Innate immunity (overview, barriers)](https://durgical.com/en/immunology/innate-immunity/)

## Connections

## Related 5

- [Patterns of acute inflammation: serous, fibrinous, purulent, abscess, ulcer](https://durgical.com/en/general-pathology/patterns-of-acute-inflammation-serous-fibrinous-purulent-abscess-ulcer/)
- [Pseudogout (CPPD disease)](https://durgical.com/en/general-pathology/pseudogout/)
- [Crystal nephropathies and nephrocalcinosis](https://durgical.com/en/general-pathology/crystal-nephropathies-and-nephrocalcinosis/)
- [Kidney stones](https://durgical.com/en/general-pathology/kidney-stones/)
- [Granulomatous inflammation: caseating vs non-caseating, the causes to know](https://durgical.com/en/general-pathology/granulomatous-inflammation-caseating-vs-non-caseating-the-causes-to-know/)

## Related conditions 4

- [Gout](https://durgical.com/en/conditions/gout/)
- [Gout of the Knee](https://durgical.com/en/conditions/gout-of-the-knee/)
- [Kidney stones (urolithiasis)](https://durgical.com/en/conditions/kidney-stones/)
- [Tumour lysis syndrome](https://durgical.com/en/conditions/tumour-lysis-syndrome/)

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Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.

Sources: [Gout](https://www.ncbi.nlm.nih.gov/books/NBK546606/) (StatPearls (NCBI Bookshelf), 2025).

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Representative model, for educational purposes only.

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Source: https://durgical.com/en/general-pathology/gout/
License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/general-pathology/gout/