Beyond medicines for gout

21 minutes to Read
30 September 2021
Gout Image Test
It is important for healthcare teams to be proactive and talk about gout and the impact it has on work, recreation and relationships.

Linda Bryant discusses gout, a chronic long-term condition that is often associated with other diseases, and with drug-related morbidity and mortality. As such, it needs to be addressed holistically as part of the psychosocial medical model.

Key points

  • Acceptance of the need for long-term treatment with allopurinol is important, so patients do not depend on short-term NSAIDs.
  • Allopurinol should be discussed at the first gout flare, and strongly recommended at the second; there is no need to wait for two gout flares annually.
  • A primary risk factor for gout is genetics – diet only plays a minor role.
  • Gout and variation in its treatment contributes to inequity.
  • Gout occurs earlier and is more severe in Māori and Pacific peoples than in non-Māori/non-Pacific peoples, so more prescribing of urate-lowering therapy, earlier, is needed to achieve equitable care.

Gout is not a benign medical condition. In addition to debilitating pain and potential long-term erosive effects on the joint, and an association with cardiovascular and renal comorbidities, there is a large impact on the social, psychological and spiritual wellbeing of the affected person and their whānau. Furthermore, there are persistent inequities because of poorly managed gout in populations that have higher prevalence of this serious condition. As there is primarily just the one medicine for controlling gout, the number of people with gout flares is helpful as a primary care quality indicator.

New Zealand has one of the highest prevalences of gout internationally.

About 208,000 or 5.7 per cent of people aged 20 or older are identified as having gout, according to 2019 New Zealand data. Gout was identified in 8.5 per cent of Māori people, close to twice that of non-Māori, non-Pacific peoples (4.7 per cent) and in 14.8 per cent of Pacific peoples, nearly three times that of non-Māori, non-Pacific peoples. Notably, fewer women than men experience gout, but Māori and Pacific women remain disproportionately affected compared with non-Māori, non-Pacific women.1

Gout prevalence increases with age. Eighteen per cent of non-Māori, non-Pacific men aged 65 or more years are estimated to have gout; however, this proportion increases to 35 per cent for Māori and 50 per cent for Pacific peoples in this age group.1

Belief – "Gout is just an old person’s disease".

Rates of regular dispensing of preventive gout medicines are very low across all ethnicities – only 36 to 43 per cent of people with gout in 2019 – and worse in young people.1 Māori and Pacific peoples are more likely to be affected by severe gout, early onset gout, tophaceous disease and accelerated joint damage than non-Māori, non-Pacific peoples.2 Additionally, over 2016–2020, they started preventive gout medicine, on average, 10–13 years earlier than non-Māori, non-Pacific peoples.3 However, given the much higher gout disease burden, this time gap may be too narrow, and Māori and Pacific peoples should perhaps be starting their gout preventive treatments even earlier to achieve equitable care.

Gout flare symptoms can be improved with NSAIDs but repeated courses of these in the absence of urate-lowering therapy can indicate poor care especially because of the potential for kidney disease and development of tophi.4 NSAID dispensing without any urate-lowering therapy has consistently decreased over time for Māori and Pacific peoples, while rates for non-Māori, non-Pacific populations have not changed.

However, overall, 41 per cent of Māori and 46 per cent of Pacific peoples with gout were dispensed an NSAID, compared with 35 per cent of non-Māori/non-Pacific peoples diagnosed with gout. Younger people, particularly Māori and Pacific peoples, were dispensed NSAIDs at significantly higher rates.1 Treatment with repeated prescriptions of NSAIDs can be a poor and potentially dangerous stopgap.4

Despite these sobering figures, we still have not achieved optimal care. Although a reduction over time has been seen in hospital admissions for the general population for gout, Māori and Pacific peoples are about 5 and 10 times, respectively, more likely to be hospitalised with a primary diagnosis of gout, relative to non-Māori, non-Pacific people.1

I had to go from working outside to working inside in a factory job…the gout was always there, eh. Sometimes, I went to work with no boot. Boy, if you got caught though! I didn’t want to miss work though, especially the overtime, eh.

Well, it does impact on your whānau. They know I’m grumpy, and they know to stay clear. They’re like, ‘oh no, here we go again’. It really impacts on the relationship side of things.

Quotes from Te Karu L, Bryant L, Elley CR (J Prim Health Care 2013;5[3]:214–22).


