The management of gout: Much has changed (2022)

Gout is not a new disease, but its management has certainly seen much change in the past five years. It is increasingly being recognised as a serious disease that causes functional disability, increased work absence, and negative economic consequences for the individual and community.1 Australian research indicates that gout is a significant and increasing problem, with at least 1.5% of the general population affected. A very high prevalence (>10%) of the disease is seen in specific groups, such as elderly men.2,3 Evidence from Australia and the rest of the world shows that the management of gout is suboptimal, as demonstrated by infrequent serum urate testing, low levels of urate-lowering therapy prescription and, when prescribed, inadequate dosing, resulting in serum urate levels above target.

There have been a number of changes to the management of gout, including dosing strategies of older drugs and availability of newer therapeutics. This review provides an update for practitioners on the management of gout.

Common misconceptions

Gout does not occur only in the great toe (podagra), although this is a common site for the initial episode. It can affect any joint in the body and can even mimic the polyarthritis of rheumatoid arthritis.

If inadequately treated, it is a condition that usually progresses rather than regresses. Accumulation of urate in the body occurs as a result of an imbalance in intake or intrinsic urate production and excretion through the kidneys and gastrointestinal tract (GIT). Kidney and GIT excretion is influenced mainly by genetics, although factors such as concomitant medications also play a role.

Gout growing in prevalence and impact

Gout has often been viewed as a nuisance and non-serious condition. It is an important condition for a number of reasons.

First, gout is increasing in prevalence as the world population becomes more overweight and obese.4

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Second, gout causes significant pain, functional impairment and reduction in work participation. Studies have found that those with gout are absent more often from work and take more sick leave than those who do not have gout.5 This has an impact not just on the patient but also on their finances, family and community as a whole.

Third, gout is associated with a number of serious comorbidities such as hypertension, diabetes mellitus, ischaemic heart disease, kidney disease and obesity. Therefore, patients who present with gout have a very high chance of another serious and treatable condition that can be screened for and treated. It is important to identify comorbid conditions as they have an impact on the therapeutic options for gout.6 The therapies used to treat comorbidities also need to be considered carefully. There are treatments that:1,7

  • raise serum urate (eg thiazide, loop diuretics)
  • impair the actions of urate-lowering drugs (eg frusemide)
  • lower serum urate (eg losartan).

Consideration of potential comorbid conditions, their treatment and their possible impact on gout is therefore critical.

Treat to target

Treating patients to a target serum urate is essential for reducing gout flares and resolving tophi. For those without tophi, a target of <0.36 mmol/L is recommended; for those with tophi, a target of <0.30 mmol/L should be considered.8 Gout flares decrease with decreasing levels of serum urate. Once the serum urate is below target, gout flares may still occur for up to 12–18 months. They should become more infrequent over time if the serum urate target is maintained, and will stop eventually.

Acute flare treatment

Treatment of acute flares should begin as soon as possible. Non-steroidal anti-inflammatory drugs (NSAIDs) or colchicine are considered first-line agents; oral corticosteroids are reserved for those who cannot tolerate, or who have contraindications, to first-line agents.9 NSAIDS are typically used at full dose. Colchicine 1.2 mg immediately followed by 0.6 mg six hours later and then 0.6mg once or twice daily for two to three days for those with normal renal function is often effective (note, the 0.6 mg tablet size is not available in Australia and the 0.5 mg tablet is usually substituted for it).9 It is not usually associated with the gastrointestinal adverse effects commonly seen with higher doses. Even lower colchicine doses are required for those with renal impairment or receiving CYP3A4 or P-glycoprotein inhibitors.10 Oral corticosteroids, such as 0.5 mg/kg prednisone for five to 10 days with gradual reduction or an intra-articular steroid injection for those with a monoarthritis due to gout, can be very effective.9

Allopurinol should not be stopped during acute flares of gout

Allopurinol should not be stopped during acute flares of gout.11 Stopping allopurinol during an acute flare means therapeutic effect is lost and the urate level will rise. In addition, there is a real risk of the allopurinol not being recommenced as well as precipitating another flare when it is recommenced.

