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BMJ. 2000 January 15; 320(7228): 132–133.
PMCID: PMC1128728

Gout

Easy to misdiagnose
R D Sturrock, professor of rheumatology

Gout is often thought to be relatively rare and therefore of not much interest to generalists. Yet it is an underdiagnosed condition that presents diagnostic and treatment challenges.

Various diagnostic criteria have been proposed for gout, depending on whether they are to be used in a clinical setting or for epidemiological surveys.1 The criteria proposed by Bennett and Wood in 19682 are still helpful in routine clinical practice. These are the presence of a clear history of at least two attacks of painful joint swelling with complete resolution within two weeks, a clear history or observation of podagra, the presence of a tophus, and a rapid response to colchicine within 48 hours of starting treatment.2 Two of these criteria are required for a clinical diagnosis, but a definitive diagnosis can be made if crystals of sodium monourate are seen in synovial fluid or in the tissues. Hyperuricaemia is a common but not obligatory feature, and it is important to realise that the serum urate concentration may be normal in an acute attack.3

Several British and American surveys have estimated the prevalence of gout to be 2.6-8.4 per 1000 overall in adults, with the prevalence increasing with age to rates of 24 per 1000 in men and 16 per 1000 in women aged 65-74.4 There is no convincing evidence that the prevalence of gout is increasing overall, although a study from New Zealand suggested that this was the case in both Maori and European men.5 For some unknown reason acute gouty attacks may be more common in the spring.6

The main predisposing factors for gout in men are a family history, obesity, an excessive alcohol intake, a high purine diet, and raised triglyceride concentrations.7 Patients may be broadly classified as overproducers or undersecretors of urate. In most cases of gout decreased urinary excretion of urate is the most common metabolic abnormality. This may be due to genetic factors, but usually drugs—including alcohol—result in the low urate renal clearance. This is a particular problem in elderly people, who are often taking thiazide diuretics and low dose aspirin, and have concomitant impaired renal function. Acute attacks of gout are less common in elderly people, in whom it presents insidiously with a chronic arthritis associated with subcutaneous tophaceous deposits on the fingers, toes, and elbows which may be misdiagnosed as rheumatoid arthritis.

Several studies have suggested a link between hypertension, coronary heart disease, and gout, and the Framingham study in particular concluded that gout was an independent risk factor for coronary heart disease.8 However, the more recent Meharry-Hopkins study has not confirmed this association.9

Gout is a rheumatic disease which has a relatively high profile but is often misdiagnosed. Idiopathic hyperuricaemia occurs more often than clinical gout, and a flare of osteoarthritis of the metarsophalangeal joint of the big toe in a patient with hyperuricaemia can lead the unwary into applying the wrong diagnostic label. Pseudogout, which often presents with a hot swollen knee in an elderly patient with pre-existing osteoarthritis, can be readily distinguished by seeing chondrocalcinosis on an x ray film and by showing positively birefringent crystals of calcium pyrophosphate dihydrate on synovial fluid analysis. Less commonly, a septic arthritis of the knee or the big toe can occur in association with gout, particularly when a tophus has ulcerated and become secondarily infected. An acute hot joint in a patient receiving chemotherapy for lymphoproliferative malignancy may be due to gout secondary to the acute tumour lysis syndrome; the differential diagnosis is osteonecrosis of bone if there is concomitant high dose steroid therapy. In transplant patients the use of cyclosporin A is associated with hyperuricaemia.

Non-steroidal anti-inflammatory drugs are the first line of therapy in the treatment of acute gout and should be given in full doses unless there is a history of a peptic ulcer, a background of renal impairment and hypertension, or cardiac failure. Colchicine given orally or intravenously is an alternative but is poorly tolerated by elderly people. Intra-articular steroids and systemic steroids are useful in older patients with impaired renal function.10 An acute attack of gout may take up to seven days to settle, and in the acute phase the patient may have a leucocytosis and a fever.

Long term prophylaxis should be with allopurinol, but this drug should not be started until one month after an acute episode, and in older people the dose should be kept low, rising to a maximum of 100-300 mg/day. Allopurinol is associated with hypersensitive skin reactions, especially when used in conjunction with ampicillin. A useful alternative in urate undersecretors, provided renal function is normal and there is no history of urate stones, is benzbromarone, a powerful uricosuric agent.11 The target urate level to aim for should be 40-70 mg/l. Recurrent attacks of gout occurring despite what seems to be adequate prophylactic therapy are almost always associated with continued alcohol abuse and poor compliance with treatment, especially in men.12

References

1. Stewart OJ, Silman AJ. Review of UK data on the rheumatic diseases—4. Gout. Br J Rheumatol. 1990;29:485–488. [PubMed]
2. Bennett PH, Wood PHN. Population studies of the rheumatic diseases. Amsterdam: Excerpta Medica; 1968. pp. 457–458.
3. Snaith ML. ABC of Rheumatology: gout, hyperuricaemia, and crystal arthritis. BMJ. 1995;310:521–524. [PMC free article] [PubMed]
4. Lawrence RC, Helmick CG, Arnett FC, Deyo RA, Felson DT, Giannini EH, et al. Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States. Arthritis Rheum. 1998;41:778–779. [PubMed]
5. Klemp P, Stansfield SA, Castle B, Robertson MC. Gout is on the increase in New Zealand. Ann Rheum Dis. 1997;56:22–26. [PMC free article] [PubMed]
6. Schlesinger N, Gowin KM, Baker DG, Beutler AM, Hoffman BI, Schumacher HR., Jr Acute gouty arthritis is seasonal. J Rheumatol. 1998;25:342–344. [PubMed]
7. Nakanishi N, Suzuki K, Kawashimo H, Nakamura K, Tatara K. Serum uric acid: correlation with biological, clinical and behavioral factors in Japanese men. J Epidemiol. 1999;9:99–106. [PubMed]
8. Abbott RD, Brand FN, Kannel WB, Castelli WP. Gout and coronary heart disease: the Framingham Study. J Clin Epidemiol. 1988;41:237–242. [PubMed]
9. Gelber AC, Klag MJ, Mead LA, Thomas J, Pearson TA, Hochberg MC. Gout and risk for subsequent coronary heart disease. The Meharry-Hopkins study. Arch Int Med. 1997;157:1436–1440. [PubMed]
10. Fam AG. Gout in the elderly. Clinical presentation and treatment. Drugs Aging. 1998;13:229–243. [PubMed]
11. Perez-Ruiz F, Alonso-Ruiz A, Calabozo M, Herrero-Beites A, Garcia-Erauskin G, Ruiz-Lucea E. Efficacy of allopurinol and benzbromarone for the control of hyperuricaemia. A pathogenic approach to the treatment of primary chronic gout. Ann Rheum Dis. 1998;57:545–549. [PMC free article] [PubMed]
12. Ralston SH, Capell HA, Sturrock RD. Alcohol and response to treatment of gout. BMJ. 1988;296:1641–1642. [PMC free article] [PubMed]

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