Gene expression of type 2 17 beta hydroxysteroid dehydrogenase in scalp hairs of hirsute women

Steroids. 2003 Sep;68(7-8):641-9. doi: 10.1016/s0039-128x(03)00093-x.

Abstract

Androgens are the main hormonal regulators of human hair growth and they are related to clinical conditions such as hirsutism. The aim of this study was to analyze the gene expression of androgen receptor (AR) and type 2 17 beta hydroxysteroid dehydrogenase (17 beta-HSD) in keratinocytes of plucked scalp hairs from hirsute patients and normal subjects. We studied 58 women with hirsutism (31 with polycystic ovary syndrome (PCOS), 27 with idiopathic hirsutism (IH)); 15 control women; and 10 control men. Hirsutism was assessed by a modified Ferriman-Gallwey method. Hormonal status was assessed between days 2 and 10 of the menstrual cycle or on any day when the patients were amenorrheic. AR and type 2 17 beta-HSD mRNA levels were estimated by reverse transcription-polymerase chain reaction (RT-PCR). AR expression was similar in all groups. Type 2 17 beta-HSD gene expression in untreated hirsute patients was lower (2.1+/-0.10) than in normal women (3.1+/-0.17), and similar to men (1.8+/-0.22). Comparing hirsute patients, type 2 17 beta-HSD expression was higher in treated PCOS (3.0+/-0.34 versus 2.2+/-0.13) and IH patients (2.5+/-0.19 versus 2.0+/-0.15); hirsutism score was lower (P=0.003, PCOS; P=0.003, IH); and SHBG levels were higher (P=0.001, PCOS; P=0.024, IH) in treated patients. The free androgen index was lower in treated women (P=0.024 for the IH group). In conclusion, the lower expression of type 2 17 beta-HSD mRNA in scalp hairs of untreated hirsute patients suggests androgen metabolism disturbances with predominance of more potent androgens, as occurs in men. The enzyme's higher gene expression in treated hirsute patients could be an indirect evidence of restored enzyme activity and intracellular androgen metabolism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 17-Hydroxysteroid Dehydrogenases / biosynthesis*
  • 17-Hydroxysteroid Dehydrogenases / genetics
  • Adult
  • Androgens / metabolism
  • Case-Control Studies
  • Estradiol Dehydrogenases
  • Female
  • Hair / cytology
  • Hair / enzymology*
  • Hirsutism / enzymology*
  • Hirsutism / etiology
  • Hirsutism / pathology
  • Humans
  • Keratinocytes / enzymology
  • Keratinocytes / pathology
  • Male
  • Polycystic Ovary Syndrome / complications
  • RNA, Messenger / analysis
  • Receptors, Androgen / biosynthesis
  • Receptors, Androgen / genetics
  • Scalp / cytology

Substances

  • Androgens
  • RNA, Messenger
  • Receptors, Androgen
  • 17-Hydroxysteroid Dehydrogenases
  • Estradiol Dehydrogenases
  • HSD17B2 protein, human