Gout

Introduction

Gout is a type of arthropathy, or joint disease, which is really painful and caused by crystal deposition of urate which forms in this super sharp needle-like structure. Flares typically manifest in the big toe and most commonly effect men following triggers like alcohol consumption.

Its pathogenesis revolves around urate which is a metabolite of purines. Remember, DNA is made up of nucleotides with four different bases: adenine, guanine, thymine, and cytosine. The first of these two are purines. When broken down, they turn into urate and as levels increase, urate begins to supersaturate. This means it starts precipitating into crystals because it’s just too concentrated. Therefore, the causes of gout are really just the causes of hyperuricaemia.

From first principles this means causes can be divided into urate over production and urate under excretion.

Overproduction is caused by the consumption of purine-rich foods, which I remember with SALT: seafood, alcohol, and meats like lamb and turkey. But it’s also caused by disorders involving high cell turnover, like malignancies.

Underexcretion is caused by poor renal elimination due to the FAT drugs (furosemide, aspirin and thiazide diuretics) and because of poor faecal excretion, which is determined mostly by genetics.

Investigation is essential because it enables us to exclude septic arthritis which is life threatening and limb threatening.

Joint aspiration or arthrocentesis provides us a means to collect synovial fluid samples. This can then be sent for polarised microscopy to check for crystals. I remember that gouty crystals are not fun at parties because they are negative needles. The fluid can also be sent for further microscopy and culture to exclude an infection and get sensitivities.

One key takeaway here is that hyperuricaemia, in the blood, is not alone diagnostic of gout. This is because levels can be high and normal during a flare.

Another investigation to consider is an xray because gout can cause characteristic joint deformities over time like Rat bite erosions.

To manage acute gout, you have three main options to PICK from.

Prednisolone, which is a steroid, Indomethacin or some other type of NSAID, or colchicine, which is an anti-mitotic drug. My K stands for keep other drugs the same. Do not try to change or start prophylaxis during an acute attack of gout.

On that note urate-lowering therapy is recommended for all patients who have had a confirmed diagnosis. First line is allopurinol which can be augmented with probenecid if it’s not doing the job.

I use GOUT itself as an acronym.

G is for Great toe. It specifically effects the first metatarsophalangeal joint but can affect elsewhere.

O is for one joint. Gout is typically monoarticular, so you should consider other differentials if multiple are effected.

U is for ultrafast. Patients can often pinpoint the onset of an attack to the hour because its often ultra painful too.

Finally, T is for Tophi. Overtime, uric acid crystals form growths around the joints. They are visible under the skin, looking like swollen hard nodules and are a sign of chronic gout.

To recap with a Mnemonic, gout is caused by SALT foods like seafood, alcohol, lamb and turkey and FAT drugs like furosemide, aspirin and thiazides. GOUT effects the great toe, and only one joint at a time, has an ultrafast onset and can eventually cause tophi.