Psoriasis vulgaris is a multifactorial heritable disease characterized by severe inflammation
resulting in poorly differentiated, hyperproliferative keratinocytes. Recent advances in
genetic analyses have implicated components regulating the interleukin (IL)-23 and nuclear
factor-B pathways as risk factors for psoriasis. These inflammatory pathways exhibit
increased activity in skin lesions, and promote secretion of various cytokines, such as IL-17
and IL-22. Unrestrained, the activated inflammatory cytokine network in psoriasis may
trigger a vicious cycle of inflammation and cellular proliferation that ultimately results in
lesion formation. These advances in genetic analyses, together with the progress made in
targeted biological therapy, pave the path to tailor treatment on the basis of an individual’s
genetic and immunologic profile.
Semin Cutan Med Surg 29:3-9 © 2010 Elsevier Inc. All rights reserved.
Psoriasis is a chronic inflammatory disorder that affects approximately 2% of the general
population. Numerous studies have evaluated the increased prevalence of comorbid diseases
and risk factors in psoriatic patients, including obesity, metabolic syndrome, cardiovascular
disease, psoriatic arthritis, autoimmune disease, psychiatric illness, liver disease,
smoking, malignancy, chronic obstructive pulmonary disease, sleep apnea, and alcohol
abuse. Insight into the overlapping pathogenesis of these comorbidities of psoriasis
highlights the importance of immune-mediated mechanisms in these disease states. Psoriasis,
with its comorbidities, must be approached in a multidisciplinary manner to effectively
and comprehensively understand, manage, and treat those with this complex
Semin Cutan Med Surg 29:10-15 © 2010 Elsevier Inc. All rights reserved.