Relationships between Anti-mullerian Hormone, Testosterone, Luteinizing Hormone and Follicle Stimulating Hormone in Men on Testosterone Therapy
- *Corresponding Author:
- Hadlow N
Department of Biochemistry, PP Building
Level 1, PathWest Laboratory Medicine
Perth, WA, 6008, Australia
Tel: +61 08 6383 4102
E-mail: [email protected]
Received Date: May 30, 2017 Accepted Date: June 15, 2017 Published Date: June 23, 2017
Citation: Hadlow N, Hamilton K, Joseph J, Millar D, Zentner A, et al. (2017) Relationships between Anti-mullerian Hormone, Testosterone, Luteinizing Hormone and Follicle Stimulating Hormone in Men on Testosterone Therapy. Clin Med Biochem 3: 128. doi: 10.4172/2471-2663.1000128
Copyright: © 2017 Hadlow N, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Aim: To assess if testosterone therapy, with suppression of LH and FSH altered AMH levels in men.
Study background: AMH is an important male hormone and is increasingly measured by laboratories for men and women’s health assessments. This prospective study was conducted in community medical centres to assess the effects of testosterone on AMH levels in men.
Methods: Men (n=15) with androgen deficiency symptoms, who were prescribed a trial of testosterone therapy by their own practitioner for at least 6 months, consented to participate in a study measuring AMH pre-therapy and post-therapy. Testosterone therapy was given to achieve LH and FSH suppression. Measurement of testosterone, LH, FSH and AMH at baseline and post testosterone therapy on at least 2 occasions including at 6 months was completed in all men. Men with abnormal baseline biochemistry (elevated LH or testosterone below age appropriate ranges) were excluded (n=5) from further study.
Results: In the study group baseline LH was normal (<8 U/L) and baseline testosterone was 7-23 (mean 12 nmol/L) and within age specific intervals. Mean baseline AMH was 36 pmol/L (range 19-89) and within age related intervals. A significant rise (p=0.001) of at least 1.5-fold in testosterone occurred post treatment (range 1.5-7.5-fold increase) with suppression of LH to <1 U/L with therapy. AMH showed variable changes after testosterone. There was no significant trend in AMH either rising or falling compared to baseline and levels were not associated with testosterone (p=0.197) nor affected by the suppression of FSH or LH (p=0.683, 0.271 respectively).
Conclusions: No significant pattern of change occurs in AMH in adult men at 6 months undergoing exogenous testosterone therapy. Laboratories do not need to adjust AMH reference intervals for effects of testosterone therapy in men with normal baseline LH and testosterone prior to therapy.