Pathophysiology – it’s not lifestyle


Usually, the first strong community belief to dispel is that having gout is the person’s fault because they have been eating the wrong food or drinking a little alcohol. There is a very strong genetic basis for hyperuricaemia, which is the cause or driver for gout. Māori and Pacific peoples typically have a genetic predisposition for gout, and when discussing the diagnosis, most Māori or Pacific men with gout will say they have relatives with gout. Conversely, those without gout will say they do not have any relatives with gout.

Belief – “It’s my fault because I eat the wrong stuff.”

It is vital to dispel beliefs about certain foods being the cause of gout and explain that some foods may be a trigger. If someone changes their diet, often by restricting foods that are culturally important, such as seafood, and still gets gout, they may feel frustrated and guilty, as though it is their fault for not being “good”. Changing diet alone rarely prevents gout flares.

The genetic predisposition is complex with different polymorphisms, but the end result is that, for some people, high serum urate levels result in precipitation of uric acid crystals in the cartilage, tendons, ligaments and, in the longer term, the larger joints.

Hyperuricaemia is due to increased production of uric acid by the liver and/or reduced renal or, to a lesser extent, non-renal excretion. Gout is primarily a result of the under-excretion of uric acid. Not all people with hyperuricaemia experience gout attacks.

Gout is a chronic inflammatory disease and inadequate treatment to reduce serum urate levels can lead to tophi (monosodium urate crystals deposited in soft tissues around joints), chronic gouty arthritis and joint destruction. Unfortunately, we still see people with tophi, which indicates poor control of serum urate for more than 10 years.

Urate-lowering treatment (eg, allopurinol) initiated early and used regularly and consistently, rather than lifestyle and dietary changes, will help patients achieve long-term symptom control.

Although the principles for treating and preventing gout appear relatively simple, it seems that we are not doing at all well. The answer is not as simple as “we need to prescribe more”, and it is not helpful to hear the rationale for poor control being “patients just don’t take their allopurinol”. We can do better, though it may require a different approach.

Interventions that promote patient education and follow-up appear successful. University of Auckland investigators conducted a systematic review of international studies that looked at outcomes of 18 interventions attempting to improve urate-lowering treatment uptake in patients with gout.5 These interventions were beyond the usual care provided in primary care and included six nurse-led, five pharmacist-led and seven multidisciplinary, multifaceted interventions. Improvement in serum urate levels was seen for all interventions, but nurse-led interventions appeared most effective. These included investigating beliefs and perceptions about gout and its management, patient education, reminders for urate level tests and prescription refills, and monitoring until target urate levels were achieved. Patient education encouraged shared decision-making and provided information on the nature of gout, its causes and consequences.

Access is an issue, but it is broader than this, and a holistic model of care is required that involves the community, greater co-design and perhaps social marketing (eg, sporting heroes advocating for taking allopurinol). Māori and Pacific men may benefit from messaging that enhances mana, empowering them to continue taking allopurinol regularly to prevent recurrent gout attacks.

There needs to be emphasis on the important role of whānau in encouraging and helping their men to engage with the health system about screening for, or managing gout. Healthcare professionals can actively encourage and expect and answer questions from whānau. Involvement of whānau and health promotion in the community both greatly contribute to improved health literacy.


Triggers for gout


Genetics and ethnicity are key risk factors for gout, along with increasing age, and male gender (Table 1). Dietary triggers for acute gout flares include foods containing high levels of purine, such as shellfish and red meat, and also alcohol – these promote the formation of lactic acid and block renal urate excretion.

More recently, fructose (used ubiquitously, but significantly as a sweetener in sugar-based beverages or fizzy drinks) has been shown to inhibit the SLC2A9-mediated renal excretion of urate. Men who consumed two or more servings of sugar-sweetened drinks per day were found to increase their risk of gout by 85 per cent compared with those who consumed less than one serving monthly. Compare this with the 49 per cent increase in risk from ingesting 15–30g of alcohol per day.6

Minor trauma and emotional or medical stress may also trigger gout. Some people may think they incurred an injury such as a sprained ankle (eg, after playing sport), but it is important to remember that injury can trigger gout.

There is debate about the significance of potential diuretic-induced gout, due to possible confounders. The effect is usually delayed, and the serum urate level may be increased by the diuretic. There may be an over-estimation of effect.7 Diuretics are not contraindicated in people with gout but would not usually be first-line blood pressure-lowering agents in people with, or at high risk of, gout. Individual benefit–risk implications should be considered. Low-dose aspirin can cause changes in renal excretion of urate, with up to a 0.01mmol/L increase in serum urate level within one week, but this effect is variable and usually very small.8 An adjustment of urate-lowering therapy may be required, but discontinuation or avoidance of low-dose aspirin is usually not necessary.

