The Doctor: how we get the gout

Most of the time, pain is invisible: you just have to take your patient’s word for it. I knew Mr W had something wrong with his foot, as I’d watched him hobble in, sucking his teeth with each step. “I’ve got the most excruciating pain in my toe,” he said. He bent down to take off his sock, and I waited for an inevitably normal-looking foot to appear. But it wasn’t normal. The first joint of Mr W’s big toe was hugely swollen, shiny and red. It looked like something a cartoonist might draw to illustrate “throbbing”: all it needed was a halo of wiggly pain lines. “It’s gout, isn’t it?” said the patient. “I Googled it. I feel like Henry VIII.”

Since Thomas Sydenham described gout in the 17th century (“So exquisite and lively meanwhile is the feeling of the part affected, that it cannot bear the weight of the bedclothes”), and James Gillray’s famous sketch of a beast gnawing on a bloated 18th-century foot, gout has actually been on the rise in the west, possibly as a result of increasing obesity and high blood pressure – though it’s unclear whether these conditions are causative or just associated.

Gout, a type of arthritis that usually affects one joint at a time, occurs when you have too much uric acid in your blood. Everyone has some circulating uric acid: it is present in many foods, and is a natural waste product of dying cells. It is normally dissolved in the blood, allowing any excess to be filtered out by the kidneys. But if the levels get very high – because you’re genetically disposed, or your kidneys aren’t working very well, for example – solid crystals of monosodium urate can precipitate out and get lodged in the joints.

This is more likely to happen at lower temperatures (uric acid is less soluble in cooler liquids); hence your chilliest joints are the most vulnerable. The big toe joint – or first metatarsophalangeal – is classic; and attacks of gout often start at night, when your body temperature drops.

Through an electron microscope, monosodium urate crystals look like pine needles, and many gout sufferers interpret this as the cause of their pain: a lot of tiny sharp things stuck in a joint is surely going to hurt. But the discomfort actually arises from the body’s reaction to the crystals, rather than from the crystals themselves: it’s the inflammatory response that’s painful. It’s easy to see inflammation in action if you consider a splinter: it’s not so much the presence of a miniature shard of floorboard that hurts, but the redness and heat and swelling that it provokes.

“Dolor, calor, rubor, tumor,” our anatomy professor used to recite, with a mystical look on his face: “Pain, heat, redness, swelling” – the hallmarks of inflammation. When the body finds spikes of monosodium urate it attacks them, dilating the blood vessels to allow lots of inflammatory cells to flood into the area, so that the joint grows tender and hot and red. Because gout is a disease of acute inflammation, the best painkillers are the non-steroidal anti-inflammatory drugs, or NSAIDs, as they work by reducing the inflammatory response (the old drug colchicine, derived from the autumn crocus, can also be effective during a flare: it interferes with the way that the white cells behave and so disrupts the inflammatory cascade).

Most sufferers will be prescribed diclofenac or naproxen for analgesia, and you may be offered the drug allopurinol (which reduces uric acid levels) as a preventative treatment for the longer term. Unfortunately, it is hard to remove the pain completely – or the rude assumption that you’ve been indulging in kingly excess.

Sophie Harrison is a hospital doctor in South Yorkshire

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