Hyperuricaemia and gout in the Pacific.

Gout is the most common form of inflammatory arthritis in adults worldwide. There has been a steady increase in prevalence, which varies across different geographic areas and is high in the Indigenous (First Nations) peoples of the Pacific region. Palaeo-archaeological studies demonstrate that gout was present in the Pacific region prior to European colonization, which is suggestive of genetic predisposition.

Integrative analysis reveals the multilateral inflammatory mechanisms of CD14 monocytes in gout.

Objectives: Gout, prevalent inflammatory arthritis caused by urate crystal deposition, involves immune cell activation, yet the precise role of CD14 monocytes in initiating the inflammatory response is poorly understood. This study aimed to characterise the molecular and cellular landscape of CD14 monocytes in gout using single-cell transcriptomic analysis.

Methods: Single-cell RNA sequencing was performed on peripheral blood mononuclear cells from 8 gout patients and 6 age- and sex-matched healthy controls.

Conducting genetic epidemiology research on hyperuricaemia and gout in an indigenous community in Guam - a feasibility study.

Background: Gout, the most common inflammatory arthritis disease, and hyperuricaemia onset are influenced by environmental and genetic factors. We sought to investigate these factors in an Indigenous community in Guam.

Methods: In this feasibility study, the University of Guam led the qualitative inquiry with the native community, training (pre-screening of participants, data collection methods, and biospecimen handling), study implementation (outreach and recruitment, data collection, and DNA extraction and quantification), and qualitative and epidemiologic data analyses.

Fatty acid oxidation-induced HIF-1α activation facilitates hepatic urate synthesis through upregulating NT5C2 and XDH.

Dyslipidemia affects approximately half of all people with gout, and prior Mendelian randomization analysis suggested a causal role for elevated triglycerides in hyperuricemia (HU), but the underlying mechanisms remain elusive. We hypothesize that dyslipidemia promotes hepatic urate biosynthesis in HU and gout and fatty acid (FA) oxidation (FAO) drives this process. Here we developed a targeted metabolomics to quantify major metabolites in purine metabolic pathway in the sera of a human cohort with HU, gout, and normaluricemic controls.