Gout ā An update of aetiology, genetics, co-morbidities and management
Introduction
Gout is a chronic urate crystal deposition disease. As patients accumulate urate crystals over time their risk of clinically manifest gout increases. Gout is not a disease that is only present during gouty flares, it is a chronic urate crystal deposition disease with flares being a symptomatic manifestation. This distinction is important as it justifies the effort to lower serum urate (SU) in patients to prevent symptoms and joint damage.
The challenges in gout care centre on diagnosis and introduction of treatment as well as maintaining adherence to urate lowering therapy (ULT). This review aims to both highlight important points in gout and provide an update since the last review of this topic in Maturitas [1].
Major papers in the field since the last published manuscript were reviewed and included if they were felt to be important to the understanding of gout or its management. Papers that marked significant changes in understanding or management from anytime were included if they sought to change long held beliefs or practice that takes an extended time to disseminate throughout the medical and scientific community. Specifically, Medline [via Web of Science] was searched from 2014 to 2018 with the topic term āgoutā (15,198 results) and restricted by āhighly sightedā and āhot papersā (73 results) which were then examined individually, initially by title and abstract review, then by full text review.
Section snippets
Aetiology
While gout has been considered by some in the past as a disease of excess and over-indulgence this view is increasingly being replaced by a more nuanced view [2]. When gout is viewed as a chronic disease of urate crystal deposition then its cause can be related back to an imbalance between urate intake/production and excretion leading to urate accumulation and crystallisation in tissues. This creates the environment for innate immune system activation and the resultant acute inflammatory state
Epidemiology
There is a steady increase in the prevalence of gout as men age with rates in elderly males well exceeding 10% in many cohorts [39,40]. Ethnicity also strongly influences gout prevalence with substantially higher prevalence rates of gout in groups like the New Zealand Maori, Pacific Islanders and Taiwanese. For example, in elderly New Zealand Maori the prevalence rate in males exceeds 40% [7]. Gout prevalence in woman is much lower until the menopause due to oestrogen causing urate loss in the
Diagnosis
The majority of gout is diagnosed and managed in primary care. In this setting the diagnosis of gout is usually made on clinical grounds, considering the age, co-morbidities, symptoms, clinical signs and laboratory results. However, the gold standard of diagnosis is joint aspiration demonstrating monosodium urate crystals on microscopy. Due to practical issues the majority of patients do not have joint aspiration. This is often due to lack of skills, lack of a polarising light microscope or
Co-morbidities
The co-morbidities of hypertension, chronic kidney disease (CKD), obesity and diabetes mellitus are common in gout patients [46,47]. CKD causes elevated SU. Many studies have demonstrated an association between gout and hypertension, diabetes and cardiovascular disease but there remains no convincing evidence that the presence of gout or raised SU contributes causally to these problems [48]. Some animal evidence has found causal relationships between raised SU and disease, for example
Treatment principles
Guidelines suggest the commencement of urate lowering therapy when people with gout have more than one flare per year, see Table 4 [59]. When treating gout with ULT it is important that the patient is aware that you are trying to deplete their body of urate crystal deposition. As such a long term, lifelong approach is required.
Patient education
It is increasingly being recognised that patient education is an important part of gout management. If patients understand that gout is a chronic disease that requires
Summary
There has been substantial progress in the strategies for the clinical management of gout, including a safer strategy for commencing allopurinol, a greater emphasis on prophylaxis of acute gout flares whilst commencing ULT and a strong focus on treating SU to target for effective gout management. This all demonstrates significant progress in managing this long neglected disease which has a huge impact on patients. There remains a number of important unanswered questions in the field, including
Contributors
Philip C. Robinson was the sole author.
Conflict of interest
The author has received research funding from AstraZeneca and speaking fees from AstraZeneca and Menarini.
Funding
No funding was received for the preparation of this review.
Provenance and peer review
This article has undergone peer review.
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