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ABSTRACT
Year : 2011  |  Volume : 3  |  Issue : 3  |  Page : 10  

Session C: Androgenetic Alopecia – Part III


Date of Web Publication16-Jun-2011

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How to cite this article:
. Session C: Androgenetic Alopecia – Part III. Int J Trichol 2011;3, Suppl S1:10

How to cite this URL:
. Session C: Androgenetic Alopecia – Part III. Int J Trichol [serial online] 2011 [cited 2017 May 27];3, Suppl S1:10. Available from: http://www.ijtrichology.com/text.asp?2011/3/3/10/82152

Androgens - A leading factor in androgenetic alopecia alter-follicular gene expression

Valerie Randall*, Saeed Al-Waleedi, Nilofer Farjo 1 , Bessam K. Farjo 1

Centre for Skin Sciences, School of Life Sciences, University of Bradford and 1 Farjo Medical Centre, Manchester, United Kingdom.

*E-mail: v.a.randall@bradford.ac.uk


Androgenetic alopecia, or male pattern baldness, is an androgen-driven, progressive minaturisation of scalp hair follicles leading to balding which normally takes place over many years. The occipital and parietal regions are usually unaffected. Although common, it causes marked psychological distress and negative effects on the quality of life in both men and women. Since androgens have contradictory stimulatory effects on hair follicles in many areas like the beard and axilla, often in the same person, the specific change must be due to the follicle's individual reactions in response to the circulating androgens. The current mechanism for androgen action in balding follicles involves intracellular metabolism of testosterone to the more potent 5α-dihydrotestosterone inside the cells of the regulatory dermal papilla. Dihydrotestosterone binding to androgen receptors activates them to form a gene transcriptional regulator complex with other coactivating proteins and this will bind to the hormone response elements of appropriate genes to alter gene expression. Altered transcription of paracine factors causing increased secretion of inhibitory factors and/or reduced secretion of stimulatory factors will reduce hair follicle activity causing balding. Such alternations have been shown in androgenetic alopecia using cultured dermal papilla cells and changes in several genes have been detected including those for paracine factors transforming growth factor-β (TGF- β) and stem cell factor (SCF). Isolated hair follicles from balding scalp also express less hepatocyte growth factor (HGF) and macrophage stimulating hormone (MSP) and some of their receptors cMet and RON. Clarification of their roles may lead to new directions in alopecia therapy.

Androgenetic alopecia: Identification of genetic susceptibility factors and first steps towards development of a predictive test

Felix F. Brockschmidt 1,2 *, Stefanie Heilmann 1,2 , Axel M. Hillmer 3 , Markus M. Nöthen 1,2

1 Department of Genomics, Life and Brain Center, University of Bonn, Bonn, Germany; 2 Institute of Human Genetics, University of Bonn, Bonn, Germany; 3 Genome Technology and Biology Group, Genome Institute of Singapore, Singapore.

*E-mail: Felix.brockschmidt@uni-bonn.de


Two essential etiological factors underlie the development of androgenetic alopecia (AGA, male pattern baldness): The pathogenesis is androgen dependent and a genetic predisposition is the major requirement for the phenotype. Several candidate gene and genome-wide studies unequivocally identified the androgen receptor gene (AR) on the X-chromosome as the first gene contributing to the development of AGA (e.g. Hillmer et al. 2005). The AR protein is a member of the nuclear receptor super family and mediates the effects of androgens. A functional AR and circulation androgens are essential requirements for the development of AGA. However, the causative variant and the underlying causative mechanism still await identification (Hillmer et al. 2009, Brockschmidt et al. 2010). In our genome-wide association study (Hillmer et al. 2008) we have identified a second contributing genetic locus on chromosome 20p11 with no obvious connection to the androgen pathway. Based on the association finding, this locus seems to confer the second strongest genetic contribution to the development of AGA. Currently, a meta-analysis of independent genome wide association studies is being performed to identify new genetic susceptibility loci which previously fell short of significance in individual studies. We have used the information on the AR and 20p11 associations to develop a new predictive test for AGA. We can demonstrate that this test allows a better risk prediction than the currently available tests.

Current and new medical treatment of pattern hair loss

Won-Soo Lee

Department of Dermatology, Institute of Hair and Cosmetic Medicine Yonsei University, Wonju College of Medicine, Wonju, Korea.

E-mail: leewonsoo@yonsei.ac.kr


Pattern hair loss (PHL, androgenetic alopecia) is the most common form of hair thinning in both men and women. Because of the social and psychological impact, patients may seek inappropriate and unproven therapies that are available in nonmedical settings, often at great expense to the consumer. The aim of treatment of PHL is to increase scalp coverage or to retard the progression of hair thinning, or both. There are effective medical treatments available currently for some men and women with PHL, but clearly further treatment options are desired, particularly for women with FPHL. Agents used to treat PHL may be nonspecific biologic response modifiers that enlarge suboptimal hair follicles regardless of the underlying pathophysiology, androgen blockers to interrupt the 5a-reductase enzymes, or androgen receptor protein inhibitors to specifically block the binding and transport of androgens to the cell nucleus. The purpose of this lecture is to provide current information on an approach to the evaluation and medical treatment of pattern hair loss. This lecture discusses therapeutic options with current and emerging new treatment modalities. Also management strategies for PHL will be covered in a setting of an algorithmic evaluation of pattern hair loss.




 

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