Abstract 14382: Psoriasis is Associated with Impaired HDL Efflux Despite Normal HDL Levels Compared to Controls
Introduction: Psoriasis is a Th-1/17 mediated inflammatory skin disease associated with increased risk of major adverse cardiac events (MACE). Systemic inflammation has been shown to be associated with inflammatory modulation of HDL which loses capacity to perform reverse cholesterol transport and “efflux” cholesterol from the arterial wall. We sought to study HDL efflux in psoriasis to examine if HDL dysfunction, which is not captured by traditional lipid panels, may link psoriasis to MACE.
Methods: We prospectively enrolled a consecutive sample of patients with psoriasis (n=78) and compared cardiometabolic risk factors with an asymptomatic age and gender matched sample from our practice (n=84). Fasting lipids were measured and HDL efflux capacity was quantified using a validated ex vivo system involving the incubation of macrophages with apolipoprotein B-depleted serum from patients. Multivariable linear regression adjusting for cardiometabolic risk factors was performed using STATA 10 software.
Results: Patients with psoriasis had lower total cholesterol (188 mg/dL (SD 36.4) vs. 208 (31.6)), LDL (110 (31.9) vs. 127 (27.1)), and HDL (47 (13.6) vs. 15 (14)) (p<0.01 for all) compared to controls, with no significant difference observed in triglycerides. However, patients with psoriasis demonstrated significantly reduced HDL efflux capacity (0.86 (SD 0.13)) compared to control patients (1.18 (0.11)) (p=0.002). This negative association observed between psoriasis and HDL efflux persisted after adjusting for traditional lipid levels and BMI.
Conclusion: We demonstrate that despite normal lipid profiles in patients with psoriasis, HDL efflux capacity is significantly abnormal in psoriasis, a finding which persists after adjustment for traditional lipid levels and BMI. The abnormal efflux capacity of HDL in psoriasis may provide a link between the association of psoriasis and MACE, however larger studies are needed to validate these findings.
- © 2011 by American Heart Association, Inc.