Chronic social stress Ameliorates psoriasiform dermatitis through upregulation of the Hypothalamic-Pituitary-Adrenal axis.

Acute stress is a physiological response of an organism to adverse conditions, contributing to survival; however, persistence through time may lead to disease. Indeed, exacerbation of inflammatory conditions such as psoriasis has been reported to follow stressors in susceptible patients. Because chronic stress cannot ethically be elicited in patients under controlled laboratory conditions, we studied genetically modified mice that naturally develop psoriasiform dermatitis, and subjected them to an ethological chronic social contact stress paradigm. Although we found elevated pro-inflammatory neuropeptide production of substance P (SP), calcitonin-gene-related peptide (CGRP) and nerve-growth factor (NGF) mRNA in the dorsal root ganglia (DRG) as well as pro-inflammatory cytokines in response to the social stressor, stress paradoxically prevented the development of the skin lesions. This effect of stress could be reversed by the treatment with glucocorticoid (GC) receptor blockers, suggesting that it was mediated through the upregulation of corticosterone secretion. Extrapolating to humans, the worsening of disease in susceptible patients with psoriasis could be attributed to a defect in the Hypothalamic-Pituitary-Adrenal (HPA) axis with an impaired production of GC during situations of adversity, thus rendering them unable to counteract the pro-inflammatory effects of chronic stressors.

Catastrophic Cutaneous Polyarteritis Nodosa Exacerbated by Emotional Stress.

We present the first case of a patient with indolent polyarteritis nodosa who suffered severe exacerbations following significant emotional stressors. This report highlights the close relationship between emotions and autoimmune diseases mediated by the deleterious effects of stressors presumptively by skewing immunity from Type 1 to Type 2.

Health providers induced iatrogenic delusions of infestation.

Patients that suffer from factitial dermatosis mutilate their skin, often lacking any consciousness of self-injury, attributing the resulting lesions to spontaneous development. The case hereby described shows how the health providers' interventions led a patient from a baseline undiagnosed factitious disorder to frank delusions of infestation with Mycobacterium Kansasii, and a relentless search for antibiotic treatments. We highlight the need for educating health practitioners on the characteristics of psycho-cutaneous disorders.

Psoriasis: Psychosomatic, somatopsychic, or both?

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.