Allopurinol may be less effective in people on furosemide,9 but this is usually overcome by increasing the allopurinol dose.

Table 1. Risk factors and triggers for gout
Click on table to enlarge

Diagnosis


The symptoms of gout are usually clear – severe throbbing or burning pain, swelling, redness and a warming of the area affected. Touching or weight-bearing can result in excruciating pain. Flares classically occur in the big toe, but ankles, knees, elbows and fingers may be affected over time. These symptoms, coupled with ethnicity and/or family history, usually provide a good basis for a clinical diagnosis.

Forms of arthritis that may mimic gout include septic arthritis, psoriatic arthritis, pseudo gout (calcium pyrophosphate or calcium phosphate arthritis), reactive arthritis or osteoarthritis as people get older, so an accurate diagnosis is important and requires ongoing review. If you can touch or press on the area without the person indicating pain, then review the diagnosis.

Although considered a gold standard, joint aspiration is usually only performed when there is doubt about the diagnosis, and particularly if septic arthritis is suspected.

Care is required to determine that gout that has “moved to the knee” is not osteoarthritis. If a patient with previously well-controlled gout and optimal serum urate levels presents with frequent “gout” in a large joint, it is important to review them for osteoarthritis or another joint disease.

Laboratory testing for serum urate concentration at the time of a gout flare will produce a lower serum urate result, by as much as 10 per cent, and approximately 40 per cent of patients will have a level within the normal range. A high serum urate level will help confirm gout, but a lower level does not discount it.

Ideally, serum urate levels should be measured at least four weeks after an acute flare. However, for many people, getting a test four weeks after an acute flare becomes a lower priority, so the blood test is unlikely to be done.

A systematic review, plus earlier primary care studies, has generated a scoring system to aid the diagnosis of gout (Table 2). A score of 8 or more meant gout was confirmed in 80 per cent of cases.10,11 This table is from the US. In New Zealand, a patient of Māori or Pacific ethnicity would have one to two points added when presenting with unilateral joint pain, given the very high prevalence of gout in these populations.

Table 2. Clinical score to increase pretest probability of gout diagnosis
Click on table to enlarge

For some people, if there is uncertainty about the diagnosis, a dual-energy CT scan detecting urate in the joints will confirm diagnosis of gout.

It is important to recognise that gout is associated with comorbidities, including metabolic syndrome, which is estimated to be present in 63 per cent of people with gout, compared with 25 per cent of people without gout.12

Also, 40 to 74 per cent of people with gout will have high blood pressure.13 Approximately one-quarter of people with gout will have diabetes, and approximately 70 per cent will have a creatinine clearance of less than 90ml/min. People with gout have an increased risk of death from cardiovascular disease.14

Hyperuricaemia and the above comorbidities are individually associated, and causation is debated. There are many clinical studies underway, but there is currently no clear recommendation to treat asymptomatic hyperuricaemia. However, other risk factors should be treated.

The multifaceted nature of gout, and the fact it rarely exists in isolation of comorbidity, are reasons why care for people with gout needs to be holistic rather than fragmented and siloed. A person presenting with gout needs to be screened and have other potential comorbidities managed (eg, cardiovascular disease, renal failure, diabetes).


Acute treatments


Belief – “I just need something to get rid of the pain when I have an attack, and then it’s all okay.”

The choice of acute medicines therapy – prednisone, an NSAID or colchicine – is influenced by comorbidities as there is little difference in effectiveness between the medicines (Table 3).15,16

The maximal dosage and hazards of excessive colchicine need to be stressed to avoid the acute toxicity likely to result from a “more is better” perception. In the Auckland area, a case series found eight people died of a colchicine overdose over 15 years, with doses between 18mg and 24mg.17

Belief– “The Voltaren tablets don’t hurt me – they get rid of the pain.”

A 2020 New Zealand study identified that, after adjusting for other risk factors, Māori and Pacific peoples were significantly more likely than European patients to be hospitalised with serious complications after being dispensed NSAIDs.18 Rate ratios for hospitalisation due to upper gastrointestinal bleed for Māori and Pacific peoples were 2.54 and 3.17, respectively, compared with European patients and rate ratios for hospitalisation due to heart failure were 2.48 and 1.97, respectively. The rate ratio for risk of acute kidney injury for Māori compared with Europeans was 1.46. The higher risk of upper gastrointestinal bleed and heart failure in Māori and Pacific peoples was more evident in males and people aged less than 60.