(Video) New Gout Guidelines: Primary Care Pointers

Allopurinol can be started during an acute attack

Historically, there has been concern that starting urate-lowering therapy such as allopurinol could worsen or prolong the acute gout flare. Two small clinical trials have now found that this is not an issue. Based on these trials, it is reasonable to start allopurinol during an acute flare of gout when combined with acute gout treatment as this does not prolong the flare.12,13 In addition, it is an ideal opportunity to initiate therapy and educate the patient while they have the acute symptoms, which are a more immediate reminder of the reason for the new therapy.

Allopurinol needs to be started low and up-titrated

Evidence suggests that it is the starting dose of allopurinol, not the maintenance dose, that increases the risk of allopurinol hypersensitivity syndrome (AHS).14 Therefore, allopurinol should be started at 50–100 mg per day (or less in those with severe renal impairment) and titrated up so patients reach their serum urate target. The American College of Rheumatology recommends that everyone commencing allopurinol start on 100 mg per day, except those with stage 4 or worse chronic kidney disease, where the recommended starting dose is 50 mg per day.8 It should then be titrated up every two to five weeks, with more caution and longer intervals in those with poorer kidney function.

For example, in a patient with gout, no tophi and normal kidney function, one might start at 100 mg a day for two to three weeks, then increase to 200 mg per day for two to three weeks, then 300mg per days for two to three weeks.8 The serum urate should then be checked and, if the target (<0.36 mmol/L) has been reached, the patient can stay on 300 mg per day. If not, the dose is then titrated up to 400 mg per day and the serum urate is checked again. In Australia, the maximum recommended dose of allopurinol is 900mg.15

The risk of AHS is increased in those who carry the HLA-B*5801 allele, which has an increased prevalence in those of Asian descent. Guidelines recommend testing for this allele in high AHS-risk individuals such as people of Asian descent with renal impairment, then avoiding allopurinol if it is present.8

Prophylaxis of acute gout flares

Prophylaxis of acute flare of gout is recommended in those commencing on urate-lowering therapy. Gout flares on starting urate-lowering therapy are very common and prophylaxis aims to prevent them from occurring. In a trial of allopurinol where prophylaxis was ceased, a flare rate of 64% was observed.16 In those receiving naproxen (250 mg twice daily) or colchicine (0.6 mg daily) prophylaxis, 20–28% of patients experienced flares on initiation of urate-lowering therapy.17 Although no head-to-head trials have been completed, the available data suggest that flare rates are substantially reduced by anti-inflammatory prophylaxis. NSAIDs or colchicine are the first-line recommended agents.8 This can be achieved by a moderate dose of an NSAID, such as naproxen 250 mg twice daily, or 0.5–1 mg of colchicine per day.9 Consideration of medication contraindications and use of gastric protection may be appropriate.

The recommended duration of prophylaxis is now longer than what has previously been used. The American College of Rheumatology recommends:

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  • at least six months’ duration, or
  • three months’ duration after achieving target serum urate in patients without tophi, or
  • six months’ duration after achieving target serum urate in patients with tophi on examination.

This recommendation is in recognition that even after the target serum urate level has been reached, flares may continue to occur for some time.8 Every clinical scenario is different and practitioners need to carefully consider the risks and benefits when prescribing prolonged courses of acute gout flare prophylaxis.

Monitoring of serum urate

Once target serum urate has been reached, six-monthly monitoring by testing serum urate is recommended to ensure continuing adequate management and adherence.8 This includes monitoring serum urate, and checking use of blister packs. Adherence with long-term allopurinol is poor and every effort should be made to encourage patients to continue to take it, including involving family members.

