No abstract

Clinical observations suggest that the nervous system, including psychological factors, can influence the onset and course of alopecia areata (AA). The aim of this study was to determine whether stressful life events, stress perception, and trait-anxiety are risk factors in the onset and course of AA. A group of 45 patients diagnosed with AA and a group of 45 healthy controls were participants in the study. The patients with AA were divided into two subgroups: patients with a first episode of AA and patients with recidivism of the disease. All participants completed questionnaires addressing sociodemographic, clinical and psychological aspects of their disorder. The frequency and types of stressful life events experienced over the previous six months were recorded. Lemyre and Tessier's Mesure de Stress Psychologique was used to measure emotional, cognitive, behavioral, and physiological aspects of distress. Anxiety was evaluated by the Spielberg's Trait Anxiety Inventory. The subgroups of AA and the control group, using the same numbers of subjects matched for age and sex, education level, marital and employment status, were statistically compared. The number of patients with four stressful life events over the previous 6 months was significantly higher in the group of AA patients with recidivism of disease compared to the control group (P=0.004). There were no differences among the other groups with respect to the frequency of life events. Examination of the relationships between the two groups regarding anxiety, as well as perceived distress, revealed that the groups differed significantly with respect to psychosocial variables studied. A significantly higher degree of trait-anxiety and perceived distress were observed among patients in both AA subgroups (first onset and recidivism of AA) than in the healthy control group. The highest scores for anxiety and stress perception among examined groups were obtained in the group with recidivism of AA (33.42 +/- 12.71 and 90.32 +/- 50.74, respectively). Trait-anxiety and stress perception constitutes risk factors that may influence the onset and exacerbation of AA. The present study does not provide evidence of a significant role of stress in the onset of AA. Life events may play an important role in triggering of some episodes.

Our findings suggest that p53 overexpression occurs mainly in neoplastic skin lesions, although it may also occur in squamous epithelium of inflammatory skin diseases such as PS, as well as in normal skin epithelium. It is associated with cell proliferation in normal as well as altered epithelium. p53 protein overexpression is an age-related process and significantly associated with sun exposure, especially in NS and PS but also in KA and SCC. Our findings suggest that Ki-67 rate and p53 protein expression reflect the degree of malignancy in the examined cutaneous neoplasms.

Lichen planus is recognized as a T-cell-mediated disease. Histologically, it is characterized by the formation of colloid bodies representing apoptotic keratinocytes. The apoptotic process mediated by CD8(+) cytotoxic T lymphocytes (CTLs) and NK cells mainly involves two distinct pathways: the perforin/granzyme pathway and the Fas/FasL pathway. So far, little is known regarding the role of perforin-mediated apoptosis in lichen planus. In the present study, the expression and distribution of perforin, T and NK cell subsets in the epidermis and dermis of lesional and nonlesional lichen planus skin were studied. Skin biopsy specimens from lesional and nonlesional skin of ten patients with lichen planus and eight healthy persons were analysed by immunohistochemistry. Significant accumulation of T cells, particularly of CD4(+) and CD8(+) subsets, was found in both epidermis and dermis of lichen planus lesions compared with nonlesional and healthy skin. There were no significant differences in the incidence of NK cells (CD16(+) and CD56(+)) between lesional, nonlesional and healthy skin. Perforin expression was significantly upregulated in the epidermis of lichen planus lesions. In conclusion, accumulation of perforin(+) cells in the epidermis of lichen planus lesions suggest a potential role of perforin in the apoptosis of basal keratinocytes.