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.
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
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).
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.
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.
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
| Risk Factors | Triggers |
|---|---|
|
Genetics:
Other:
|
Dietary:
Drugs:
Other:
|
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.
| Variable | Clinical Score |
|---|---|
| Serum urate level >0.36mmol/L* | 3.5 |
| First metatarsophalangeal joint involvement | 2.5 |
| Male gender | 2.0 |
| Previous patient-reported arthritis attack | 2.0 |
| Hypertension or ≥1 cardiovascular disease | 1.5 |
| Joint redness | 1.0 |
| Onset within 1 day | 0.5 |
| Maximum score | 13 |
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 (eg, cardiovascular disease, renal failure, diabetes) managed.
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
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.
| Medicine | Advantages | Disadvantages | Dosage |
|---|---|---|---|
| Prednisone |
As effective as naproxen 500mg twice daily
|
Short-term increase in blood glucose for people with diabetes, usually in the afternoon Potential for short-term fluid retention and increased appetite |
0.5mg/kg for 5–10 days 40mg every morning for 5 days, then 20mg daily for 5 days is usually considered the “standard” dosage |
| NSAIDs | Effective |
Adverse effects, such as gastrointestinal bleeding, renal impairment and increased cardiovascular risk Avoid in renal impairment (eGFR <60ml/min/1.73m2); use a lower dose if eGFR 45–60ml/min/1.73m2 Avoid in people with heart failure or high cardiovascular risk, and 12–24 months after myocardial infarction There appears to be a tendency for patients to exceed the prescribed dosages due to the severe pain of gout |
Use at full dosage (e.g., naproxen 500mg twice daily) In people with creatinine clearance <60 ml/min, reduce dose and use with caution due to risk of renal failure, especially in Māori and Pacific peoples Minimise use to 5 days or less if possible Only prescribe or dispense small volumes (e.g., no more than 20 tablets) – experience indicates that diclofenac tablets are frequently shared; hence, there is risk of adverse effects in vulnerable people |
| Colchicine |
Specific for gout Effective when started early |
Preferable to start within 12–24 hours Toxic in overdose, which occurs with a small number of tablets and has resulted in deaths in New Zealand Dose reduction in renal impairment Potential interactions with cytochrome P450 3A4 inhibitors (diltiazem, macrolides, itraconazole, cyclosporin) and take care with statins Do not use in pregnancy |
1mg stat followed by 0.5mg every 6 hours; maximum of 2.5mg on the first day, 1.5mg on subsequent days (dosing reduced to 3 times daily), and no more than 6mg in 4 days Low-dose alternative: 1mg stat, followed by 0.5mg 1 hour later; a further 0.5mg may be taken once or twice daily for 2–3 days more (studies show 0.5mg twice daily is better than 3 times daily with fewer adverse effects) Dosage is reduced for people <50kg or who have a creatinine clearance <50ml/min: maximum dosage is 1mg in 24 hours, and no more than 3mg over 4 days |
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.
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 a couple of weeks.
Understanding some of the factors that result in stopping preventive therapy is important. These include:
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 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.
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.
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.
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.
| eGFR (ml/min/1.73m2) | Starting dose | Titration |
|---|---|---|
| >60 | 100mg daily | Increase by 100mg monthly |
| 30-60 | 50mg daily | Increase by 100mg monthly |
| 10-30 | 50mg on alternative days | Titrate 1-2 monthly (discuss with a rheumatologist) |
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.
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 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.
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.
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.
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.
Any drug–drug interactions should be checked, but some clinically important interactions are presented below.
Prednisone
NSAIDs
Caution is also required with selective serotonin reuptake inhibitors, including tramadol, due to the effect on platelet serotonin.
Colchicine
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
Febuxostat
Probenecid
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 appropriate 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, it would be helpful if the pharmacist discussed the importance of long-term adherence every time allopurinol is dispensed.
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.
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?
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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*New audit section*
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