The Psoriasis Pathogenesis and the Metabolic Risk
Rosalba Buquicchio1, Caterina Foti1, Maria Teresa Ventura2, *
Identifiers and Pagination:Year: 2018
First Page: 70
Last Page: 79
Publisher Id: TODJ-12-70
Article History:Received Date: 20/5/2018
Revision Received Date: 20/6/2018
Acceptance Date: 2/7/2018
Electronic publication date: 31/7/2018
Collection year: 2018
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: (https://creativecommons.org/licenses/by/4.0/legalcode). This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Psoriasis is a multifactorial disease that can be related to genetic, environmental and immunological causes. Therefore, not only a single factor but different aspects contribute to the onset of the disease, varying from individual to individual. It would be characterized by an abnormal proliferation and differentiation of keratinocytes, mediated by a dysregulation in the auto-immune T cell response in which several cytokines participate, including Interleukin (IL)-17, IL-17A, IL-12, IL-22, IL-23. These cells and cytokines are responsible for the aggression on skin cells, inflammation and accelerated reproduction of the cells of the epidermis. Due to the chronic inflammation, psoriasis is frequently associated with other concomitant non-dermatological morbid conditions such as arthropathy which can be complicated by a disabling evolution. Psoriasis is also frequently associated with comorbidities such as Cardiovascular Diseases (CVD), hyperlipidemia, diabetes and obesity.
The knowledge of common inflammatory pathways and of the potential links between psoriasis and other diseases should encourage dermatologists to a multidisciplinary approach to psoriasis and to an optimal management also in the light of new therapeutic possibilities.