Psoriasis, like atopic eczema, is an inflammatory skin disease with a multifactorial aetiology. It is a chronic, immune-mediated disorder (Kreuger, 1989) associated with significant physical and psychological morbidity. The psychological factors have been summarised by Ginsburg and Link (1989) and instruments have been developed to measure psoriasis-related stress (Wang et al., 1990; Fortune et al., 2002).
In psoriasis there is an overexpression of INF gamma and TNF alpha and a relative underexpression of the Th2 cytokines, IL-4 and IL-10. It appears that the T-cells involved are Th1 lymphocytes and that the disease may be influenced by a cell-mediated autoimmune process.
There is an early influx of T-cells into psoriatic lesions, increased antigen presentation in psoriatic cells and ablative effect with anti-T cell therapy, and the common antigens considered in the pathogenesis of psoriasis are bacterial proteins and superantigens.
However, clinical and histological features in psoriasis show the Koebner phenomenon on trauma, clearance of psoriatic plaque after desensitising injury, symmetry of clinical lesions and increased nerve density in psoriatic plaques, which have led to the proposal of a neurogenic hypothesis for the disease (Raychaudhuri et al., 1995; Raychaudhuri & Farber, 2000).
Nerve growth factor (NGF) is a peptide whose functions have been shown to stimulate and direct nerve growth. At a cellular level in skin it is mitogenic for ker-atinocytes and promotes the migration and degranulation of mast cells leading to dilated vessels and oedema. In addition to this promotion of the release of inflammatory mediators via mast cells, NGF also induces keratinocytes to produce the cytokine RANTES, a key participant in the activation of memory T-cells in psoriasis (Raychaudhuri & Farber, 2000). NGF, together with neuropeptides, have been shown to produce neutrophil response in psoriasis via CGRP and IL-8. They are mitogenic for keratinocytes and inhibitors of apoptosis (cell death) via SP, CGRP and VIP, and thus probably contribute to the influences producing the epidermal proliferation in psoriasis (Pincelli et al., 1997).
These sophisticated measurements in cutaneous biology are not matched by clinical correlations during non-pharmacological interventions in skin disease.
However, it was shown that a structured programme in the management of psychological distress with cognitive-behaviour management reduced relapse of disease. Furthermore, psychological distress impairs the clearance of psoriasis treated with photochemotherapy (Fortune et al., 2002). This is indirect evidence that these putative stress mechanisms have clinical importance.
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Do You Suffer From the Itching and Scaling of Psoriasis? Or the Chronic Agony of Psoriatic Arthritis? If so you are not ALONE! A whopping three percent of the world’s populations suffer from either condition! An incredible 56 million working hours are lost every year by psoriasis sufferers according to the National Psoriasis Foundation.