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We often come across differences in the severity of androgenetic alopecia (AGA) as assessed subjectively by the patients themselves and objectively by the attending physicians. For the purpose of examining the differences in the assessment of AGA between patients and physicians, we presented the Norwood classification to male patients and the Shiseido classification to female patients and asked them to assess the degree of hair loss by themselves. We compared the results with the severity as assessed by 2 specified dermatologists. The results show that the assessments of the severity of AGA were consistent between the patients and physicians in 42% (15/36) of cases, the physicians reported a higher grade of severity than the patients themselves in 30% (11/36) of cases, and the patients reported a higher grade of severity than the physicians in 28% (10/36) of cases; however, the Wilcoxon signed rank statistical analysis showed no significant difference between the patients and physicians assessments. AGA should be treated in accordance with individual symptoms and wishes and not a standardized treatment protocol. [ABSTRACT FROM AUTHOR]

5α-dihydrotestosterone is known to play a crucial part in the regulation of hair growth and in the development of androgenetic alopecia. 5α-dihydrotestosterone is formed locally within the hair follicle from the systemic precursor testosterone by cutaneous steroid 5α-reductase. Moreover, adrenal steroids such as dehydroepiandrosterone are converted to 5α-dihydrotestosterone by isolated hair follicles, which may provide an additional source of intrafollicular 5α-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 5α-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. [ABSTRACT FROM AUTHOR]