Gout: Diagnosis and Management in Primary Care

This transcript has been edited for clarity.

In this podcast, I'm going to talk about the diagnosis and management of gout in primary care. Let's start with a typical case we might all see in primary care.

Henry is a 58-year-old man working in marketing. He presents to us in duty surgery with a very sore and red left big toe. He's never had this before. Past medical history includes hypertension, and he's never smoked. He admits that he enjoys alcohol liberally and regularly, particularly his craft ales. Current medications are lisinopril 20 mg once a day and bendroflumethiazide 2.5 mg once a day, which he also admits he takes only sporadically for his hypertension.

Bloods done at his previous hypertension review demonstrated normal kidney function. On examination, blood pressure was 154/92 mm Hg, and there was clear evidence of gout affecting his right first metatarsophalangeal, or MTP, joint.

Henry's case raises a number of questions for us in primary care. First, how do we manage Henry's symptoms of acute gout? Second, what lifestyle advice should we offer Henry to prevent future gout flares? Do we need to review his medications? Next, when do we offer Henry urate-lowering therapy, and what are our available options? If we do treat Henry with urate-lowering therapy, what target serum uric acid level should we aim for? Finally, does Henry require long-term follow-up of his gout?

Let's answer these questions. Gout is increasing in prevalence, incidence, and severity, yet it remains underrecognized and undermanaged by both healthcare professionals and patients. It's actually the most common cause of inflammatory arthritis globally. Gout commonly affects the first MTP joint, or base of the big toe, as is the case with Henry, but can also affect the midfoot, ankle, knee, hand, wrist, and elbow.

Hyperuricemia is the most important risk factor for gout and leads to deposition of monosodium urate crystals in various tissues and joints, leading to inflammation and subsequent destruction. Any medical condition that causes high cell turnover, such as psoriasis and myeloproliferative disorders, also leads to increased serum urate levels. Urate excretion is partially undertaken by the kidney, so any impairment in kidney function also increases serum uric acid levels.

Overall, a change of thinking is required for gout — a shift away from a troublesome, largely self-inflicted recurrent condition due to lifestyle, to a common, chronic inflammatory arthritis that can lead to joint destruction, long-term pain, and disability. Recently updated United Kingdom NICE guidance on the diagnosis and management of gout reinforced this shift, and I'll be drawing on key take-home messages from this guideline throughout this podcast.

Additionally, cardiovascular disease is the major cause of increased mortality in patients with gout. Cardiovascular risk assessment and mitigation of cardiovascular risk factors should also be a key focus of management, alongside treatment of acute symptoms and consideration of urate-lowering therapy to prevent gout flares.

The first question is, what do we offer Henry for his acute attack of gout? Gout is a clinical diagnosis. We need to exclude septic arthritis and other forms of crystal arthritis, such as pseudogout, which involves deposition of calcium pyrophosphate crystals predominantly in the wrist and knee. Serum uric acid levels often fall during an acute attack of gout, so they have limited diagnostic value. If the diagnosis is uncertain, we should consider joint aspiration and microscopy, looking for crystals.

Acute attacks of gout should be treated promptly. We should advise rest, ice, and elevation. Pharmacologic treatment of gout should be guided by comorbidities, current therapies, kidney function, and patient preference.

UK NICE guidance suggests that first-line therapy should be either a nonsteroidal anti-inflammatory drug, with or without PPI cover, or colchicine, or a short course of oral steroids. If using colchicine, I usually prescribe 500 μg twice a day for 3-5 days as tolerated. Usual side effects limiting use of colchicine are abdominal pain, diarrhea, nausea, and vomiting. If eGFR is less than 50 mL/min, colchicine should be used with caution at a lower dose.

If using steroids for gout, I usually prescribe prednisolone 30 mg once a day for 3-5 days. Intra-articular or intramuscular steroids can also be considered if nonsteroidal anti-inflammatory drugs and colchicine are contraindicated, not tolerated, or ineffective.

Our next questions are, what lifestyle advice should we offer Henry, and do we need to review his medications? All patients with gout should be given verbal and written information about their gout. The Versus Arthritis charity in the UK produce an excellent patient information booklet on all aspects of gout.

Lifestyle interventions to discuss include weight management and reducing intake of high-purine foods, such as red meat; game, such as venison; offal, such as liver and kidney; seafood, particularly shellfish; oily fish; Marmite; and Vegemite. Interestingly, vitamin C, cherries, cherry extract, and low-fat dairy products have all been shown to reduce serum uric acid levels; intake should be encouraged where possible.