This study highlights the need to be especially wary of prescribing NSAIDs in Māori and Pacific peoples who have an estimated glomerular filtration rate (eGFR) that is lower than would be expected for their age.

Table 3. Advantages and disadvantages of medicines for acute gout flares
Click on table to enlarge

Preventive medicines


Preventive medicines include allopurinol and febuxostat, which inhibit xanthine oxidase, the enzyme that catalyses the conversion of purine to xanthine, before it is converted to uric acid. Probenecid and benzbromarone increase the excretion of uric acid, although benzbromarone is no longer available in New Zealand. And the two biologics not readily available in New Zealand, rasburicase and pegloticase, promote the conversion of uric acid to allantoin, which is then excreted.

Allopurinol is still the first-line preventive urate-lowering medicine in New Zealand and internationally.

Belief – “You need two gout flares a year before you consider allopurinol.”

In our high-risk population of Māori and Pacific peoples, preventive urate-lowering therapy should be discussed when someone presents with their first gout flare, and strongly recommended after the second flare. New Zealand and international studies have found urate-lowering therapy, although indicated, is often delayed, sometimes for a period of several years following symptom appearance.19 For the majority, and especially Māori and Pacific people with a family history, gout is not going to go away, and every flare will be causing damage to the joints. Māori and Pacific peoples also require a full assessment for comorbidities.

The resistance to taking a lifelong tablet is understandable. Patients often stop and restart allopurinol several times. Patience is required, especially as the process requires slow titration with each restart if the patient stops taking allopurinol for more than one month. If they stop for less than one month, then the previous dose can be restarted.

Belief– “Taking tablets every day means I am sick and weak.”

Understanding some of the factors that result in stopping preventive therapy is important. These include:

  • difficulty developing a medicines-taking habit
  • beliefs and attitudes to medicines
  • misunderstanding of the need for lifelong therapy
  • wanting to “test” if allopurinol is still needed
  • confusing preventive therapy with acute therapy.

Studies have found that people take allopurinol only about 62 per cent of the time.20 Those who are younger and those who do not take other regular medicines are less likely to take their allopurinol.

This emphasises that it is not necessarily the prescribing of allopurinol that is the issue. It is imperative that ongoing, consistent advice and education is given, addressing the individual’s concerns. Ensure medicine and lifestyle conversations/interventions happen at distinct times in the patient/whānau journey: at initiation, flare occurrences, and when working towards stabilisation on long-term treatment.

There is much to consider when encouraging people to take allopurinol life-long. Rather than just giving information, advice and instructions, it is important to develop a relationship with the person - determine their beliefs, values and understanding, and the factors that may reduce the likelihood of taking allopurinol continuously.

The Ask Build Check tool (smstoolkit.nz/ask-build-check-model) may also be helpful. This model comprises three steps: ask what the person knows, thinks, believes or does; build new information onto what is already known, and check how clearly and effectively you have communicated.


Allopurinol


Initiation

Traditionally, allopurinol has been started once an acute flare has resolved. This required the person to remember not only to start the allopurinol but also the instructions for titration. This requirement plus the need to take prophylactic medicine, such as a low-dose NSAID or colchicine, for at least three months could be seen as confusing and inconvenient. Further, it could lead to people forgetting to start allopurinol after the acute flare, or thinking it unnecessary because the gout is “cured”. Initiation of allopurinol usually requires three prescription fees: for the allopurinol, the prophylactic medicine, and the treatment for the acute flare.

Belief– “You can’t start allopurinol during an acute gout flare.”

Delaying the initiation of urate-lowering therapy until a flare is no longer painful is only supported by scant evidence. A meta-analysis found moderate-quality evidence that initiation of urate-lowering therapy during an acute gout flare did not increase pain severity,21 and other studies included in the American College of Rheumatology 2020 gout management guidance have found that initiating a urate-lowering treatment during a flare has no significant impact on the duration of the flare or its severity.22

Initiating allopurinol along with prophylactic medicine increases complexity, but using blister packaging for the first three months of therapy is very helpful for managing acute treatment, titration of allopurinol and short-term use of prophylactic medicine. The importance of education and advice, even with blister packaging, cannot be underestimated.

