Psoriasis: Psychosomatic, somatopsychic, or both?

Abstract Psoriasis is a chronic inflammatory disorder characterized by substantial psychiatric comorbidity. Historically, anecdotal observations have suggested that psychosocial distress can trigger flares of psoriasis, but over the past several decades, high-quality data from experimental studies support the assertion that stress plays a critical role in the pathogenesis of psoriasis. There may be a subset of patients unable to elicit an appropriate immunosuppressive response to stress through upregulation of cortisol, with resultant exacerbation of their psoriasis. Other notable studies revealed that key neuromodulators, including substance P, calcitonin gene–related peptide, vasoactive intestinal peptide, and nerve growth factor may be potent regulators of neurogenic inflammation that induce psoriasis flares through a stress-mediated mechanism. Preliminary trials in humans that examine psychosocial interventions to reduce stress, as well as animal studies targeting specific neuropeptides, provide support for the concept that alteration of pathways mediated by the stress response represents novel forms of therapy in the management of psoriasis.