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Clin Exp Dermatol 2002 Jul;27(5):405-9
Epidemiology and genetics of alopecia areata.
The frequency of alopecia areata and observed patterns of heritability are in keeping with a polygenic inheritance model but the genetics of alopecia areata is still poorly understood. The role of environmental factors in triggering disease initiation or exacerbation remains almost entirely speculative. Using the candidate gene approach, three susceptibility/severity factors have been identified. HLA alleles were the first to show a strong association with alopecia areata and some DQB and DR alleles have been demonstrated to confer a high risk for disease by both case-control and family-based studies. Interleukin (IL)-1 cluster genes, mainly the IL-1 receptor antagonist, show a strong association with disease severity in alopecia areata and a number of other autoimmune and inflammatory diseases. Finally, the association of alopecia areata with Down's syndrome, the high frequency of alopecia areata in autoimmune polyglandular syndrome type I due to mutations of the autoimmune regulator (AIRE) gene on chromosome 21q22.3 and the finding of association with MX1, another gene in the Down's syndrome region of chromosome 21 indicate this area of the genome as a promising target for future-family based investigations. The role of individual genes of the MHC, IL-1 cluster or chromosome 21q22.3 is difficult to establish and further genetic and functional investigations are needed to confirm their involvement in the pathogenesis of alopecia areata.
Australas J Dermatol 2002 Aug;43(3):221-3
Lupus panniculitis clinically simulating alopecia areata.
A 27-year-old woman with a known history of lupus erythematosus presented with two circumscribed patches of non-scarring alopecia closely resembling alopecia areata. Scalp biopsy showed a predominantly subcutaneous and deep dermal lymphocytic infiltrate that surrounded the deep follicular segments and hair bulbs, as well as the eccrine glands. There was associated hyaline fat sclerosis. The epidermis, infundibular and isthmus segments of follicles were relatively spared and lacked the lichenoid inflammation and fibrosis seen with lupus erythematosus. The biopsy findings illustrate that the deep variant of lupus panniculitis may be concentrated around the hair bulbs and deep temporary segments of hair follicles and spare the permanent stem cell-rich follicular segments. This pattern is capable of producing a temporary hair-loss, clinically simulating alopecia areata. The clinical history, presence of subtle erythema and scalp tenderness on physical examination, as well as the biopsy findings, were important clues in distinguishing our case from a true combination of alopecia areata and lupus erythematosus.
Ther Umsch 2002 May;59(5):233-7
Alopecia areata
Alopecia areata is a frequent cause of hair loss. The origin of disease is not fully understood. However there are indications for a T-cell mediated autoimmune process. Genetic, immunologic and psychologic factors are important for the outbreak of disease. Most patients show localized patches of acute hair loss, where regrowth is observed spontaneously or with simple topical treatment within few months. In up to 15% of patients severe forms of disease can develop with total scalp (alopecia totalis) or scalp and body hair loss (alopecia universalis). There are only few known risk factors for development of a severe form. Although spontaneous remission is possible in these cases, it occurs rarely and treatment is difficult. Multifocal alopecia areata responds to intravenous high-dose corticosteroids. Topical immunotherapy with diphenylcyclopropenone (DPC) or PUVA therapy may be effective in longstanding and widespread disease. The unpredictable course of disease is a major handicap for clinical trials and treatment recommendations. Contact of patients with self-help organisations may be of help for coping with the disease.
Eur J Dermatol 2002 May-Jun;12(3):236-9
HLA class II alleles in patients with alopecia areata.
Our purpose was to determine which HLA class II alleles are associated with Turkish alopecia areata patients. Also we investigated whether there was a relationship between the age of onset and severity of disease and HLA alleles or not. Sixty-five patients with alopecia areata were included in this study, and 50 healthy transplant donors were used as a control group. The total group of alopecia areata patients as well as various subgroups according to scalp hair loss were compared to the control group. HLA DNA typing was performed by polymerase chain reaction/sequence specific primer method. The frequency of DQB1*03 allele was 86.1% in all patients compared to 62.0% in controls (P = 0.005). While the frequency of DQB1*03 was significantly increased, the frequency of DRB1*03 was decreased in the all patients group (4.6% versus 22.0%, P = 0.01). In the group of scalp hair loss less than 25%; the frequency of DRB1*03 was decreased (3.2%, P = 0.02). The group of patients with 25-75% scalp hair loss was compared to control group; the frequencies of DRB1*04 (66.7% versus 28.0%, P = 0.02) was increased. When the alopecia totalis, alopecia universalis or alopecia totalis/alopecia universalis group was compared to control group; DQB1*03 was associated with an increased frequency in this group versus control group (90.9%, P = 0.03). There were no significant differences for the other DQ alleles and the DR alleles tested in the patients and in the controls. When patients with early onset were compared to patients with late onset; no significant allele differences were found. Our findings suggested that DQB1*03 allele is a marker for general susceptibility to alopecia areata and may also serve as special genetic marker for susceptibility for the severe form of alopecia areata in our population. However, this association is not related to age at onset of the disease.
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