Are YOU getting the right pills to help beat crippling gout?
Why hundreds of thousands like Sue are missing out on treatment that could beat agony of attacks
For seven years, Sue McDonagh struggled with agonising gout attacks so intense, it felt as though shards of glass were pressing into her right big toe, and at one point had her begging for an amputation.
‘Each attack caused me excruciating pain,’ says Sue, 62, an artist. Then, three years ago, in 2017, she finally got her symptoms under control.
rather than a case of misdiagnosis, she had simply not been given the right treatment. Taking the correct drug, two tablets daily, has changed her life.
‘I’ve had only one attack since,’ says Sue, who lives in Llantwit Major, Glamorgan, with her partner. ‘But why did it take seven years for my GP to put me on effective treatment?’
research suggests that hundreds of thousands of gout patients in the UK are, like Sue, missing out on the medication they need to avoid attacks.
Unchecked, gout can leave patients not just in pain, but unable to walk. It may even lead to joint damage and, in severe cases, amputation.
Cases of gout, the intensely painful and most common form of inflammatory arthritis, are on the rise, according to a review published in August by the University of Sydney. It found that cases have risen by 7 per cent globally since 1990. In the UK, one in 40 — around 1.5 million people — now suffers from the condition.
Gout is caused by high levels of uric acid (or urate) — a waste product created by the breakdown of cells and the digestion of certain foods — that is normally excreted via the kidneys. High levels can trigger the formation of needle-like crystals in joints, typically in the big toe, ankle, knees, hands and shoulders. It is these crystals that cause pain and other problems if left untreated.
The rise in gout cases is being driven in part by higher levels of obesity and soaring numbers of people with metabolic syndrome, a cluster of conditions including high blood pressure, raised blood sugar, abnormal cholesterol and excess fat around the waist, which increase your risk of heart disease, stroke, and type 2 diabetes.
DR TIM TAIT, a consultant rheumatologist at the United Lincolnshire Hospitals NHS Trust and a trustee of the UK Gout Society, explains: ‘obesity and metabolic disorders all slow down the excretion of uric acid from the kidneys.
‘There is good evidence that gout increases the risk of cardiovascular disease and kidney disease, and vice versa (as gout is an inflammatory illness and increases the risk of other inflammatory illnesses including heart disease), so these are other reasons, apart from preventing joint damage, why it needs to be treated and controlled.’
Under guidelines from the British Society for rheumatology, published in 2017, all gout patients should have early, aggressive, long-term drug treatment to reduce their uric acid levels, typically with allopurinol or febuxostat, which reduce uric acid production in the blood.
However, a study published in The BMJ in 2016 by researchers from Nottingham and Keele universities revealed that only 48 per cent of gout patients who visited their doctors about gout symptoms between 1997 and 2012 were treated for it.
Shockingly, just over a third of those (37.6 per cent) were receiving urate-lowering therapy. This means more than 750,000 gout patients in the UK may not be on effective treatment to treat the cause of the condition — instead, they manage with painkillers.
‘Part of the problem is gout is seen as self-inflicted through overindulgence and it’s just not taken seriously enough,’ says Dr Alastair Dickson, GP trustee of the UK Gout Society. ‘People think gout just affects old men who eat too much rich food and drink port — but that’s not true. For a start, women get it, too, although not as much as men (it’s not known why), and while diet does play a role, it’s one of the least important factors.’
Diet affected uric acid levels by less than 1 per cent, whereas genes controlled 23.9 per cent of a person’s uric acid levels, according to a 2018 study by the University of otago, New Zealand published in the journal BMJ open.
‘Genes are now seen as increasingly important in determining whether you will develop gout,’ explains Dr Dickson. ‘There are 28 different groups of genes involved in gout — some control production of uric acid, others its reabsorption and excretion. You may have a genetic predisposition, and then an environmental stress such as being overweight turns it on.’
And when it comes to ‘rich’ food, certain foods such as offal, game, oily fish, shellfish, meat and beer are high in purines, proteins which, when broken down in the body, form uric acid. However, as Dr Tait explains: ‘Around 70 per cent of uric acid is actually produced by metabolic processes in the body and only 30 per cent ingested from food or drink.’
Patients diagnosed with gout are often just given non-steroidal anti-inflammatory drugs (NSAIDs) painkillers such as ibuprofen or naproxen, or a drug called colchicine or steroids, to reduce the inflammation. ‘They may also be told to change their diet,’ says Dr Dickson.
This was Sue McDonagh’s experience after her first attack ten years ago. Her big toe throbbed so much she assumed she had broken it and went to A&E. ‘But I was told the pain was due to “arthritic” changes,’ she says. ‘The pain stopped after five days taking ibuprofen, but I couldn’t walk for ten days.’
After 18 months with no symptoms, Sue suffered another attack and this time her GP diagnosed her with gout. She was told to change her diet and was treated with anti-inflammatory drugs, including diclofenac, a prescription-only NSAID. She was also told to lose weight and stop drinking alcohol and eating red meat.
‘But I wasn’t overweight. I weigh only 10st 7lb and I’m 5ft 5in, so within the healthy range for BMI. I also ate little red meat and drank moderately,’ says Sue.
She continued to have two gout attacks a year, each lasting seven to ten days. ‘I dreaded them — the pain was so bad I couldn’t walk or go to work,’ she says.
HER case was most likely related to genes — she discovered her late father had gout, too. Three years ago, Sue suffered her worst-ever gout attack. ‘It lasted weeks,’ she says. ‘I wanted my toe amputated it was so bad.
‘I hobbled to see my GP with a walking stick and he finally arranged blood tests, which found my uric acids levels were high, so he prescribed me allopurinol.’
Dr Dickson says early treatment with drugs such as allopurinol to lower uric acid levels will dissolve the crystals and cure the gout, although this can take five years. ‘My other frustration is even when drugs are prescribed, many are just left on a low dose and they don’t get the follow-up blood tests needed to check if the drugs are working,’ he says. ‘This is why the British Society for rheumatology set a target of reducing uric acid levels to less than 300 millimoles per litre of blood.’
Some people cannot tolerate allopurinol — around 10 to 15 per cent of patients experience side-effects such as feeling generally unwell, but they can take febuxostat. other options include sulfinpyrazone, which increases the amount of uric acid excreted by the kidneys.
Another problem, says Dr Tait, is that research indicates 50 per cent of patients stop taking the tablets after 12 months.
‘If they feel better, some patients stop treatment,’ he says. ‘What many don’t realise is uric acid is building up and silently damaging their joints.’
Having found something that ends her painful attacks, Sue says she needs no persuading to continue taking her treatment.
‘Life without pain is amazing — but why did I have to suffer unnecessarily for so long?’