Psychological Stress in Atopic Dermatitis

Fig. 13.1

Cohort questionnaire study of Osaka University students with AD (n = 288) who were followed for 4 years from 2012 to 2016

Fig. 13.2

The change in patient symptoms of AD from 2013 to 2015. This diagram indicates the ratio of students with AD who were cured, under treatment, untreated, and without medical checkup

Fig. 13.3

The frequency of psychological stress through college life. The frequency of stress was scored as follows: 0, very little; 1, sometimes; 2, often; and 3, always. Each bar represents the mean ± SD. Key (***) P < 0.001 by paired t-test

There are three psychosocial factors that affect AD symptoms. (1) Emotional factors can determine the natural course of the disease from onset through recurrence and protraction in some cases [2, 4]. Psychosocial stress (stressors) and poor coping mechanisms exacerbate AD. (2) The loss of sleep, appearance of diseased skin, intractable clinical course, and burden of treatment secondary to disabling pruritus may elevate the patient’s level of psychological stress. The psychosocial problems derived from AD contribute to an impaired quality of life [7]. (3) Patients with AD may suffer from other mental disorders, such as depression and anxiety [8]. Overall, studies indicate that AD is a skin disease associated with increased anxiety levels [9].

13.2 Assessment of Psychological Stress

Psychosomatic evaluation is very important for patients with AD because the ability to cope with psychological stress varies among individuals. Personalized psychological treatment based on an exact evaluation may be effective in successfully treating the dermatitis. Several important psychosomatic scales and measures of coping with stress are described below.

13.2.1 Psychosomatic Scales

The Psychosomatic Scale for Atopic Dermatitis (PSS-AD) is a 12-item scale consisting of the following three factors: exacerbation triggered by stress, disturbances due to AD, and ineffective control [10].

The Depression-Anxiety-Stress Scale (DASS) is a 42-item self-reporting instrument designed to measure the three related negative emotional states of depression, anxiety, and tension/stress [11].

The Inventory of Stress Symptoms for Adults Lipp (ISSL) assesses symptoms of stress, the patients’ stress level (alarm, resistance, near exhaustion, and exhaustion), and the kind of predominant symptoms present (physical or psychological) in the preceding 24 h, the preceding week, and the preceding month [12].

The Trier Inventory for the Assessment of Chronic Stress (TICS) consists of 57 items to evaluate different aspects of chronic stress in the following nine subscales: work overload, social overload, excessive demands from work, lack of social recognition, work discontent, social tension, pressure to perform, social isolation, and chronic worrying [13].

The Screening Scale for Chronic Stress (SSCS) consists of 12 items to assess the following five aspects of the experience of chronic stress: chronic worrying, work overload, social overload, excessive demands from work, and lack of social recognition [13].

13.2.2 Measure of Coping Skills

The Brief COPE tool assesses the following 14 dimensions of effective and ineffective coping strategies: self-distraction, active coping, denial, substance use, use of emotional support, use of instrumental support, behavioral disengagement, venting, positive reframing, planning, humor, acceptance, religion, and self-blame [14].

13.3 Influence of Stress on Skin Function and Immunity

13.3.1 Influence of Stress on Skin Function

Stressful events influence cutaneous functions. Stressful life events preceding the onset of itching were found in >70% of the patients with AD [15]. Aioi et al. demonstrated that stress induces impairment of the barrier function and water retention property in stratum corneum in mice [16]. This impairment is concomitant with a decline in ceramide and pyrrolidone carboxylic acids, which are intensely hygroscopic amino acids. Moreover, Garg et al. reported that psychological stress delays recovery of the skin barrier [17].

13.3.2 Influence of Stress on Immunity

The systemic stress response affects two central biological systems. One system is the hypothalamic-pituitary-adrenal axis (HPA), in which various neuroendocrine mediators (i.e., adrenocorticotropin, β-endorphin, and cortisol) are produced in response to stress [18]. The other system is the sympathoadrenal medullary system, which regulates the release of epinephrine and norepinephrine [18]. Catecholamines and cortisol, which are stress hormones, mediate the differentiation of T-helper (Th) cells to Th2 cells. This differentiation results in an increased allergic inflammatory response [19, 20]. IL-31, which is produced by activated Th2 cells, causes pruritus [21, 22]. Elias et al. reported that an increase in endogenous glucocorticoids disrupts the barrier function of the skin, stratum corneum cohesion, and epidermal antimicrobial function [23].

Nerve terminals in cutaneous sensory nerves release neuropeptides, such as calcitonin gene-related peptide (CGRP) and substance P (SP), both of which have a variety of effects on the local inflammatory response [24, 25]. Mast cell stimulation by SP and corticotropin-releasing hormone (CRH), which are secreted under stress and regulate the HPA, results in the release of proinflammatory cytokines [26, 27]. Mast cells also play a central role in neurogenic inflammation [28]. SP increases expression of functional CRH receptor-1 [27]. The correlation between neurotransmitters in psychodermatological pathways and skin inflammation is now well known, and mast cells, CRH, and SP have been implicated in a brain-skin connection [27]. Some degree of brain-skin connection underlies any inflammatory skin disease [18, 29]. Moreover, SP was shown to be involved in stress-induced hair loss in mice [30].

13.4 Treatment

Most treatments of AD, such as topical corticosteroid, oral antihistamines, and phototherapy for skin inflammation, have been prescribed using a standard medical approach. Adherence to treatment is difficult for a patient during the chronic course of AD, which has frequent flare-ups, but can be improved with a good relationship between the doctor and patient. Supportive psychotherapy by a clinician, with respect, acceptance, and empathy, is widely used with standard psychological therapy. To achieve success with this approach, the patient needs to clarify the level of his or her stress and what he or she defines as stressors. Using this information, the doctor analyzes the coping behavior of the patient and advises the patient regarding what would be an effective coping mechanism. For example, relaxation exercises may be of help in preventing habitual rubbing and improving symptoms of skin inflammation [31].

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