The role of stress in the pathogenesis of Alopecia Areata: an objective assessment via hair cortisol level

BACKGROUND The pathogenesis of alopecia areata (AA) is poorly understood and multifactorial. There seems to be a strong belief, but conflicting evidence that stress causes or exacerbates AA. Hair cortisol measurement has been proven to be a reliable biological marker for cumulative prior stress. This measurement has up to date not been used in AA cases and may provide convincing evidence in the debate of stress and AA. OBJECTIVES: The primary aim of this project was to determine whether stress triggers onset of hair loss (OOHL) in AA by analysing the relationship between hair cortisol concentrations (HCCs) pre-OOHL in cases vs controls. Three secondary objectives were identified: • To determine whether there is a difference in HCC of lesional skin versus perilesional skin in cases. • To determine whether there is a correlation between disease activity (as determined by the hair pull test) and HCC. • To determine whether validated stress questionnaires correlate with HCC. METHODS A case control study was performed. Fourteen patients, fulfilling the inclusion criteria were recruited from the GSH and RXH outpatient departments. For each case consent was obtained, a data sheet was filled out, stress questionnaire(s) and two strands of hair, one lesional and one peri-lesional, were collected. Next, 14 healthy controls were recruited from whom a hair strand each was collected. On the hair samples, the position of onset of hair loss (OOHL) was determined by measuring one centimetre per month after OOHL, from the proximal (scalp near) end. Then three sections of three centimetres each were cut, two distally (representing the six-month period before OOHL) and one proximally (representing the three months post OOHL). In six of these cases a fourth or “current” section was obtained. This represented the section on the scalp and thus reflected current stress by measuring the most recent HCC. Next, the HCC’s of these sections were measured using the Salivary ELISA Cortisol kit©. An additional 44 cases, not meeting the inclusion criteria, were recruited for acquisition of additional stress questionnaires and data sheets. RESULTS HCC’s on average were higher in cases than in controls (before, during and after OOHL). The difference in HCC’s, however, was not statistically significant. There was no statistical difference between HCC’s in lesional and peri-lesional scalp samples. Distal section HCC’s were the highest. HCC’s correlated positively with disease activity, but was nonsignificant. There was no statistically significant relationship between HCC’s and stress questionnaires. CONCLUSIONS: Although the result was not statistically significant, likely due to small sample size, stress as measured by HCC may trigger OOHL in AA. HCC does not play a role in whether an area of the scalp is affected or not. Disease activity may be cause for stress. A larger study is warranted to validate these findings