Relationship of galectin‐3 in psoriasis patients

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This study looked at the relationship of galectin‐3 in psoriasis patients.

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Background:
Psoriasis has been shown to increase cardiovascular risk, and a contributor to this might be enhanced myocardial fibrosis promoted by the disease‐associated proinflammatory milieu.

Objective:
We sought to investigate the relationship of galectin‐3 (Gal‐3) – a recognized mediator of fibrosis with inflammatory activation and left ventricular (LV) systolic and diastolic function in patients with psoriasis.

Methods:
We enrolled 102 psoriatic patients (mean age: 52.5±12.6 years). Sixty‐five age‐ and sex‐matched healthy subjects served as controls. Echocardiographic assessment of myocardial function included estimation of LV longitudinal systolic deformation (GLS), and diastolic indices: tissue e’ velocity and E/e’ ratio. Laboratory measurements encompassed blood Gal‐3, creatinine, glucose, insulin, CRP and erythrocyte sedimentation rate (ESR).

Results:
Patients with psoriasis were characterised by elevated Gal‐3 (12.3 [9.3‐13.4] vs. 6.3 [5.5‐9.4] ng/ml in healthy controls, P <0.001), ESR (17.0 [11.0‐29.0] vs. 8.5 [6.0‐13.0] mm respectively, P <0.001) and CRP (3.1 [1.7‐10.6] vs. 1.9 [1.5‐4.0] mg/l respectively, P <0.001), and reduced GLS (19.9±3.7 vs. 22.0±3.0% respectively, P <0.001). Progressive deterioration of GLS was demonstrated across Gal‐3 tertiles. Significant associations between GLS and age (beta=‐0.21, P <0.04), Gal‐3 (beta=‐0.27, P <0.01), CRP (beta=‐0.22, P <0.03), ESR (beta=‐0.25, P <0.01), waist circumference (beta=‐0.22, P <0.03) and waist‐to‐hip ratio (beta=‐0.20, P <0.05) were found. Stepwise multiple regression analysis revealed that the independent determinants of GLS in psoriatic patients were Gal‐3 (beta=‐0.24, P <0.01) and ESR (beta=‐0.21, P <0.03). Regression‐based mediation analysis demonstrated that the relationship between ESR and GLS was partially mediated by Gal‐3.

Conclusions:
Subclinical left ventricular systolic dysfunction in psoriasis, as evidenced by reduced GLS, is linked with the inflammatory up‐regulation, and enhanced pro‐fibrotic activity (as reflected by elevated serum Gal‐3) may be involved in this process. These putative mechanisms may be responsible for the observed higher incidence of heart failure in this disease condition and should be considered as a potential target for preventive and therapeutic measures.

Source: onlinelibrary.wiley.com

*Early view funding unknown.