Maslach, Schaufeli and Leiter identified six risk factors for burnout in 2001: mismatch in workload, mismatch in control, lack of appropriate awards, loss of a sense of positive connection with others in the workplace, perceived lack of fairness, and conflict between values.Although job stress has long been viewed as the main determinant of burnout, recent meta-analytic findings indicate that job stress is a weak predictor of burnout. These findings question one of the most central assumptions of burnout research. In a systematic literature review in 2014, the Swedish Agency for Health Technology Assessment and Assessment of Social Services (SBU) found that a number of work environment factors could affect the risk of developing exhaustion disorder or depressive symptoms:

People who experience a work situation with little opportunity to influence, in combination with too high demands, develop more depressive symptoms. People who experience a lack of compassionate support in the work environment develop more symptoms of depression and exhaustion disorder than others. Those who experience bullying or conflict in their work develop more depressive symptoms than others, but it is not possible to determine whether there is a corresponding connection for symptoms of exhaustion disorder. People who feel that they have urgent work or a work situation where the reward is perceived as small in relation to the effort develops more symptoms of depression and exhaustion disorder than others. This also applies to those who experience insecurity in the employment, for example concerns that the workplace will be closed down. In some work environments, people have less trouble.
The disrupted skin barrier leads to transdermal water loss (leading to the xerosis or dry skin commonly seen in AD) and antigen and allergen penetration of the epidermal layer. Filaggrin mutations are also associated with a decrease in natural antimicrobial peptides found on the skin; subsequently leading to disruption of skin flora and bacterial overgrowth (commonly Staphylococcus aureus overgrowth or colonization).Atopic dermatitis is also associated with the release of pruritogens (molecules that stimulate pruritus or itching) in the skin. Keratinocytes, mast cells, eosinophils and T-cells release pruritogens in the skin; leading to activation of Aδ fibers and Group C nerve fibers in the epidermis and dermis contributing to sensations of pruritus and pain. The pruritogens include the Th2 cytokines IL-4, IL-13, IL-31, histamine, and various neuropeptides. Mechanical stimulation from scratching lesions can also lead to the release of pruritogens contributing to the itch scratch cycle whereby there is increased pruritus or itch after scratching a lesion. Chronic scratching of lesions can cause thickening or lichenification of the skin or prurigo nodularis (generalized nodules that are severely itchy). Diagnosis
AD is typically diagnosed clinically, meaning it is based on signs and symptoms alone, without special testing. Several different criteria developed for research have also been validated to aid in diagnosis. Of these, the UK Diagnostic Criteria, based on the work of Hanifin and Rajka, has been the most widely validated. Treatments
No cure for AD is known, although treatments may reduce the severity and frequency of flares.