Serum level of interleukin-17A in patients with alopecia areata and its relationship to age
Background There is strong evidence for an autoimmune etiology of alopecia areata (AA). Interleukin‐17A (IL‐17A) is a Th17 proinflammatory cytokine that has been linked to the pathogeneses of diverse autoimmune and inflammatory diseases. Objectives This study aimed to measure serum IL‐17A in AA pati...
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Veröffentlicht in: | International journal of dermatology 2016-08, Vol.55 (8), p.869-874 |
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Sprache: | eng |
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Zusammenfassung: | Background
There is strong evidence for an autoimmune etiology of alopecia areata (AA). Interleukin‐17A (IL‐17A) is a Th17 proinflammatory cytokine that has been linked to the pathogeneses of diverse autoimmune and inflammatory diseases.
Objectives
This study aimed to measure serum IL‐17A in AA patients and to study associations between IL‐17A levels and AA severity, duration, and age of onset, and patient gender and age.
Methods
The study enrolled 39 AA patients and 37 healthy control subjects. Scalp involvement was assessed using the Severity of Alopecia Tool (SALT), and clinical disease severity was determined. Serum IL‐17A was measured using ELISAs.
Results
Serum IL‐17A was significantly higher in AA patients than in control subjects (P < 0.001). Correlations between serum IL‐17A and gender, disease duration, SALT score, and disease severity were non‐significant. Serum IL‐17A was significantly higher in patients aged ≤30 years than in patients aged >30 years (P = 0.045). Age and serum IL‐17A were significantly negatively correlated in patients with AA (rs = −0.363, P = 0.023) but not in control subjects (rs = −0.294, P = 0.077). Patients with juvenile‐onset AA had significantly higher IL‐17A levels than those with maturity‐onset disease (P = 0.034). There was a significant negative correlation between age at disease onset and serum IL‐17A (rs = −0.349, P = 0.029).
Conclusions
It is possible that IL‐17A plays a role in the pathogenesis of AA. Serum IL‐17A may be influenced by patient age and age of onset of AA but does not seem to influence disease severity. |
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ISSN: | 0011-9059 1365-4632 |
DOI: | 10.1111/ijd.12994 |