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Conflicts of interest: none declared. Sir, We read with great interest the article by Richards et al.1 regarding an attenuated psychological stressor response in the hypothalamic–pituitary–adrenal (HPA) axis in patients with psoriasis, especially in those with an apparent stress‐sensitive disease. In 1985, we reported a similar attenuation in the HPA axis in patients with psoriasis compared with healthy controls following stressor exposure similar to that used in the eloquent laboratory set‐up by Richards et al.2 Moreover, despite standardized stressor exposures, the psoriatic group in our study reported higher mental strain levels during stress, which was also reflected in higher blood glucose and urinary adrenaline levels during stressor exposures vs. controls. Thus, the greater cortisol attenuation might be due to changes in the HPA and other stress‐responsive systems and/or how patients with psoriasis interpret challenges, that is, differences in the stress appraisal process. In recent years, there has been an increasing focus on the importance of suboptimal stressor activation of the HPA axis during acute stressor exposures and its implications to health.3 Studies of patients with psoriasis indicate that heightened stress responsiveness of the sympathetic nervous system is accompanied by an inability to activate the HPA axis. This might have important implications for the dermatological health of patients and be of special interest in light of the fact that for many years cortisone has been the mainstay in psoriasis treatment.
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Arnetz et al. (2006) studied this question.
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