It is imperative patients accept the need for long-term treatment with allopurinol and not depend on short-term NSAIDs. Learning this acceptance takes time and can be a challenging process for the patient and their whānau. A few false starts along the way are likely before the lifestyle or behaviour change has been achieved. Multiple health professionals and community care workers can support interventions that involve patient engagement. These must empower patients to share decisions about their care and make the sustained behavioural changes required to take long-term medication and accept and adapt to living with a long-term health condition.

Dosing

Gout flare reduction is on a continuum of serum urate levels, but the target that provides a good balance between gout flares and pill burden is less than 0.36mmol/L, and less than 0.30mmol/L if the patient has tophi. Ideally, the main clinical outcome of urate-lowering therapy is no gout flares, although if gout does occur, it is less frequent and less severe. Some people may require lower serum urate levels to prevent gout flares, while others may avoid gout flares at slightly above the target level.

Allopurinol starting dose is based on renal function (Panel 1) and is equal to 1.5mg allopurinol per unit of eGFR, rounded to a convenient dose. Monthly titration is an easy way to remember the dosing increases and reduces the risk of both a gout flare and allopurinol hypersensitivity syndrome (AHS).19

Traditionally, the dosage of allopurinol was considered to be 300mg daily. However, in New Zealand, to achieve a target serum urate level of less than 0.36mmol/L, a mean dosage of 360mg daily, or median dosage of 450mg daily, is required.

The maximum dosage of allopurinol is 900mg daily, but specialist advice is recommended if a dosage greater than 600mg daily is required to achieve the target serum urate level, as there are possible explanations other than gout, or an alternative medicine may be required.

Panel 1 | Allopurinol initiation

Dosing

Table Four

Prophylactic cover
  • NSAID at half dose (eg, naproxen 250mg twice daily for six months).
  • Alternatively, colchicine 0.5mg once or twice daily for six months depending on renal function. Note this is off-label (unlicenced) use.
  • Stop if a rash occurs (2-4% risk of minor rash; 0.4% due to hypersensitivity).
Starting during a gout flare

Use prednisone to treat the acute flare for five to 10 days. In people with diabetes, balance the risk of a short-term increase in blood glucose with the corticosteroid (usually in the afternoon) against the risks of taking NSAIDs, as to which is preferred.

Prophylactic cover

If someone starts allopurinol and a gout flare is precipitated, it is very difficult to convince them to restart allopurinol as, in their mind, it becomes associated with causing gout. Therefore, prophylactic cover is needed when initiating allopurinol (eg, colchicine 0.5mg daily or an NSAID, such as naproxen 250mg twice daily).

Without prophylactic cover, approximately two-thirds of people will experience a gout flare when starting allopurinol. With prophylaxis, the risk of a flare is reduced to 20 to 30 per cent. One study found that colchicine prophylaxis reduced the number of gout flares from 2.9 to 0.5 in the three months after initiation of allopurinol.23

This is an off-label (unlicenced) use of colchicine, but for people in whom NSAIDs should be used cautiously (renal impairment, high cardiovascular risk, history of peptic ulceration), it is effective cover. However, it needs to be clear that one colchicine tablet daily is preferred, and two tablets daily should not be exceeded.

Prophylactic cover needs to be continued for at least six months, or for three months after achieving target serum urate levels.

Monitoring

Monitoring serum urate levels for dosing adjustment is inconvenient. Further, in New Zealand, the median dosage of allopurinol required to achieve a serum urate level of less than 0.36mmol/L is approximately 450mg daily. Thus, titrating the allopurinol monthly to 300mg daily and then checking serum urate is easier for patients who find it difficult to access testing.

Once at the target serum urate level, periodic checks are usually helpful for adherence to therapy, though gout flares will usually indicate poor adherence. Finger-prick testing for serum urate levels may be available in some pharmacies and general practices.

Adverse effects

Allopurinol is usually well tolerated. AHS is the most concerning adverse effect, due to a mortality of approximately 25 per cent. It is estimated to occur in 0.1 per cent of people, although this is variable in different populations due to genetic variation. It is more common in the Han Chinese population, in which genetic testing is recommended before starting allopurinol.

AHS is a delayed hypersensitivity reaction, usually occurring within 30 days, and with 90 per cent of cases occurring within 90 days.24 It presents as a toxic epidermal necrolysis or Stevens–Johnson syndrome-type rash with fever, eosinophilia, leucocytosis and possibly hepatic and renal dysfunction.

