Human leukocyte antigen region involvement in the genetic predisposition to alopecia areata
Dermatology, ISSN: 1421-9832, Vol: 175, Issue: 1, Page: 10-14
1987
- 59Citations
- 7Captures
- 1Mentions
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Metrics Details
- Citations59
- Citation Indexes59
- 59
- CrossRef39
- Captures7
- Readers7
- Mentions1
- References1
- Wikipedia1
Article Description
Human leukocyte antigens (HLA) of classes 1 and II were studied in 127 patients with alopecia areata (AA). The patients were subdivided into different groups depending on (1) hair loss area, (2) sex, (3) pathogenesis, (4) response to topical immune modulators (squaric acid dibutylester and diphencyprone) and (5) age of onset of the disease. The frequencies of class I HLA markers (loci A, B, C) were not significantly different from the controls. However, among the class II antigens (loci DR, DQ), the frequency of DR5 was in-creased in both alopecia areata and alopecia universalis when compared with the control group. In particular, DR5 was strongly linked to the early-onset form. The highest DR5 fre-quency (62%) was found in the group of patients which presented both the early onset and the most severe form of the disease (p < 0.01; RR = 3.14). A decrease of the HLA-B8 pheno-type frequency was found in the alopecia areata group versus the alopecia universalis one. No significant deviation was found between the female patients and the control group. However, an increase of CW3 and a decrease of DR1 was seen in the males. In the group including ‘combined’, ‘prehypertensive’, ‘atopic’ alopecia of Ikeda’s classification the frequency of HLA-A28 and DR5 was increased and that of DR1 was decreased in comparison with the ‘common’ type of alopecia and the controls. It was not possible to find any relationship between these genetic markers and the response to topical immune modulators. © 1987 S. Karger AG, Basel.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0023083880&origin=inward; http://dx.doi.org/10.1159/000248775; http://www.ncbi.nlm.nih.gov/pubmed/3497062; https://karger.com/DRM/article/doi/10.1159/000248775; http://www.karger.com/doi/10.1159/000248775; http://www.karger.com/Article/Abstract/248775
S. Karger AG
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