The larger number of T-lymphocytes in the periphery of vitiligo lesions and their association with angiogenesis are reported. The objective of this study was to investigate angiogenesis, VEGF and mast cell in vitiligo lesions. Specimens of 30 patients' biopsies, from lesional and perilesional nondepigmented skin were stained for mast cells, CD34 and VEGF. The evaluation was made by image analysis and the measured variables were statistically analyzed. A significantly increased number of CD34 and VEGF positive vessels and mast cells were detected in the centre of the lesion than in the periphery (p < 0.0001, p < 0.0001 and p = 0.001). There was a positive correlation of CD34, VEGF and mast cell number between the centre and the periphery of the lesions (r = 0.877, p < 0.0001; r = 0.946, p < 0.0001 and r = 0.863, p < 0.0001, respectively). The increased angiogenesis and mast cell numbers in the area where lymphocyte number is lower may be explained with the stepwise inflammatory process in vitiligo.
To evaluate variations in sexual and erectile function in subjects taking 1 mg of finasteride for androgenetic alopecia by administering the abridged 5-item version of the International Index of Erectile Function (IIEF-5) questionnaire before and during treatment.Design: In a multicenter study, 186 patients with androgenetic alopecia were asked to complete the IIEF-5 regarding the domain of erectile function before (at baseline) and 4 to 6 months after beginning finasteride treatment. The test was self-administered.
Setting:The study was conducted in 7 institutional dermatology departments in Italy
Androgenetic alopecia (AGA) is the most common cause of hair loss, affecting up to 80% of men and 50% of women in their lifetime. Genetic predisposition to the disease is well known but the responsible genes have not been identified. Polymorphism in the androgen receptor gene has been recently detected in AGA.(1) Although the role of androgens, and particularly dihydrotestosterone (DHT), in causing the disease has been established for a long time, the natural history of AGA is still not completely understood. This paper reviews recent data about natural progression of the disease, as well as factors that may interfere with its course and long-term prognosis.
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