Elevated Serum Leptin Levels in Nonobese Patients With Psoriasis

February 2013 | Volume 12 | Issue 2 | Original Article | e25 | Copyright © 2013

Dalia G. Aly MD,a Ihab Y. Abdallah MD,b Noha S. Hanafy MD,a Mohamed L. Elsaie MD,a,c and Neveen A. A. Hafizd

aDepartment of Dermatology and Venereology, National Research Center, Giza, Egypt bDepartment of Dermatology and Venereology, Benha University Hospital, Benha, Egypt cDepartment of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL dDepartment of Clinical Pathology, Benha University Hospital, Benha, Egypt

Abstract

Background: Leptin, an adipocyte-derived hormone, has been shown to have several immunological effects similar to those of proinflammatory cytokines. The relationship between serum leptin, psoriasis, and obesity is still conflicted, and very few studies have investigated its role in skin diseases other than psoriasis.
Aim: To evaluate the possible relationship between serum leptin in nonobese patients with psoriasis and other randomly selected skin diseases.
Subjects and methods: Eighty subjects (40 patients with psoriasis, 20 patients with other randomly selected skin diseases, and 20 healthy controls) were included in the study. Fasting serum leptin levels of the study groups were examined by sandwich enzyme-linked immunosorbent assay.
Results: Elevated serum leptin levels were detected in both nonobese patients with psoriasis (P=.004) and those with other randomly selected skin diseases (P=.05). Leptin levels failed to correlate to the Psoriasis Area and Severity Index score of psoriatic patients. Both sexes demonstrated comparable levels of serum leptin in psoriatic patients, while female patients suffering from other skin diseases showed higher levels of serum leptin than did males of the same group.
Conclusion: Leptin may play a role in the immunopathogenesis of psoriasis and other skin diseases, even in the absence of obesity as a cofactor.

J Drugs Dermatol. 2013;12(2):e25-e29.

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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.


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