Shared pathways linking hyperuricemia, obesity, and psoriatic disease.
| Domain | Key elements | Shared mechanisms | Clinical implications |
|---|---|---|---|
| Psoriatic inflammation | Th17/Th1 (IL-17, TNF-α, IFN-γ); neutrophils (NETs/ROS); IL-1 family | Endothelial activation, oxidative stress, innate-adaptive crosstalk | Amplifies vascular injury beyond classic risk factors; higher cIMT/plaques in PsA cohorts. |
| Hyperuricemia/gout | Elevated SUA; NLRP3 → IL-1β/IL-18; XO-ROS | ↓ NO, endothelial dysfunction; inflammasome-driven vascular inflammation | Tracks with subclinical atherosclerosis; causal role plausible but not definitive; ULT neutral for CV outcomes in non-gout CAD. |
| Obesity/metabolic dysfunction | Adipokines (leptin, resistin, IL-6, TNF-α); NAFLD; insulin resistance | Raises SUA (overproduction/under-excretion); sustains psoriatic inflammation | Central driver of hyperuricemia in psoriatic disease; weight loss likely improves inflammation and urate handling. |
| Integrative phenotype (PsO/PsA) | Clustering of hyperuricemia, obesity, metabolic syndrome, systemic inflammation | Feedback loops linking IL-17/TNF, adipokines, and SUA | Elevated hyperuricemia/gout prevalence; higher CV risk—supports combined inflammatory-metabolic targeting (e.g., anti-IL-17 + GLP-1/GIP). |
Shared pathways linking hyperuricemia, obesity/metabolic dysfunction, and psoriatic disease. Domains summarize dominant immune and metabolic actors, the key crosstalk mechanisms, and their clinical implications for vascular risk in psoriatic phenotypes. PsA: psoriatic arthritis; PsO: psoriasis; SUA: serum uric acid; ULT: urate-lowering therapy; NAFLD: non-alcoholic fatty liver disease; XO: xanthine oxidase; ROS: reactive oxygen species; NETs: neutrophil extracellular traps; IFN-γ: interferon-gamma; cIMT: carotid intima-media thickness; CV: cardiovascular; GIP: glucose-dependent insulinotropic polypeptide; GLP-1: glucagon-like peptide-1; ↓: reduction/diminishing; →: activation signal.