Febuxostat as an alternative urate-lowering therapy

Febuxostat is a newer agent used to treat gout that works by inhibiting xanthine oxidase – the same mechanism as allopurinol. It is now available on the Pharmaceutical Benefits Scheme (PBS) as an ‘authority required drug’ for patients with gout who have a contraindication to allopurinol or a documented history of AHS, or intolerance to allopurinol necessitating permanent treatment discontinuation.18 This would therefore be appropriate in patients with allopurinol rash or AHS. In addition, it would be appropriate therapy for those who have HLA-B*5801.

Management of gout in those with severe chronic renal impairment

The evidence guiding the management of those with gout requiring urate-lowering therapy and an estimated glomerular filtration rate (eGFR) <30mL/min is limited. One approach is to start the patient on a very low dose of allopurinol (eg 1.5 mg per mL eGFR) with very gradual up-titrating (eg 25–50 mg per month). An alternative is the use of low‑dose febuxostat, although evidence to support this approach is currently sparse.19 Referral to a rheumatologist is recommended.

Patient education

Research has suggested that patients with gout who lack confidence in their treatments have reduced adherence to their medications. A lack of confidence in treatment can result from their gout flaring after initiation of urate-lowering therapy.20 Education about this and other aspects of gout is important to make sure patients understand that although their gout may flare in the short term, they are moving towards a shared goal of no gout attacks in the long term.21,22 In addition, equipping patients who have gout with the skills and motivation to be adherent with medication is likely to also be very important.

A large intake of sugar or sweetened soft drinks, such as cola or lemonade, is a recognised risk for gout. Patients with gout are advised to limit their intake of these beverages.8

(Video) The TRUTH about GOUT & URIC ACID that no one really talks about.

Although epidemiological evidence suggests that a high-purine diet increases the risk of gout, there is scant evidence that introducing a low-purine diet in those with gout results in a clinically meaningful reduction in gout flares or serum urate.

A comprehensive approach is best, including providing patients with a schema to help them understand important aspects of gout management (Box 1).

Box 1. Gout treatment schema23
  • Set urate target
  • Start urate-lowering therapy with prophylaxis
  • Ensure patient has acute flare plan (see text for further details)
  • Monitor serum urate until target reached
  • Titrate urate-lowering therapy to achieve target
  • Once target achieved, monitor 6–12 monthly

Treatment of asymptomatic hyperuricaemia

No current guidelines or recommendations in the US, UK, Australia or New Zealand support treatment of asymptomatic hyperuricaemia.

Conclusion

The increasing prevalence and impact of gout mean that greater focus is required to ensure best outcomes for patients. Newer therapeutic agents are on the horizon, but gout can still be well treated with our current agents, especially in light of recent insights into treatment strategies, such as commencing allopurinol during acute attacks and starting at a low dose and titrating up. Generally speaking, the most important strategy is to treat to a serum urate target (<0.36 mmol/L in most people) as this is critical to preventing gout flares and resolving tophi.

Authors

Philip C Robinson MBChB, PhD, FRACP, Senior Lecturer, University of Queensland School of Medicine, QLD, and Staff Specialist in Rheumatology, Royal Brisbane and Women’s Hospital, Herston, QLD. philip.robinson@uq.edu.au

Lisa K Stamp MBChB, PhD, FRACP, Professor of Medicine, Department of Medicine, University of Otago, Christchurch, New Zealand, and Rheumatologist, Rheumatology Department, Christchurch Hospital, Christchurch, New Zealand

(Video) Gout Management

Competing interests: Philip C Robinson has received research funding and consulting fees from AstraZeneca, and consulting fees from Menarini and Novartis. Lisa K Stamp has received consulting fees from AstraZeneca.
Provenance and peer review: Not commissioned, externally peer reviewed.

FAQs

How was gout treated in the past? ›

Many different methods have been used to manage gout over the years. Early treatments from Hippocrates' day included barley water, purging and counterirritation (scorching the veins near the affected joint). Bloodletting was also very popular among physicians at the time.

What is the management of gout? ›

Your doctor may recommend colchicine (Colcrys, Gloperba, Mitigare), an anti-inflammatory drug that effectively reduces gout pain. The drug's effectiveness may be offset, however, by side effects such as nausea, vomiting and diarrhea. Corticosteroids.

