Gene array profiling and immunomodulation studies define a cell-mediated immune response underlying the pathogenesis of alopecia areata in a mouse model and humans.

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J Invest Dermatol 2002 Aug;119(2):392-402

Gene array profiling and immunomodulation studies define a cell-mediated immune response underlying the pathogenesis of alopecia areata in a mouse model and humans.

Alopecia areata is a suspected autoimmune hair loss disease. In a rodent model, alopecia areata can be induced in normal haired C3H/HeJ mice by transfer of skin grafts from mice with spontaneous alopecia areata. At weeks 2, 4, 6, and 10 after surgery, grafted mice were euthanized, skin collected and processed for histology, and RNA extracted. Age-matched sham-grafted mice, and mice with and without spontaneous alopecia areata, were similarly processed. For comparison, skin biopsies from alopecia areata and androgenetic alopecia affected humans were also collected. Skin mRNA processed to cDNA was analyzed using Affymetrix mouse 11K and human 6800 gene chip(R) array technology. Microarray results indicated 42 known genes upregulated or downregulated during onset of mouse alopecia areata consistent with an inflammatory cell-mediated disease pathogenesis involving antigen presentation, costimulation, and a T helper 1 lymphocyte response. In contrast, 114 genes, many regulating immunoglobulin response, were altered late in disease development. In alopecia areata affected humans, 95 genes were significantly modulated. As confirmation of microarray analysis results, lymph node and spleen cells from alopecia areata affected mice injected into normal haired littermates transferred the alopecia areata phenotype. Alopecia areata onset could be inhibited in skin-grafted mice by modulation with B7.1- and B7.2-specific monoclonal antibodies. In addition, depletion of CD4+ CD8+ expressing cells in chronic alopecia areata affected mice using monoclonal antibodies permitted hair regrowth. The results consistently demonstrated the importance of an immune cell-mediated disease mechanism in alopecia areata pathogenesis and suggested targeting antigen-presenting cells and reactive lymphocytes may be effective in alopecia areata treatment.

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.

Schweiz Rundsch Med Prax 2001 Nov 29;90(48):2087-93

Photographic documentation of the effectiveness of 1 mg. oral finasteride in treatment of androgenic alopecia in the man in routine general practice in Switzerland

A 6-month, prospective, open, multicenter cohort study in 265 men with male pattern hair loss treated with oral finasteride 1 mg/day (Propecia) was conducted in the office of 52 Swiss dermatologists. The patient's head was placed in a stereotactic device, and Polaroid photographs were taken of the vertex and frontal areas. Endpoints used to determine treatment efficacy were patient self-assessment, investigator clinical assessment, and blinded assessment of the serial Polaroid photographs by a panel of 2 experienced dermatologists. Significant improvements were stated on the photographs by both clinical investigators and the blinded expert panel: 54% of patients showed improvement of hair growth at 6 months of treatment in the vertex region, and 48.7% in the frontal area. No progression of hair loss was found in an additional 38% (vertex) and 47% (frontal region), respectively. Clinical investigator and expert assessment yielded comparable results. Independently, patient self-assessment and investigator clinical assessment confirmed the progress. Propecia was well-tolerated, and no significant safety concerns were identified during the study. The photographic method was well accepted by the physicians. The office-based Polaroid photographic system allowed reliable assessment of change during treatment of male pattern hair loss with Propecia. The data generated in this manner corresponded to the antecedent results of the multicenter, placebo-controlled studies with oral finasteride.

Dermatology. 2003;206(3):189-91.

Association between Smoking and Hair Loss: Another Opportunity for Health Education against Smoking?

Besides being the single most preventable cause of significant morbidity and an important cause of death in the general population, tobacco smoking has been associated with adverse effects on the skin. Smoke-induced premature skin ageing has attracted the attention of the medical community, while only recently an observational study has indicated a significant relationship between smoking and baldness. The mechanisms by which smoking causes hair loss are multifactorial and are probably related to effects of cigarette smoke on the microvasculature of the dermal hair papilla, smoke genotoxicants causing damage to DNA of the hair follicle, smoke-induced imbalance in the follicular protease/antiprotease systems controlling tissue remodeling during the hair growth cycle, pro-oxidant effects of smoking leading to the release of pro-inflammatory cytokines resulting in follicular micro-inflammation and fibrosis and finally increased hydroxylation of oestradiol as well as inhibition of the enzyme aromatase creating a relative hypo-oestrogenic state. In view of the psychological impact of androgenetic alopecia on affected men and women, increasing public awareness of the association between smoking and hair loss offers an opportunity for health education against smoking that may be more effective than the link between smoking and facial wrinkles or grey hair, since the latter can be effectively counteracted by current aesthetic dermatologic procedures, while treatment options for androgenetic alopecia are limited.

Seeing is believing. Learning by anecdotal observations is an old way of science. It is not reasonable to stop taking daily food and herbal supplements altogether just because of scietific/clinical support: our life must go on until we have better understandings of food and herb. There are two merits that Hair Million enjoys: Firstly, Hair Million is relatively inexpensive, and secondly, it is made only of edible herbs that are known to be safe when consumed in regular quantities. Propecia is a clincally validated prescription medication for hair loss.

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