In regard to alcohol, of course, excessive alcohol intake should be avoided, but it's actually particularly beers and spirits that increase the risk for gout rather than, traditionally, red wines and port. We should also remind Henry to maintain adequate hydration, around 2-2.5 L of clear fluids daily, not including tea, coffee, or alcohol.

Do we need to review Henry's medications to reduce his risk for a future flare-up of his gout? Diuretics, and particularly thiazide diuretics, such as Henry's bendroflumethiazide, are indeed associated with increased serum uric acid levels. Switching his bendroflumethiazide to an alternative class of antihypertensive agent would be beneficial to him.

Interestingly, losartan and calcium channel blockers, such as amlodipine, are better options, as they have uricosuric properties and may actually help reduce serum uric acid levels. If individuals are on low-dose aspirin for secondary prevention of cardiovascular disease, this can be continued, as the benefits outweigh the risk in terms of reduced uric acid excretion.

Next, when do we offer Henry urate-lowering therapy, and what are our available options? There's growing consensus that urate-lowering therapy should be discussed and offered to all patients with gout at the time of diagnosis, and not just to those with recurrent flares, very high serum uric acid levels, gouty tophi, kidney impairment, or those with gout at a younger age. There is, however, no strong evidence to support the use of urate-lowering therapy in people with asymptomatic hyperuricemia.

Overall, there persists poor uptake of urate-lowering therapy by healthcare professionals and patients. Only one third of people living with gout receive urate-lowering therapy, and only one third of these individuals use it effectively.

A move to a treat-to-target principle is strongly advocated in many gout guidelines globally, including the UK guidance. Lifestyle modification shouldn't be the prime focus of the management of gout. Pharmacologic modification with urate-lowering therapy should also be given equal priority.

The UK NICE guidance advocates offering urate-lowering therapy using a treat-to-target strategy to people with gout at their first or subsequent flare who have multiple or troublesome flares; to people with CKD stages G3 to G5 — that's an eGFR below 60 mL/min; to those who are on diuretic therapy; to those who have evidence of gouty tophi; or to those who have evidence of chronic gouty arthritis.

Urate-lowering therapy is best delayed until the acute inflammation and pain are settled. We should usually wait at least 2-4 weeks after the acute flare and then check serum uric acid levels. If individuals are experiencing more frequent flares, urate-lowering therapy can be started during a flare. Importantly, we should not stop established urate-lowering therapy during any acute gout attacks.

UK NICE guidance suggests offering allopurinol or febuxostat first line as urate-lowering therapy, taking into account comorbidities and preferences. Allopurinol should be the first-line option in people with gout and cardiovascular disease, and I'll discuss this shortly. When prescribing allopurinol, it should be initiated at 100 mg daily and can be increased at four weekly intervals, up to 900 mg daily in divided doses. However, if eGFR is less than 60 mL/min, the dose should be capped at 100 mg daily.

In contrast, febuxostat is safe in kidney impairment, is initiated at 80 mg once a day, and can be increased to 120 mg once daily after 2-4 weeks if serum uric acid levels are still above target. Of note, in patients with preexisting major cardiovascular diseases (for example, myocardial infarction or stroke), febuxostat therapy should be used cautiously due to past conflicting cardiovascular safety evidence for febuxostat.

When initiating urate-lowering therapy, individuals should be offered prophylaxis for up to 6 months to prevent an acute flare-up of their gout. We can offer either colchicine 500 μg once daily or twice daily, or a low-dose nonsteroidal anti-inflammatory drug with PPI cover, or a low-dose steroid, again, if colchicine and nonsteroidal anti-inflammatory drugs are not tolerated or contraindicated.

Once we've started Henry on urate-lowering therapy, what target serum uric acid level should we aim for? Once again, a treat-to-target approach is strongly advocated in all global gout guidelines. The UK NICE guidance recommends treating to a serum uric acid target of less than 360 μmol/L to prevent further crystal formation and to dissolve existing crystals.

However, we should consider a lower target of less than 300 μmol/L if individuals have evidence of gouty tophi or chronic gouty arthritis, or if individuals continue to suffer frequent flares of their gout despite a serum uric acid level of less than 360 μmol/L.

Finally, does Henry require long-term follow-up of his gout? Guidelines are quite clear; urate-lowering therapy should be considered as a long-term treatment for Henry, and UK NICE guidance recommends at least annual assessment of his serum uric acid levels.

Additionally, at each annual assessment, lifestyle modification can be reinforced, as we've already discussed. Also, the opportunity can be taken to reassess Henry's cardiovascular risk factors, offer him advice, and try to manage any significant risk factors as appropriate.

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Any views expressed above are the author's own and do not necessarily reflect the views of WebMD or Medscape.

Cite this: Gout: Diagnosis and Management in Primary Care - Medscape - Dec 12, 2024.