A random study of Asian male androgenetic alopecia in Bangkok, Thailand.

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Dermatol Surg 2002 Sep;28(9):804-7

A random study of Asian male androgenetic alopecia in Bangkok, Thailand.

BACKGROUND: Androgenetic alopecia remains the most common cause of male pattern baldness (MPB) in all races. The prevalence of MPB in Caucasians is well documented. The prevalence of MPB in Asians is believed to be very low, only one-fourth to one-third on average compared to Caucasians. However, according to my previous study, there is a clear trend indicating that it is approaching that of Caucasians. OBJECTIVE: To assess the prevalence of MPB in the Asian population in Bangkok, Thailand; to compare this prevalence to previous studies conducted on Asians; and to compare the results to previous studies conducted on Caucasian. METHODS: This study was conducted by two physicians and assisted by two registered nurses. The questionnaire included age, sex, Norwood classification, diet, family history of baldness, income, and education. The physicians examined the scalp of each interviewee upon completion of each questionnaire. The ethnic focus group in this study was Thai and Chinese who reside in Bangkok, Thailand. The interviews were conducted in hospitals, nursing homes, classroom, medical meetings, temples, parks, and villages. RESULTS: A total of 1124 men were randomized in this study. The prevalence of cosmetically significant MPB (Norwood III-VII) was 38.52% and steadily increasing with age, approaching that of Caucasians. Variant MPB was found to be 0.67% and other types of androgenetic alopecia was 0.6%. From an ethnic point of view, the majority of the groups were of mixed blood and mostly of Chinese origin, thus we were unable to distinguish between Chinese and Thai. CONCLUSION: This study shows that the prevalence of MPB in Asians is not as low as previously thought. The cause of this increasing prevalence is uncertain. There are no past studies in Thailand for comparison, however, it can be extrapolated that the socioeconomic environment and westernized diet may contribute to this prevalence.

Eur J Dermatol 2002 Jul-Aug;12(4):327-34

Diphencyprone immunotherapy alters anti-hair follicle antibody status in patients with alopecia areata.

Alopecia areata (AA) is a relatively common reversible hair loss disorder usually manifesting as patchy areas of complete hair loss on the scalp and other body parts that can progress to complete loss of all body hair. This condition is now generally assumed to be an autoimmune disease with the hair follicle (HF) as the principal target tissue. AA may be passively transferred by T cells and there is some evidence that serum IgG may also disturb hair cycling. Here, we examine whether the status of anti-HF antibody reactivity is altered during hair regrowth associated with topical immunotherapy using the contact sensitizer diphencyprone. Eleven patients with severe AA of the scalp were treated with diphencyprone on one side of the scalp and serum was obtained from each patient before the start of therapy, after unilateral hair regrowth, during continuing hair regrowth and in some cases after complete and sustained regrowth. The presence and titer of circulating antibodies to HF was assessed by indirect immunofluorescence and immunoblotting analysis. A striking reduction was detected in both the titer and range of HF components/antigens targeted by anti-hair follicle IgG antibodies in those patients that exhibited complete and sustained hair regrowth after DCP-treatment. By contrast, unilateral hair regrowth was associated with no change, or even an increase, in anti-HF antibody titer and reactivity. Therefore we can conclude that the down-regulation of antibody reactivity is likely to be a result rather than the cause of hair regrowth induction by topical immunotherapy. As this immunotherapy is associated with a reduction in the titer/pattern of anti-HF antibodies, these may hold the key to the identity of the HF antigen targets in AA. Moreover, the presence/titer of anti-HF antibodies may be a marker of clinical disease activity or opportunity for spontaneous regrowth.

Arch Dermatol 2002 Jul;138(7):916-22

Mediation of alopecia areata by cooperation between CD4+ and CD8+ T lymphocytes: transfer to human scalp explants on Prkdc(scid) mice.

OBJECTIVE: To determine the role of CD4+ and CD8+ T lymphocytes in the pathogenesis of alopecia areata. DESIGN: Relapse of alopecia areata was induced in autologous human scalp grafts on Prkdc(scid) mice by injection of activated T lymphocytes derived from lesional skin. CD4+ and CD8+ T cells were separated by magnetic beads before injection. SETTING: University-based dermatology practice. PARTICIPANTS: Eleven patients with either alopecia totalis or severe alopecia areata. MAIN OUTCOME MEASURES: Hair regrowth, hair loss, and immunohistochemical findings of scalp explants. INTERVENTION: Transfer of scalp T cells to autologous lesional scalp explants on Prkdc(scid) mice. RESULTS: Injection of unseparated T cells and mixed CD4+ plus CD8+ T cells resulted in significant hair loss (P<.01) in 5 of 5 experiments. However, injection of purified CD4+ or CD8+ T cells alone did not result in reproducible hair loss. CD4+ and CD8+ T cells induced follicular expression of intercellular adhesion molecule 1 (CD54), HLA-DR, and HLA-A, HLA-B, and HLA-C after injection into scalp grafts. CONCLUSIONS: CD4+ and CD8+ T cells have a role in the pathogenesis of alopecia areata. It is hypothesized that CD8+ T cells act as the effector cells, with CD4+ T cell help. It is now necessary to look for HLA-A, HLA-B, and HLA-C associations with alopecia areata. Therapeutic manipulations that interfere with CD8+ activity should be examined.

J Invest Dermatol 2001 Dec;117(6):1342-8

Steroid sulfatase in the human hair follicle concentrates in the dermal papilla.

5 alpha-dihydrotestosterone is known to play a crucial part in the regulation of hair growth and in the development of androgenetic alopecia. 5 alpha-dihydrotestosterone is formed locally within the hair follicle from the systemic precursor testosterone by cutaneous steroid 5 alpha-reductase. Moreover, adrenal steroids such as dehydroepiandrosterone are converted to 5 alpha-dihydrotestosterone by isolated hair follicles, which may provide an additional source of intrafollicular 5 alpha-dihydrotestosterone levels. Elevated urinary dehydroepiandrosterone and serum dehydroepiandrosterone sulfate have been reported to be present in balding young men. These reports suggest that dehydroepiandrosterone sulfate may act as an important endocrine factor in the development of androgenetic alopecia. Hence the question arises whether the dehydroepiandrosterone sulfate can be metabolized within the hair follicles to yield dehydroepiandrosterone by the microsomal enzyme steroid sulfatase, and where steroid sulfatase might be localized. We therefore performed immunostaining for steroid sulfatase on human scalp biopsies as well as analysis of steroid sulfatase enzyme activity in defined compartments of human beard and occipital hair follicles ex vivo. Using both methods steroid sulfatase was primarily detected in the dermal papilla. Steroid sulfatase activity was inhibited by estrone-3-O-sulfamate, a specific inhibitor of steroid sulfatase, in a concentration-dependent way. Furthermore, we show that dermal papillae are able to utilize dehydroepiandrosterone sulfate to produce 5 alpha-dihydrotestosterone, which lends further support to the hypothesis that dehydroepiandrosterone sulfate contributes to androgenetic alopecia and that steroid sulfatase inhibitors could be novel drugs to treat androgen-dependent disorders of the hair follicle such as androgenetic alopecia or hirsutism.

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