Michael H Ellman1, Michael A Becker. 1. University of Chicago, Pritzker School of Medicine, Rheumatology Section, Department of Medicine, University of Chicago Medical Center, Chicago, Illinois 60637, USA.
Abstract
PURPOSE OF REVIEW: To highlight recent investigations that have stimulated renewed interest in crystal-induced arthropathies. RECENT FINDINGS: Specific diet-related and alcohol-related risks for gout have been clarified, and alternative urate-lowering treatments likely to benefit patients with difficult-to-treat gout are in development. Progress toward understanding mechanisms underlying the renal deficits defining most cases of gout includes characterization of a urate-specific renal tubule transporter explaining many aspects of renal uric acid handling and identification of mutations in the UMOD gene, resulting in altered uromodulin protein in the gout-associated disorders familial juvenile hyperuricemic nephropathy and medullary cystic kidney disease type 2. A genetic marker associated with the risk for severe allopurinol toxicity has been reported. Hyperuricemia and gout are increasing in incidence, as is complicated gout, especially among the elderly and patients with cardiovascular and renal comorbidities, organ transplants, or complex concomitant medication regimens. Asymptomatic hyperuricemia is clearly associated with hypertension, chronic kidney disease, cardiovascular disease, and the insulin resistance syndrome, and the pathogenetic significance of these associations is under intensive study. Mutation in the ANKH gene has been found among some patients with sporadic as well as familial calcium pyrophosphate deposition disease. SUMMARY: The results of these clinical, epidemiologic, experimental, and therapeutic investigations presage advances in the management of crystal-induced arthropathies.
PURPOSE OF REVIEW: To highlight recent investigations that have stimulated renewed interest in crystal-induced arthropathies. RECENT FINDINGS: Specific diet-related and alcohol-related risks for gout have been clarified, and alternative urate-lowering treatments likely to benefit patients with difficult-to-treat gout are in development. Progress toward understanding mechanisms underlying the renal deficits defining most cases of gout includes characterization of a urate-specific renal tubule transporter explaining many aspects of renal uric acid handling and identification of mutations in the UMOD gene, resulting in altered uromodulin protein in the gout-associated disorders familial juvenile hyperuricemic nephropathy and medullary cystic kidney disease type 2. A genetic marker associated with the risk for severe allopurinoltoxicity has been reported. Hyperuricemia and gout are increasing in incidence, as is complicated gout, especially among the elderly and patients with cardiovascular and renal comorbidities, organ transplants, or complex concomitant medication regimens. Asymptomatic hyperuricemia is clearly associated with hypertension, chronic kidney disease, cardiovascular disease, and the insulin resistance syndrome, and the pathogenetic significance of these associations is under intensive study. Mutation in the ANKH gene has been found among some patients with sporadic as well as familial calcium pyrophosphate deposition disease. SUMMARY: The results of these clinical, epidemiologic, experimental, and therapeutic investigations presage advances in the management of crystal-induced arthropathies.
Authors: Débora Mara Fortes Bartoli; Airton Luiz Felizatti; Fernando Russo Costa do Bomfim; Julia Leme Bovo; Andrea Aparecida de Aro; Maria Esméria Corezzola do Amaral; Marcelo Augusto Marretto Esquisatto Journal: Lasers Med Sci Date: 2020-06-10 Impact factor: 3.161