It was once thought that impaired renal function increased the risk of AHS due to an increase in the allopurinol active metabolite, oxypurinol. This is no longer the case as no association between oxypurinol concentration and AHS has been found.

Belief – “Allopurinol dose is limited by renal function.”

Renal function is still important, but this is to establish the starting dose of allopurinol. Starting at a high dose, or titrating too quickly, can increase the risk of both gout flares and AHS.19,24 The final dose of allopurinol is now the dose that achieves a serum urate level of less than 0.36mmol/L, rather than a maximum dose according to renal function. Once the optimal allopurinol dose is obtained, there is no need to reduce the dose if renal function declines.

There are non-AHS rashes that may occur in approximately 2 per cent of people, but the risk of AHS means anyone with a rash should seek immediate advice.


Other urate-lowering medicines


Febuxostat is similar to allopurinol in its mechanism of action. The dosing regimen is a starting dose of 80mg daily, increasing to 120mg daily after four weeks if the target serum urate level is not achieved. Avoid treatment with febuxostat in patients with pre-existing major cardiovascular diseases (eg, myocardial infarction, stroke or unstable angina).25

Losartan is not a specific urate-lowering agent but may reduce serum urate levels by approximately 0.02–0.04mmol/L. It works by inhibiting the renal urate transporter URAT1, hence increasing urate excretion.26,27 If an ACE inhibitor or angiotensin II receptor blocker is being considered for a patient with gout, then losartan may be preferable. Similarly, atorvastatin and empagliflozin may be helpful adjuncts, but it is important to remember they are not treatment per se.

Other preventive therapies are available. Consult a rheumatologist if the patient does not tolerate allopurinol or if allopurinol has not been effective.


Interactions


Any drug–drug interactions should be checked, but some clinically important interactions are presented below.

Prednisone

  • NSAIDs – increased gastrointestinal bleeding risk.

NSAIDs

  • Medicines that increase the risk of bleeding, such as antiplatelets (aspirin, clopidogrel, ticagrelor) and anticoagulants (dabigatran, rivaroxaban, warfarin).
  • Prednisone – increased gastrointestinal bleeding risk.
  • ACE inhibitor or angiotensin II receptor blocker plus diuretic combinations should be avoided.
  • The effect of blood pressure-lowering medicines may be reduced.

Caution is also required with selective serotonin reuptake inhibitors, including tramadol, due to the effect on platelet serotonin.

Colchicine

  • CYP3A4 inhibitors (eg, itraconazole, diltiazem, verapamil, macrolides).
  • P-glycoprotein inhibitors (eg, cyclosporin).
  • Statins, especially simvastatin, may have a pharmacodynamic interaction.

Care is required with statins as there are reports of colchicine toxicity and there is an increased risk of myopathy (pharmacodynamic interaction). If colchicine needs to be used with a statin, use the low-dose colchicine regimen.

Allopurinol

  • Azathioprine and 6-mercaptopurine - the dose of azathioprine needs to be reduced with specialist advice.
  • Warfarin.
  • Diuretics - a higher dose of allopurinol is likely to be needed.
  • Theophylline.
  • Penicillins - there may be a small increased risk of a penicillin skin rash.

Febuxostat

  • Azathioprine and 6-mercaptopurine - the dose of azathioprine needs to be reduced with specialist advice.

Probenecid

  • Methotrexate (increased concentrations).
  • Penicillins and cephalosporins (increased concentrations).


How can we do better?


While gout is a “canary in the mine” for cardiovascular disease, it is a health condition for which inequity pervades. Māori and Pacific peoples are much more likely to get gout (genetic prevalence). In these populations, it is also a more severe health condition, occurring at an earlier age with a greater burden of pain, frequency of pain, and sequelae. Therefore, earlier detection of gout and initiation of preventive treatment is needed.

Nevertheless, Māori and Pacific peoples are less likely to be able to access care, to be prescribed appropriate medicines, to be followed up and to be provided with understandable education.4,18

Initial explanation about gout and the long-term nature of complications and treatments is important, plus the emphasis that allopurinol treatment is for life. This should be reiterated at each appointment. Some practices are starting the concept of shared medical consultations for gout. Practices with health improvement practitioners and health coaches may find these people can get engagement and provide good understandable information.