How was gout treated in the 18th century? ›

Gout was sought by some who did not have it. In the 18th century, patients suffering from consumption or melancholy were sent by their physicians to the waters at Bath in the hope of acquiring gout and so ousting their other sickness.

What is the gold standard treatment for gout? ›

The drugs of first choice for acute gouty arthritis are nonsteroidal anti-inflammatory drugs (NSAID), corticosteroids, and colchicine. Treatment with xanthine oxidase inhibitors (XOI) or uricosuric drugs is indicated for patients with a recurrent or severe course; the target uric acid value is <6 mg/dL.

Is there any permanent solution of gout? ›

Patients can never be cured of gout. It is a long-term disease that can be controlled by a combination of medication to control the uric acid level, and anti-inflammation drugs to treat a flare-up. “Lowering the level of uric acid is key to treating gout, and patients must understand this.

Does gout ever fully heal? ›

An acute gout attack will generally reach its peak 12-24 hours after onset, and then will slowly begin to resolve even without treatment. Full recovery from a gout attack (without treatment) takes approximately 7-14 days.

What is the first treatment for gout? ›

First-line therapy for acute gout is nonsteroidal anti-inflammatory drugs or corticosteroids, depending on comorbidities; colchicine is second-line therapy. After the first gout attack, modifiable risk factors (e.g., high-purine diet, alcohol use, obesity, diuretic therapy) should be addressed.

Why is gout called Kings disease? ›

Gout has long been known as the "disease of kings" because of the lavish diet and alcohol consumption of the wealthy, like King Henry VIII, who suffered from it. Gout is also the "king of arthritic diseases" because the pain of an acute gout attack is so severe, it often leads to a visit to the emergency department.

Why did so many kings get gout? ›

Historically, gout was thought to be a disease of only the wealthy or royal class, and it was called the “disease of the kings.” Overindulgence in diets rich in meats, seafood, and alcohol has long been associated with gout, and the people who could afford such a lifestyle were the people typically affected.

Which medication is the oldest medication and was used to treat gout and bladder stones? ›

Perhaps the most important historical advance in the treatment of hyperuricemia was the development of allopurinol, the first xanthine oxidase inhibitor [39].

What is the safest gout medication? ›

Allopurinol is considered very safe to take for a long period of time. There are unlikely to be any long-term effects. What will happen if I stop taking it? If you stop allopurinol treatment suddenly, there is a high risk that gout may get worse or you will get serious side effects.

Can you reverse gout damage? ›

Gout is one of the most common inflammatory arthritides. The disease is due to the deposition of monosodium urate crystals. These deposits are reversible with proper treatment, suggesting that gout is a curable disease.

What is the fastest way to flush gout? ›

Drinking water may flush uric acid crystals out of your system. Preliminary research suggests that adequate water consumption during the 24-hour period before a gout flare can decrease recurrent gout attacks.

Does apple cider vinegar help cure gout? ›

There is no proof that consuming or using apple cider vinegar can help prevent or treat gout. However, certain chemicals in apple cider vinegar, namely acetic acid, may lower the risk of developing conditions that can increase the likelihood of gout, such as obesity, diabetes, and high blood pressure.

What is the last stage of gout? ›

Chronic tophaceous gout

This is the final stage of gout, which is a form of chronic arthritis characterized by permanent damage to the cartilage and bone in the joint.

How do you break up gout crystals? ›

Drink at least 10-12 eight-ounce glasses of non-alcoholic fluids daily, especially if you have had kidney stones. This will help flush the uric acid crystals out of your body.

Which fruit is best for uric acid? ›

Grapefruit, oranges, pineapples, and strawberries are all great sources of vitamin C, which lowers your uric acid levels and helps prevent gout attacks.

Is lemon good for uric acid? ›

Lemon juice may help balance uric acid levels because it helps make the body more alkaline. This means it slightly raises the pH level of blood and other fluids. Lemon juice also makes your urine more alkaline.

