Effect of stress and other psychological factors on the pathophysiology and treatment of dermatoses

Abstract

Psychological factors precipitate or increase the morbidity of many dermatoses (1). There is increasing evidence that stress influences disease processes (2) and contributes to the inflammation through vasoactive neuropeptides (3,4), lymphokines or other chemical mediators (5). Experimental results indicate that the endocrine, nervous and immune systems can no longer be considered autonomous, but involve complex bidirectional interactions between them (6-8). Dermatology holds a distinct position in psychosomatic medicine because it deals with an organ that can be readily seen and touched. The psychological states of anxiety, fear, shame, pleasure, and sexual excitation are visibly indicated by blushing, hair-rising, growing pale, itching or hyperhidrosis. The skin, therefore, clearly responds to many psychologic and stressful stimuli. As the skin is exposed to view, dermatoses elicit reactions from the patients' environment and the easy accessibility of the skin allows patients to interact directly with their lesions. In addition to the classic stress response involving increased levels of neuroendocrine hormones and autonomic neurotransmitters, stress also affects the immune system (6-8). Stress has been reported to cause decreased natural killer cell cytotoxicity, depressed mitogenic responses in lymphocytes, increased IgA levels, enhanced neutrophil phagocytosis and activation of interferon synthesis in lymphocytes (9). Psychodermatological syndromes can be classified according to the type and degree of causal relationship between the psychological etiology and the dermatosis. There is some overlap between the groups, but there is a satisfactory classification under three magor headings that suggests an approach to treatment (1,11).