Community pharmacists’ input can be of particular value with this latter point of understandable education. As well as explaining the role of prophylactic cover when allopurinol is initiated, every time allopurinol is dispensed it would be helpful if the pharmacist discussed the importance of long-term adherence.

Work by Leanne Te Karu (Muaūpoko/Whanganui), PhD candidate at the University of Auckland, and colleagues has identified many barriers involving the system. A multifaceted, multidisciplinary and culturally driven model of care is being investigated to improve the delivery of care for gout, as an example, and then ultimately holistic healthcare (personal communication).

As healthcare providers, being proactive and talking about gout and the impact it has on work, recreation and relationships is important. All members of the team can contribute, including GPs, pharmacists, nurses, physiotherapists, podiatrists and the kaiāwhina workforce. We all need to give consistent advice (Panel 2) and recognise barriers to access – often not a lack of prescribing but the ongoing, patient and whānau-centred encouragement and reinforcement that is required.

Panel 2 | Considerations and patient resources

Keep front of mind:
  • Try to improve access to regular dispensing of preventive gout medicine (persistence and adherence).
  • Help people to accept and stick with allopurinol to prevent recurrent attacks.
  • Reduce inappropriate prescribing and use of NSAIDs.
  • Earlier detection and initiation of preventive treatment is important, particularly for Māori and Pacific peoples.
  • Women are also affected by gout.
  • Gout may present as a traumatic injury.
Provide consistent advice:
  • Gout is caused by genetics – it runs in the family. Dispel beliefs about food and alcohol being a major cause. Food is just a trigger.
    • Once on allopurinol and the serum urate level is at target, small amounts of trigger foods may be eaten.
    • Even if gout is controlled, do not drink sugar-sweetened drinks, such as fizzy drinks and high-fructose drinks, as they reduce excretion of urate.
  • Do not take more than the maximum doses of tablets prescribed, even when there is a gout flare.
    • Explain about the risks of excessive doses of NSAIDs and colchicine.
    • Do not give or lend medicines for gout to friends, whānau or neighbours because people with some medical conditions may be harmed by the medicines.
  • Allopurinol titration takes three to six months, and an extra medicine is taken during initiation of therapy but is stopped when the serum urate level is at target.
    • Confirm what the target serum urate level is and how this is monitored.
    • So that there are realistic expectations, explain that flares may still occur in the first year of treatment, but these reduce over time and are less severe.
    • Advise not to stop allopurinol, even during an acute flare.
    • Explain that treatment with a preventive therapy is lifelong – stopping the medicine will cause the serum urate level to increase again.
  • Describe the symptoms of allopurinol hypersensitivity syndrome, especially the rash, and the importance of stopping the allopurinol and seeing a doctor immediately for a blood test to confirm the diagnosis.
  • Provide written information amd a website link for patients to find out more.
Resources for patients:
Free support and advice are available to people who want to talk about their gout. They can call Arthritis New Zealand educators on 0800 663 463 or fill out an online form to request a call back.

And here's a challenge: start with an audit of all people in your practice with a diagnosis of gout, plus those who have been prescribed allopurinol or colchicine. What are their serum urate levels? How much prednisone or NSAID have they received in the last 24 months? What can you do to improve the management of gout for these people?

Dr Linda Bryant is a prescribing pharmacist working in two general practices: Newtown Union Health Service, Wellington, and Porirua Union and Community Health Service. Her focus is on inequity, particularly around long-term conditions such as cardiovascular disease, diabetes, respiratory diseases and gout.

Professional development - Assessments for pharmacists, GPs and nurses

Pharmacists - a set of CLASS reflection and peer group guides has been prepared for you in relation to this article and is available for download here.

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This activity is endorsed by the College of Nurses Aotearoa (NZ) Inc for 60 minutes' professional development (CNA084).

This activity has been endorsed by the Pharmaceutical Society of NZ Inc (PSNZ) as suitable for inclusion in a pharmacist’s CE records for Continuing Professional Development (CPD) purposes.

This activity has been endorsed by The Royal New Zealand College of General Practitioners (RNZCGP) and has been approved for 1 CME credit for Continuing Professional Development (CPD) purposes. To claim your credits, log in to your RNZCGP dashboard to record this activity in the CME component of your CPD programme.

Professional College Endorsements

References

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  3. Ministry of Health: Pharmaceutical Collection. People starting preventative gout medication for the first time between 1 June 2016 and 30 June 2020 aged 15+ years. https://tinyurl.com/hlthstats
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