In a primary care‐derived population, the treatment of chronic gout appears to be suboptimal and poorly concordant with recent EULAR recommendations for the management of gout.5
Lifestyle‐modification advice is infrequently offered and allopurinol is only prescribed for a minority of patients despite ongoing hyperuricaemia and recurrent acute attacks in allopurinol non‐users. Although other UK studies2,9
have identified higher rates of allopurinol use in primary care, our finding of 30% is consistent with the findings of a recent large study undertaken in the General Practice Research Database.1
Uricosuric use is commonly limited to secondary care in the UK.
Even in allopurinol users, disease control is often suboptimal. Almost one‐third of allopurinol users had experienced acute attacks of gout in the preceding year despite a median duration of therapy of 10 years. Recent evidence suggests that the aim of ULT should be to lower SUA to <360 μmol/;6,7
yet 23% of allopurinol users had not attained this goal. Our finding that 300 mg is the most commonly prescribed dose of allopurinol is consistent with a number of studies from the UK and abroad, in both primary and secondary care.2,9,10,11,12
The maximum dose of allopurinol in the UK is 900 mg ,and the suboptimum degree of control identified suggests that higher doses are warranted. Poor adherence is often cited as an important reason why treatment of gout may fail and, although self‐reported adherence was reasonable in our survey, studies undertaken in prescribing databases suggest adherence to ULT to be low.13,14
Another commonly stated barrier to successful use of allopurinol is hypersensitivity. This is thought to be a particular problem in the elderly and in those with impaired renal function.15,16
However, none of the 65 patients who had ever taken allopurinol in this study had experienced a severe hypersensitivity reaction and only one patient had experienced a milder allergic reaction necessitating discontinuation of the drug. It is likely that hypersensitivity is a less significant problem in the spectrum of gout patients seen in primary care compared with hospital clinics, as shown by the infrequent finding of tophi.
Recent prospective epidemiological studies have confirmed the role of lifestyle factors such as excess alcohol, high‐purine diet and obesity in the development of gout.17,18,19
To our knowledge, however, only one study has previously examined the frequency with which advice to modify such risk factors is offered to patients with gout. In a review of UK general practice medical records, Pal et al
found that advice concerning alcohol and diet was offered to <30% of patients.9
Our study differs in that we assessed patient recall of lifestyle modification advice, often many years after the event, and although we identified similar results, this approach risks underestimating the frequency of such advice because of poor recall. However, given that patient education is vital for lifestyle modification behaviours to be adopted, it is noteworthy that patient recall of provision of written information and lifestyle modification advice was modest.
Diuretics are widely acknowledged to be a risk factor for hyperuricaemia and subsequently gout,1,19
yet almost two‐thirds of patients with presumed diuretic‐induced gout were still taking a diuretic at the time of the study. Although diuretic cessation should be considered in all patients with gout, this may not be possible in many patients, particularly those with cardiac failure, and an important caveat to the finding that diuretics were frequently continued in the long term is that data regarding the indications for diuretic therapy were not available.
The diagnosis of gout by general practitioners appeared to be reasonably accurate in terms of according with the “specialist” diagnosis based on clinical assessment. The main error encountered was a tendency towards overdiagnosis, rather than underdiagnosis. For such a painful condition, it is perhaps surprising that 12% of gout sufferers had never consulted a doctor about their gout. Although it is not always easy to differentiate primary from secondary gout, the proportions of those with secondary gout (30%) and with tophi (6%) were less than might be expected in hospital‐based series, which have a bias towards inclusion of more complex and severe secondary gout cases. It implies, however, that most gout sufferers in the community have the type of gout that is most easily managed and “cured” by standard treatment approaches, making the relative undertreatment in this survey all the more disappointing.
The major limitation to our study is the low overall response rate to the postal questionnaire. In addition to the 164 gout cases identified, there were a further 89 patients who reported in the questionnaire having gout but did not consent to a face‐to‐face clinical assessment. Another limitation might be the use of a clinical case definition. Without doubt, the gold standard for diagnosis of gout is identification of crystals on aspirates from synovial fluid or tophus. However, although intercritical joint aspiration is a useful diagnostic technique,20,21,22,23,24,25
the requirement to undergo aspiration might have further reduced the number of people agreeing to participate in the clinical assessment, particularly as only 4% had experienced joint aspiration previously (data not shown). As an alternative to crystal identification, many studies of gout have used the 1977 ARA preliminary criteria as diagnostic criteria.8
However, these classification criteria are limited to the acute arthritis of primary gout, thus they are not helpful for either chronic or secondary gout, and have never undergone further validation as suggested by the authors in the original report. They were included as a secondary diagnostic criterion. The 14 cases of clinically confirmed gout that did not fulfil the 1977 ARA criteria may reflect either cases of secondary gout or misclassification by the clinical approach.
The treatment of chronic gout, a curable form of arthritis, in a primary care‐based population appears to be suboptimal and poorly concordant with the recent EULAR recommendations for the management of gout.5
The explanation for this observation is likely to be multifactorial. Despite its significant associated comorbidity, gout appears not to be considered an important disease. Previously, doctors have received mixed messages concerning the indications and aims of ULT, the timing of ULT in relation to acute attacks, and the need for and duration of NSAID or colchicine prophylaxis. For example, exactly how many acute attacks of gout constitute “recurrent acute attacks” (proposition 7) indicating a need for ULT remains a subject of much debate. The need to aim for SUA levels well below the saturation threshold of urate (proposition 8) is not widely appreciated. As discussed above, adherence to ULT is thought to be poor.13,14
There is a need for an education programme to raise the profile of gout and to educate doctors who manage gout about the importance of a multi‐faceted treatment strategy and the appropriate use of ULT. Wider dissemination of the EULAR recommendations should be a priority in order to optimise the management of chronic gout.