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Both Schmidt's abstracts show elevation of cortisol for balding & acne in both male & females.Could cortisol be acting as an anti-inflammatory response to acne or bacterial problems in baldness? If so, do the dermal papilla pay the price of cortisol's anti-insulin actions? Endocrinol Exp 1990 Dec;24(4):457-64 Endocrine parameters in acne vulgaris. Schmidt JB, Lindmaier A, Spona J Department of Dermatology II, University of Vienna, Austria. Hormonal parameters (see below) were determined in 78 male acne patients of both sexes (mean age 21.2 +/- 3.8 years; (mean +/- S.D.) and compared with 63 controls (25.0 +/- 4.2 years). In a female group consisting of 60 patients acne (23.2 +/- 5.0 years) and 28 controls (26.1 +/- 5.7 years) of age, blood sampling was performed in the luteal phase of the menstrual cycle. Testosterone (T), dehydroepiandrosterone-sulfate (DHEAS), androstenedione (A), free testosterone (FT) and 17-hydroxy-progesterone (17-OHP) were determined by standard radioimmunoassay methods. In addition, sex hormone binding globulin (SHBG), follicle stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), 17 beta-estradiol (E2) and cortisol (F) were evaluated. Moreover, the counts of acne lesions in the face were performed in 34 males and females patients in order to investigate possible correlations between hormones and acne lesions. The results in the male group revealed a significant elevation only for F but not for the other hormones. However, the female acne group significantly elevated levels of T, DHEA and F and a decrease of E became apparent. In addition, the correlation between both free and total T and acne lesions were found in the total of males and females. In the female group, free T and total A were found to correlate with acne lesions. The evaluation of these results indicates that androgens play a more important role in female than in male acne at the hormonal and at the peripheral level in skin. Another interesting finding was the significant increase of F in both male and female acne subjects, thus stressing the role of suprarenal involvement. PMID: 2151388, UI: 91256933 Dermatologica 1991;182(4):214-7 Hormonal parameters in androgenetic hair loss in the male. Schmidt JB, Lindmaier A, Spona J Department of Dermatology II, University of Vienna, Austria. Alopecia in the male is considered as a genetically determined disorder. Increased local androgen _meta_bolism and androgen receptor binding in the balding areas confirm the importance of the target organ hair follicle as regulative of androgen influences. In our study the hormonal parameters of 65 male patients with male pattern hair loss with a mean age of 24.31 years were compared with those of 58 age-matched controls. Determinations of the androgens, sex-hormone-binding globulin, the hypophyseal hormones luteinizing hormone, follicle-stimulating hormone and prolactin, 17 beta-estradiol and cortisol were performed by standard radioimmunoassay. Significant differences in serum levels of androstenedione, cortisol, 17 beta-estradiol and luteinizing hormone were noted between hair loss patients and control subjects. Suprarenal stimulation as well as hypophyseal feedback mechanisms therefore seem to be involved in male pattern alopecia. PMID: 1832108, UI: 91357216 A broad range of hormones was determined in males and females with androgenic hair loss (AH). The androgens testosterone, androstenedione, dehydroepiandrosterone sulfate, 17-hydroxyprogesterone and sex hormone binding globulin were evaluated in 65 male and 46 female patients. Besides estradiol (E2), cortisol (F), and the hypophyseal hormones LH, FSH, and prolactin (PRL) were investigated. Hormone levels were compared with those of 58 age-matched male and 45 female controls. In 38 of the 46 female AH patients, hypophyseal function was moreover evaluated by the 'TRH test', which detects slight, secondary hypothyroidism and/or hyperprolactinemia. Our findings showed a significant elevation of F in both male and female AH patients compared to controls, pointing to the suprarenes as a contributing factor in AH. This is confirmed by the observation of exacerbated AH in periods of increased stress. Concerning specifically male androgens, a significant elevation of androstenedione was noted. The mainly peripheral activity of this hormone and elevated E2 levels in males stress the importance of androgen _meta_bolism especially at the peripheral level. Additional TRH tests in females demonstrated significant hypophyseal hypothyroidism. Mult_i_layer__ed interaction between thyroid hormones and androgens may contribute to the development of AH in hyperthyroid patients. Another significant finding was elevated PRL after TRH stimulation. Thus, the androgen-stimulating effect of PRL may also play a role in female AH. Our findings show mult_i_layer__ed hormonal influences in AH. Broad-range hormone determination demonstrated a differentiated hormonal situation in this disorder.
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