Gout, Hyperuricemia and Psoriatic Arthritis: An Evolving Conundrum.

Abstract

Purpose of review: The co-existence of gout and psoriatic disease (PD) is long standing but more recently frequently encountered in clinical settings due to increased awareness of their shared comorbidities and clinical phenotypes, often posing diagnostic and management challenges. Here we review the overlap in gout and PD focusing on shared clinical features, common inflammatory pathophysiology and comorbidities which may prompt a diagnosis of 'Psout' and lead to changes in management.

Recent findings: Several epidemiological studies have highlighted the increased incidence of hyperuricemia and gout in those with PD and vice versa. Although the role of monosodium urate (MSU) crystals is well recognized in activation of innate immunity via inflammasome and NETosis, it is likely that they have a role in triggering adaptive immunity via antigen presenting cells and their autocrine effect on keratinocytes in psoriasis (PSO), ultimately leading to T cell secretion of proinflammatory cytokines such as IL17. Hyperuricemia (HU) is common in PD (up to 30%) and underpins metabolic syndrome comorbidities that are common to both gout and PD. Shared clinical phenotypes and co-morbidities are routinely observed in clinical practice yet there is a paucity of evidence evaluating the effect of treating hyperuricemia/gout on PD activity, with small scale clinical trials showing a positive effect. There were no studies to our knowledge assessing gout disease activity with concurrent treatment of PD. The association between gout and PD is likely due to shared multimorbidity and perhaps to a smaller extent, the direct role of HU in triggering the release of proinflammatory cytokines in PD. There is often a significant overlap in clinical and radiological presentation of gout and Psoriatic arthritis (PsA). In those with atypical response to standard treatments of the primary condition (either gout or PsA), it would be plausible to investigate and treat for the other 'secondary' condition. This is particularly relevant and relatively feasible in those with PsA (and features of HU and multimorbidity) who respond poorly to standard immunomodulating treatments.