The role of xenobiotics in triggering psoriasis

Psoriasis is a common inflammatory skin disease affecting approximately 2% of the world population. A complex interplay of genetic predisposition and risk factors contributes to the risk of its onset. Several xenobiotics have been implicated in the pathogenesis of psoriasis. Drugs are among the most investigated trigger factors; strong association with disease induction or exacerbation has been reported for β-blockers, lithium, NSAIDs and ACE inhibitors, all of which are commonly used in the management of various comorbidities in psoriasis patients. Furthermore, inhibitors of TNF have a well-documented potential for triggering new-onset psoriasis when used for other indications (e.g. Crohn's disease or rheumatoid arthritis), while post-marketing data have revealed the same association for ustekinumab. Several other drugs have been connected with psoriasis, but the evidence is less compelling. Smoking and alcohol have been reported to increase the risk for occurrence of psoriasis, but can also affect unfavorably the course of the disease and its response to treatment. Furthermore, exposure to secondhand smoke, especially in childhood, also mediates the risk. Emerging data now suggest that air pollution also has a detrimental effect on skin disease, including psoriasis, but this association needs further investigation. Understanding of the toxic effect of xenobiotics on the initiation and clinical course of psoriasis can contribute to its better control, as it can help with the avoidance of triggering factors and, in some cases, influence the success of pharmacological treatment. It, therefore, has an important place in the comprehensive management of psoriasis.