[Alopecia areata and alexithymia]
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Ayça Cordan Yazici1, Ayşe Başterzi, Senel Tot Acar
1Mersin U Tip Fak., Dermatoloji AD., Mersin. aycacordan@yahoo.com
Objective:
Whether or not psychological factors play an important role in the pathogenesis of alopecia areata (AA) is a controversial issue. AA has had a tendency to be associated with high avoidance in attachment relationships, high alexithymic characteristics, and poor social support. Some studies have suggested that personality characteristics might modulate individual susceptibility to AA. The role of stressful life events in the appearance of AA is uncertain. In addition to reports associating anxiety and affective disorders with the onset of AA, there have also been studies that have not confirmed such an association. This case-control study was undertaken with the aim of determining the significance of stressful life events and other psychological factors in the etiopathogenesis of AA.
Method:
A total of 43 patients (26 male, 17 female) with AA and 53 age-and gender-matched healthy controls selected from hospital staff and their relatives (28 male, 25 female) were enrolled in the study. Both patients and controls were evaluated using the Hospital Anxiety and Depression Scale (HADS), Stress Scale, and Toronto Alexithymia Scale (TAS).
Results:
There was no statistically significant difference between the patient and control groups with regard to the total scores of stressful major life events, depression, and anxiety (p>0.05). However, TAS scores in patients with AA were higher than in controls (p=0.013).
Conclusion:
The present study found no evidence that stressful major life events, depression, or anxiety have a role in the etiopathogenesis of AA, but AA tended to be associated with alexithymia. It has been suggested that alexithymics may suffer from unnoticed chronic stress with physiological, endocrine, and immune consequences, and that alexithymia is associated with impaired immune response. We suggest that alexithymia may play a role in the pathogenesis of AA via stress-induced immunological mechanisms.
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