1 October 2011

Gout is an extremely painful recurring arthritic disease affecting a great number of New Zealanders, and is the main focus of the Arthritis & Inflammation Group, led by Dr Jacquie Harper.

Gout is caused by the build-up of crystals of uric acid in the joints, which trigger an inflammatory immune response.  It is this immune response that is responsible for the swelling, heat and intense pain felt in the affected joint.

The main risk factor for gout is hyperuricaemia or high levels of uric acid in the blood. Hyperuricaemia can occur for a number of reasons including genetics, poor renal function or excessive cell death following injury. In 20% of hyperuricaemics, uric acid crystallises in the extremities resulting in gout. 

Acute gout is the most common form of the disease, where an individual will often go to bed feeling fine, but wake in the morning with a painful swollen toe that stays that way for up to two weeks.  If acute gout doesn’t self-resolve, it can progress into tophaceous gout – a crippling and debilitating condition where excessive crystal build-up can lead to irreversible joint damage. 

Dr Harper’s research is currently focussed on understanding how the immune system reacts to these crystals.  Previously it was believed that particular immune cells called monocytes enter the inflamed joint and change into cells that resolve inflammation.  However her team has now shown that these cells in fact develop into proinflammatory macrophages and are primed to exacerbate inflammation in the presence of ongoing crystal deposition in the joint.  Their work suggests that these monocytes might be an effective drug target for future therapies aimed at easing the pain of acute gouty arthritis. 

Call for volunteers for gouty arthritis clinical study

Dr Harper’s research group are undertaking a gouty arthritis clinical study in collaboration with Wellington Rheumatologists Dr Andrew Harrison and Dr Rebecca Grainger, and they are currently seeking volunteers. 

This study builds on previous clinical work published by this team in the Journal of Rheumatology last year, which revealed vital information showing that hyperuricaemia may increase inflammatory immune responses to the uric acid crystals.  Gout patients about to commence urate lowering therapy are now being recruited for a follow-up clinical study that will investigate the effects of lowering blood uric acid levels on their inflammatory immune response to uric acid crystals. 

Please contact Dr Harrison on [email protected] if you would like information on how to be involved in this study.