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.

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.

Am Fam Physician. 2003 Mar 1;67(5):1007-14.

Alopecia in women.

Alopecia can be divided into disorders in which the hair follicle is normal but the cycling of hair growth is abnormal and disorders in which the hair follicle is damaged. Androgenetic alopecia is the most common cause of hair loss in women. Other disorders include alopecia areata, telogen effluvium, cicatricial alopecia, and traumatic alopecias. The diagnosis is usually based on a thorough history and a focused physical examination. In some patients, selected laboratory tests or punch biopsy may be necessary. Topically administered minoxidil is labeled for the treatment of androgenetic alopecia in women. Corticosteroids and other agents are typically used in women with alopecia areata. Telogen effluvium is often a self-limited disorder. Because alopecia can be devastating to women, management should include an assessment for psychologic effects.

Australas J Dermatol. 2003 Feb;44(1):62-6.

Androgenetic alopecia in a postmenopausal woman as a result of ovarian hyperthecosis.

A 65-year-old woman presented with an 8-year history of progressive frontotemporal alopecia and hirsutism. She had elevated serum levels of testosterone, androstenedione and estradiol. Ultrasound and computed tomography imaging suggested a right ovarian mass, while bilateral ovarian venous sampling demonstrated increased testosterone levels originating from both ovarian veins. Histology obtained following bilateral oophorectomy demonstrated bilateral ovarian hyperthecosis. Six months after surgery, the patient remains well with no progression of the alopecia. Ovarian hyperthecosis is a rare cause of androgenetic alopecia in postmenopausal women. The role of hyperthecosis and its relationship to androgenetic alopecia is reviewed.

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