IMMUNOLOGICAL MECHANISMS FOR THE DEVELOPMENT OF NONALCOHOLIC FATTY LIVER DISEASE IN PATIENTS WITH GOUT AND PSEUDOGOUT: A REVIEW OF LITERATURE

Abstract

The current ideas of gout include both the traditional metabolic theory of disorders of purine metabolism and environmental exposure and the involvement of immunoinflammatory factors in the pathological process. Inflammation is a hallmark of an acute tissue reaction to monosodium urate the crystals in gout and to calcium pyrophosphate crystals in pseudogout. The crystals interact with the membranes of plasma cells, with the activation of NLRP3, the proteolytic cleavage of pro-interleukin 1β, and the secretion of mature interleukin-1β that modulates a sequence of events leading to the activation of endothelial cells and neutrophils, which is also preceded by fatty degeneration of the liver. This review details recent data on the pathogenetic mechanisms that serve as predictors of metabolic changes and nonalcoholic fatty liver disease in patients with gout.

Keywords

• gout
• non-alcoholic fatty liver disease
• inflammation
• comorbidity