INTRODUCTION
Psoriasis is a complex chronic inflammatory skin disorder affecting approximately 2% to 3% of the population, and it poses a lifelong burden for those affected. There is increasing awareness that psoriasis as a disease is more than skin deep, and that it is associated with multiple systemic disorders.1 Patients with psoriasis have been found to be at greater risk of developing comorbid diseases such as metabolic syndrome, vascular disorders, and, in particular, obesity.2 It is believed that the cooccurrence of obesity and psoriasis could lead to interactions of both diseases in which adipokines, at least in part, are involved.3
Leptin, a 16-kD nonglycosylated polypeptide product of the obese (ob) gene, is an adipocyte-derived hormone that has long been recognized as a key factor in regulating a wide range of biological responses, including energy homeostasis, neuroendocrine function, angiogenesis, bone formation, and reproduction. In addition to being a hypothalamus modulator of food intake, body weight, and fat stores, leptin has been increasingly recognized as a cytokine-like hormone with pleiotropic actions in modulating immune responses.4 It plays a role in acute and chronic inflammation via regulation of cytokine expression that modulates the balance of types 1 and 2 T helper cells (TH). Therefore, leptin has been implicated in the pathogenesis of autoimmune inflammatory conditions such as type 1 diabetes mellitus, rheumatoid arthritis, and chronic bowel disease.5,6
Since psoriasis is an immune-mediated inflammatory disease, characterized by hyperproliferation of keratinocytes and infiltration of mostly T lymphocytes, leptin is considered to provide a link between T-cell function and the inflammation noted in psoriasis.6 It has been shown that both CD4+ and CD8+ T lymphocytes detected in the papillary dermis and the epidermis of the psoriatic lesions express leptin receptors.7 Moreover, stimulus through the leptin receptor promotes both TH17 and TH1 immune responses, with enhanced production of tumor necrosis factor (TNF)–α and interleukin (IL)-6 by monocytes and IL-2 and interferon-γ by T lymphocytes, while at the same time impairing the function of regulatory T cells.8,9
Numerous clinical studies have suggested leptin secretion to be positively correlated with body mass index (BMI), and that obese psoriatic patients have inordinately high levels of circulating leptin.6,10-12 However, the potential pathophysiological pathways that may be responsible for this association are not yet clear.
