by Gerard Hall
The ancient condition of gout is on the increase – we are seeing more and more patients, mostly due to changes in our lifestyle. Our understanding continues to improve and yet patients are not being treated as well as they could be.
Not all patients get the right diagnosis, for a number of reasons. The classical presentation is easy to recognise: a man developing sudden onset, excruciating pain in the joint of the big toe, often starting at night. The joint becomes red, shiny, swollen and hot. An attack lasts for a few days before settling and the symptoms usually respond well to anti-inflammatory drugs.
But big toe pain is not the only manifestation of this miserable condition. Other joints can be involved and we see gout affecting the knee, ankle or even the whole foot. Sometimes the appearance looks like an infection and this is a common misdiagnosis. The pain is usually very severe – when a patient thinks he’s broken his foot, without any preceding trauma, then he’s probably got gout! It mostly affects lower limb joints but we can sometimes see it in the hands and wrists. It may cause swelling behind the elbow, like a golf ball, called olecranon bursitis. Men of any age can be affected but it’s extremely rare in premenopausal women.
Gout is all about the development of uric acid crystals in joints and adjacent tissues. The crystals can sheer off, resulting in a massive inflammatory response and acute gouty arthritis (arthritis being the term used for inflammation of a joint and can have numerous aetiologies). Crystals have settled in the joints due to the presence of high uric acid levels in the bloodstream. By far the commonest cause of a high blood level is the kidney’s inability to excrete uric acid efficiently and this is usually an inherited problem. The kidney otherwise works well, it just has an isolated problem with uric acid excretion.
Uric acid is a breakdown product of the metabolism of purines, which themselves come from day to day cell turnover. We also consume purines in our diet and this will increase the purine load on the kidney. Purine rich foods include offal meat and seafood.
Most gout sufferers aren’t guilty of rich living, consuming platefuls of scallops, foie gras and sweetbreads but many are overweight due to a high calorie diet and many also drink too much alcohol. Being overweight will raise your uric acid level. Alcohol acts directly on the kidney to cause inhibition of uric acid excretion, thus raising blood levels further. All alcoholic drinks will do this. Beer has the additional problem of having a high purine content so is probably the worst drink of all. Some foods can lower the blood urate level, especially cherries and dairy produce.
The diagnosis should be confirmed by a doctor. Don’t let the doctor rely on a blood test taken during an attack of gout – the uric acid level can fall during an acute episode and is not reliable. It’s best done once the attack has settled.
There are several ways of treating an acute attack of gout, non-steroidal anti-inflammatories (NSAIDs) being the most commonly used. Ibuprofen and Diclofenac can be bought over the counter – you’ll need high doses to tackle gout, 800mg of Ibuprofen 3 times daily and 50mg of diclofenac 3 times daily are the maximum doses. Caution if there is a history of asthma or stomach ulcers. There are other NSAIDs that can be prescribed by a doctor. I use short courses of steroids in patients with particularly severe attacks, either tablets or by injection. Colchicine (one tablet 2or 3 times a day) is also effective in acute gout.
Once the attack ahs settled, it is important to tackle the high blood level of uric cid. Dietary changes are important but do not always result in prevention of future attacks and most patients end up taking medication to lower urate levels.
If the patient is overweight, the focus of treatment should be on weight reduction through a low calorie diet and increased exercise. One study showed a 17% fall in urate levels following a 1200 kCal diet and a low purine diet may also lower the level by 10-20%. But even with weight reduction, a low purine diet and cutting back on alcohol, most patients won’t be able to lower their blood urate level sufficiently to allow the joint crystals to dissolve. Once a target blood level of 350 umol/l has been reached, the crystals will be reabsorped thus preventing further gout attacks. This is best achieved using a tablet called Allopurinol that acts directly to lower the urate level. It’s been used for decades and is generally safe and extremely well tolerated. I’ve never encountered a serious side effect yet. But convincing an otherwise fit man to take a daily tablet for the long term; well that’s a different matter….
Gout should be easy to diagnose and easy to treat. It’s a shame that so many patients with gout are suffering unnecessarily.
For further dietary advice, try ukgoutsociety.org