Abstract
While "omics" studies have advanced our understanding of inflammatory skin diseases, metabolomics is mostly an unexplored field in dermatology. We sought to elucidate the pathogenesis of psoriatic diseases by determining the differences in metabolomic profiles among psoriasis patients with or without psoriatic arthritis and healthy controls. We employed a global metabolomics approach to compare circulating metabolites from patients with psoriasis, psoriasis and psoriatic arthritis, and healthy controls. Study participants were recruited from the general community and from the Psoriasis Clinic at the University of California Davis in United States. We examined metabolomic profiles using blood serum samples from 30 patients age and gender matched into three groups: 10 patients with psoriasis, 10 patients with psoriasis and psoriatic arthritis and 10 control participants. Main outcome(s) and measures(s): Metabolite levels were measured calculating the mean peak intensities from gas chromatography time-of-flight mass spectrometry. Multivariate analyses of metabolomics profiles revealed altered serum metabolites among the study population. Compared to control patients, psoriasis patients had a higher level of alpha ketoglutaric acid (Pso: 288 ± 88; 209 ± 69; p=0.03), a lower level of asparagine (Pso: 5460 ± 980; 7260 ± 2100; p=0.02), and a lower level of glutamine (Pso: 86000 ± 20000; 111000 ± 27000; p=0.02). Compared to control patients, patients with psoriasis and psoriatic arthritis had increased levels of glucuronic acid (Pso + PsA: 638 ± 250; 347 ± 61; p=0.001). Compared to patients with psoriasis alone, patients with both psoriasis and psoriatic arthritis had a decreased level of alpha ketoglutaric acid (Pso + PsA: 186 ± 80; Pso: 288 ± 88; p=0.02) and an increased level of lignoceric acid (Pso + PsA: 442 ± 280; Pso: 214 ± 64; p=0.02). The metabolite differences help elucidate the pathogenesis of psoriasis and psoriatic arthritis and they may provide insights for therapeutic development.
Highlights
Psoriasis is a chronic, inflammatory skin disease associated with significant morbidity and mortality[1]
When comparing the metabolite profiles of psoriasis patients and control patients, the key differences that reached univariate significance were characterized by an increase in alpha ketoglutaric acid, and decreases in asparagine, glutamine, and beta-sitosterol in psoriasis patients compared to control patients (Figure 1, Dataset)
Patients with psoriasis and psoriatic arthritis compared to patients with psoriasis Upon comparing the metabolite profiles of patients with both psoriasis and psoriatic arthritis to patients with skin-limited psoriasis, the top metabolite differences were characterized by a decrease in alpha ketoglutaric acid, and increases in arabinose, lignoceric acid, phosphoric acid, and glycerol-3-galactoside in psoriasis patients with concomitant psoriatic arthritis compared to patients with psoriasis alone (Figure 2, Dataset)
Summary
Inflammatory skin disease associated with significant morbidity and mortality[1]. One-third of psoriasis patients develop psoriatic arthritis[2,3]. The exact mechanisms underlying psoriasis remain under investigation. A complex interplay between genetic and environmental factors initiates a cascade of events that lead to activation of dendritic cells[4]. The activated dendritic cells stimulate differentiation and migration of effector T cells (Th1 and Th17) to the skin. The subsequent release of inflammatory cytokines promotes further recruitment of immune cells, stimulates keratinocyte proliferation and sustains a state of chronic inflammation[4]
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