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Endocrinology and Metabolism Unit, Developmental Origins of Health and Disease Division, School of Medicine (I.E.-M., C.M., R.S., B.C., V.W., K.H., P.H.S., R.I.G.H.), University of Southampton, Southampton SO16 6YD, United Kingdom; Institute of Mathematics, Statistics, and Actuarial Science (E.E.B.), University of Kent, Canterbury, Kent CT2 7NZ, United Kingdom; and Department of Forensic Science (C.B., D.C.), Drug Monitoring, Drug Control Centre, Kings College London, London SE5 9RS, United Kingdom
Address all correspondence and requests for reprints to: Dr. Richard I. G. Holt, The Institute of Developmental Sciences (IDS Building), MP887, University of Southampton, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, United Kingdom. E-mail: r.i.g.holt{at}soton.ac.uk.
Context: A method to detect exogenously administered growth hormone (GH) based on the measurement of two GH-dependent markers, IGF-I and type 3 procollagen (P-III-P) has been proposed. Skeletal or soft tissue injury may alter these markers. Elevations in either of these proteins after injury might lead to a false accusation of doping with GH.
Objective: The objective of the study was to assess the effect of musculoskeletal or soft tissue injury on IGF-I and P-III-P concentrations in amateur and elite athletes and assess the effect of injury on the proposed GH detection method.
Design: This was a longitudinal observational study after sporting injury.
Setting: The study was conducted at Southampton General Hospital and British Olympic Medical Centre.
Subjects: Subjects included elite and amateur athletes after an injury.
Intervention: Interventions included measurement of IGF-I and P-III-P and application of the GH-2000 discriminant function score up to 84 d after an injury as well as classification of injury by type and severity.
Outcome Measures: IGF-I and P-III-P concentration and ability to detect GH abuse in athletes without the risk of false accusation because of an injury were measured.
Results: There was no change in IGF-I concentration after an injury. By contrast, P-III-P concentrations rose by 41.1 ± 16.6%, reaching a peak around 14 d after an injury. The rise in P-III-P varied according to injury type and severity. This rise had a trivial effect on the GH-2000 discriminant function score, and no subject reached the threshold needed for a doping offense.
Conclusions: Although there was a rise in P-III-P after injury, this was insufficient to invalidate the GH-2000 detection method based on IGF-I and P-III-P concentrations.
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