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This version published online on April 1, 2008
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2008-0402
A more recent version of this article appeared on June 1, 2008
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Submitted on February 21, 2008
Accepted on March 20, 2008

Pharmacodynamics of GH abuse biomarkers and the influence of gender and testosterone: a randomized double-blind placebo-controlled study in young recreational athletes

Anne E Nelson, Udo Meinhardt, Jennifer L Hansen, Irene H Walker, Glenn Stone, Christopher J Howe, Kin-chuen Leung, Markus J Seibel, Robert C Baxter, David J Handelsman, Rymantas Kazlauskas, and Ken K Ho*

Garvan Institute of Medical Research and St Vincent's Hospital, Sydney, Australia; CSIRO Mathematical and Information Sciences, North Ryde, Australia; Australian Sports Drug Testing Laboratory, National Measurement Institute, Sydney, Australia; ANZAC Research Institute, University of Sydney, Concord Hospital, Sydney, Australia; Kolling Institute of Medical Research, University of Sydney, Royal North Shore Hospital, Sydney, Australia

* To whom correspondence should be addressed. E-mail: K.Ho{at}garvan.org.au.

Context: IGF axis proteins and collagen peptides are promising markers of GH abuse.

Objective: To investigate whether responses of serum IGF axis and collagen markers to GH differ between men and women, and are influenced by testosterone.

Design: Randomized double-blind placebo-controlled study of 8 weeks treatment followed by 6 weeks washout.

Setting: A clinical research facility.

Participants: 96 recreationally trained healthy athletes (63 men, 33 women), aged 18–40 years.

Intervention: All subjects received GH (2mg/day sc) or placebo for 8 weeks; men also received testosterone (250 mg/week IM) or placebo for 5 weeks.

Main outcome measures: Serum IGF axis proteins (IGF-I, IGFBP-3, ALS) and collagen peptides (PINP, ICTP, PIIINP).

Results: GH induced significant increases in IGF axis and collagen markers which were greater in men than women (P<0.001). Of the IGF axis markers, IGF-I showed the greatest increase. The relative incremental responses of the collagen markers in general were greater than the IGF markers, especially for PIIINP. The collagen markers rose and fell more slowly with most remaining elevated (P<0.01) after 6 weeks, in comparison to IGF markers which returned to baseline within 1 week. Addition of testosterone to GH amplified the response of PIIINP by >1.5-fold, but did not affect any other marker. Testosterone alone did not affect IGF axis markers but modestly increased collagen markers.

Conclusions: These markers of GH abuse are less responsive in women. The increases in collagen markers have a different time course to the IGF markers and extend the window of detection in both sexes. The response of PIIINP is increased by co-administration of testosterone.







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