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.