Does Covid trigger gout? ›

Results. Among 5,904 patients with gout (mean age: 63·1 years; 85·5% male) who experienced gout flares within one month, the risk of gout flares slightly increased on the second day after COVID-19 vaccination (odds ratio: 1·44; 95% CI: 1·02 to 2·07).

Is it good to walk with gout? ›

It is safe for people to walk with gout. In fact, doing joint friendly activities such as walking can help improve gout-related pain. Gout is a form of arthritis that usually affects the big toe joint, but it can also affect the lesser toes, ankles, and knees. It normally affects one joint at a time.

Does stress cause gout? ›

For some people, stress can trigger gout attacks. That's because high levels of stress and anxiety are associated with increased uric acid levels. 10 Taking action to manage your stress can also support a more calm state of mind and reduce the inflammation associated with stress.

Is gout from inbreeding? ›

Gout is not a measure of your breeding or status. There have been plenty of aristocrats and geniuses who have never had gout--but then again the European upper classes were so inbred that if they didn't get gout they contracted just about everything else.

What famous person has gout? ›

Sir Laurence Olivier, one of the best actors of the 20th century was diagnosed with gout at the age of 58. In the sports world, we have soccer player Harry Kewell from Australia who was actually diagnosed with gout while playing in the 2006 World Cup and a gout flare kept him out of a game.

What ethnicity gets gout the most? ›

Black race was associated with greater odds of gout during this period among women (odds ratio [OR], 1.81 [95% CI, 1.29-2.53]), among men (OR, 1.26 [95% CI, 1.02-1.55]) (Table 2), and overall (OR, 1.46 [95% CI, 1.22-1.74]).

What is the best long term medication for gout? ›

Allopurinol is used for the long-term treatment and prevention of gout. Taken regularly, it can stop attacks of gout and help prevent damage to your joints. Gout occurs in people who have high levels of urate in their blood.

Which one is not a first line treatment option for gout? ›

Which of the following is NOT a first-line option for the pharmacologic treatment of acute gout? Please click below for answer and next question. The correct answer is D. Aspirin.

Can colchicine damage kidneys? ›

Nonsteroidal anti-inflammatory drugs and colchicine are recommended first-line treatments for acute gouty arthritis attacks. However, in patients with CKD, nonsteroidal anti-inflammatory drugs are not recommended because their use can exacerbate or cause acute kidney injury.

What painkiller is better for gout? ›

Take an NSAID (but not aspirin)

Over-the-counter non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen or naproxen, can help relieve gout pain. Avoid aspirin and other medications that contain acetylsalicylic acid, which can make your gout worse.

Is turmeric good for gout? ›

If you have gout, try turmeric as a home remedy. Its most active chemical, curcumin, has potent anti-inflammatory and antioxidant properties. This may help ease gout-related inflammation and pain. When eaten in foods, turmeric is generally safe.

Do bananas trigger gout? ›

Bananas are low in purines and high in vitamin C, which makes them a good food to eat if you have gout. Changing your diet to include more low-purine foods, like bananas, can lower the amount of uric acid in your blood and reduce your risk of recurrent gout attacks.

What is the number one food that causes gout? ›

Foods that commonly trigger gout attacks include organ meats, red meats, seafood, alcohol and beer. They contain a moderate-to-high amount of purines ( 11 , 12 ). However, there is one exception to this rule. Research shows that high-purine vegetables do not trigger gout attacks (13).

Is cheese OK for gout? ›

Dairy. Dairy products, such as milk, cheese, and yogurt, are low in purines, and they are a good fit for a diet to manage or prevent gout. They are good protein alternatives to meat, and reduced-fat dairy products are lower in saturated fat than full-fat ones.

Why was gout so common in the past? ›

Rates of gout approximately doubled between 1990 and 2010. This rise is believed to be due to increasing life expectancy, changes in diet and an increase in diseases associated with gout, such as metabolic syndrome and high blood pressure.

