Conflicts of interest None declared.
Obesity in psoriasis: leptin and resistin as mediators of cutaneous inflammation
Version of Record online: 28 JUN 2008
© 2008 The Authors. Journal Compilation © 2008 British Association of Dermatologists
British Journal of Dermatology
Volume 159, Issue 2, pages 342–350, August 2008
How to Cite
Johnston, A., Arnadottir, S., Gudjonsson, J.E., Aphale, A., Sigmarsdottir, A.A., Gunnarsson, S.I., Steinsson, J.T., Elder, J.T. and Valdimarsson, H. (2008), Obesity in psoriasis: leptin and resistin as mediators of cutaneous inflammation. British Journal of Dermatology, 159: 342–350. doi: 10.1111/j.1365-2133.2008.08655.x
- Issue online: 17 JUL 2008
- Version of Record online: 28 JUN 2008
- Accepted for publication 26 February 2008
Background Obesity is a significant risk factor for psoriasis and body mass index (BMI) correlates with disease severity.
Objectives To investigate the relationship between obesity and psoriasis, focusing on the role of adipokines such as leptin and resistin.
Patients/methods Patients with psoriasis (n = 30) were recruited and their BMI, waist circumference and disease severity [Psoriasis Area and Severity Index (PASI)] were recorded. Fasting serum samples were obtained on enrolment and after a course of ultraviolet (UV) B treatment. Age-, sex- and BMI-matched healthy controls were also recruited.
Results On enrolment, serum leptin and soluble leptin receptor levels were not raised compared with the controls. However, resistin, interleukin (IL)-1β, IL-6, and chemokines CCL2, CXCL8 and CXCL9 were all significantly elevated in the patient group and serum resistin correlated with disease severity (r = 0·372, P = 0·043). Improvement after UVB treatment was accompanied by decreased serum CXCL8. In vitro, both leptin and resistin could induce CXCL8 and tumour necrosis factor-α production by blood monocytes, and leptin could additionally induce IL-1β and IL-1 receptor antagonist production. Leptin also dose dependently increased secretion of the growth factor amphiregulin by ex vivo-cultured lesional psoriasis skin.
Conclusions These data support the view that leptin and resistin may be involved in the pathogenesis of psoriasis in overweight individuals, possibly by augmenting the cytokine expression by the inflammatory infiltrate.