A review of uric acid, crystal deposition disease, and gout

Abstract

There has been increased interest in gout in both academic and clinical practice settings. Several reasons may explain this. The prevalence of both hyperuricemia and gout has risen in the last decades in developed countries and therefore the burden of gout has increased. The association of hyperuricemia and gout with cardiovascular outcomes and the opportunity of further benefits of intervention on hyperuricemia have been recently highlighted in the literature. Imaging techniques have proven to be useful for detection of urate deposition, even prior to the first clinical symptoms, enabling the evaluation of the extent of deposition and providing objective measurement of crystal depletion during urate-lowering treatment. Treating to target is increasingly used as the approach to treatment of diverse diseases. Therefore, different targets have been recommended for different stages of the burden of disease and for different stages of treatment. The final strategic target, to which any effort should be taken into consideration, is to completely dissolve urate crystals in tissues and therefore avoid further symptoms and structural damage of involved musculoskeletal structures. In summary, evidence suggest that an early approach to the treatment of gout and associated comorbidities is advisable, that new imaging techniques may help to evaluate both the burden of deposition and response to urate-lowering treatment in selected patients, and finally that the final strategic objective of healthcare for patients with gout is to completely resolve urate crystal deposits.

Fig. 1

Diagram showing the path from hyperuricemia to structural joint damage. Long-standing hyperuricemia may lead to monosodium urate deposits, with no symptoms and sometimes associated to subclinical inflammation; intermittent acute inflammation is caused by crystal shedding into the joint space, inflammation persisting between flares, bone erosions may appear; untreated or improperly treated deposition will lead to further persistent inflammation, increase in the number of flares and structural joint damage with permanent joint space narrowing

Fig. 2

Three-dimensional volume rendered reconstruction of a dual-energy CT scan of the right foot in a patient with tophaceous gout, demonstrating the extent of urate crystal deposition throughout the foot, and particularly at the 1st metatarsophalangeal joint and Achilles tendon. Urate crystals are shown in green

Fig. 3

Two-dimensional DECT sagittal image demonstrating urate crystal deposition within an erosion at the 1st metatarsophalangeal joint in a patient with tophaceous gout. Urate crystals are shown in green