Why did so many kings have gout? ›

Gout has long been known as the "disease of kings" because of the lavish diet and alcohol consumption of the wealthy, like King Henry VIII, who suffered from it. Gout is also the "king of arthritic diseases" because the pain of an acute gout attack is so severe, it often leads to a visit to the emergency department.

Did Romans have gout? ›

The bacchanalian appetites of ancient Rome caused a widespread incidence of gout among the aristocracy, including most of the emperors, and therein lies a strong clue, according to a Canadian researcher, that lead poisoning contributed to the fall of the Roman Empire.

When was the first case of gout? ›

Gouty arthritis was among the earliest diseases to be recognized as a clinical entity. First identified by the Egyptians in 2640 BC [1], podagra (acute gout occurring in the first metatarsophalangeal joint) was later recognized by Hippocrates in the fifth century BC, who referred to it as 'the unwalkable disease'.

Why is gout called a rich man's disease? ›

Gout has been dubbed a “disease of kings” or a “rich man's disease.” It gets those monikers because gout is often linked to a “rich” diet – one heavy on meat.

What is the number one thing that causes gout? ›

Drinking alcohol. The risk of gout is greater as alcohol intake goes up. Eating or drinking food and drinks high in fructose (a type of sugar). Having a diet high in purines, which the body breaks down into uric acid.

Which country has the highest gout rate? ›

The prevalence of gout is greater than 1% in most developed countries, including the USA (3.9%), Australia (5.2%), Canada (3.8%), Greece (4.75%), Germany (1.4%), and the UK (2.5%). However, the prevalence of HUA in Thailand and Bangladesh was 10.6% and 9.3%, respectively.

What is the spiritual root of gout? ›

In popular consciousness, developing gout was also a sign of spiritual superiority. This popular belief was clearly mentioned by the 16th century physician, Geronimo Cardano: “What a man gout makes! Devout, morally pure, temperate, (and) circumspect.

Is gout a lifetime? ›

Gout is considered a chronic disease, meaning it does not have a cure and will usually last your whole life. Gout comes in sudden, and sometimes severe attacks, also called flares, or flare-ups.

Is gout a disease from royalty? ›

Gout has been called the disease of kings because European royalty appears to have been disproportionately afflicted by the disease. Monarchs and other luminaries were described as having arthritic attacks that are strongly suggestive of gout attacks.

Can gout make you disabled? ›

It's unfortunate, but gout is not listed as an automatic qualifying condition on the SSA's list of disabling conditions. It is, however, listed as an associated condition with inflammatory arthritis. This means if your doctor diagnoses you with the latter illness, you can apply under that listing.

Can Covid trigger gout? ›

Abstract. Objectives COVID-19 vaccination often triggers a constellation of transitory inflammatory symptoms. Gout is associated with several comorbidities linked to poor outcomes in COVID-19, and gout flares can be triggered by some vaccinations.

What organ causes gout? ›

Normally, uric acid dissolves in your blood and passes through your kidneys into your urine. But sometimes either your body produces too much uric acid or your kidneys excrete too little uric acid.

Can gout affect the brain? ›

In this study, we found that patients with gout have thickening or thinning of cortical thickness in multiple brain regions that function in sensory processing, emotional processing, language understanding, hearing, etc.

Videos

1. Why Gout has Quadrupled Globally in 40 years: How to reverse it
(Dr Karl Goldkamp - Keto Naturopath)
2. The Sad Truth About Uric Acid & Gout - What You Need to Know
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3. Disease Management: Understanding Gout and Kidney Disease
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4. Detoxify Uric Acid From Kidneys – Uric Acid Gout & Kidney Stones – Dr. Berg On Kidney Cleanse
(Dr. Eric Berg DC)
5. In Virtuo Live w/ Dr. Randolph Sanchez "Clinical Management of Gout"
(In Virtuo)
6. Recent NICE Guideline Changes: Dr Jade Holway cover key updates
(Dr. Aman Arora - Arora Medical Education)

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