Shannon D Sullivan1, Mark S Nash2, Eshetu Tefera3, Emily Tinsley4, Marc R Blackman5, Suzanne Groah6. 1. Center for Drug Evaluation and Research, US Food and Drug Administration, 10903 New Hampshire Ave, Building 22, Room 3373, Silver Spring, MD 20993(∗). Electronic address: Shannon.sullivan@fda.hhs.gov. 2. Departments of Neurological Surgery and Rehabilitation Medicine, University of Miami Miller School of Medicine, Miami, FL(†). 3. Department of Biostatistics and Bioinformatics, Medstar Health Research Institute, Hyattsville, MD(‡). 4. Department of Rehabilitation Medicine, Medstar National Rehabilitation Hospital, Washington, DC(§). 5. Research Service, Washington, DC VA Medical Center, Washington, DC; Departments of Medicine and Rehabilitation Medicine, Georgetown University School of Medicine, Washington, DC; Departments of Medicine, Biochemistry and Molecular Medicine, George Washington University School of Medicine, Washington, DC(¶). 6. Department of Rehabilitation Medicine, Medstar National Rehabilitation Hospital, Washington, DC; Department of Rehabilitation Medicine, Medstar Georgetown University Hospital, Washington, DC(#).
Abstract
BACKGROUND: Spinal cord injury (SCI) triggers an "accelerated aging" process that may include development of hypogonadism, even among younger men with SCI; however, few studies have investigated the prevalence or etiology of hypogonadism in men with SCI. Young men with SCI also are at increased risk for developing metabolic dysfunction after injury, which may be exacerbated by concomitant testosterone (T) deficiency, thus identifying the prevalence and risk factors for T deficiency in men with SCI is important for their long-term health. OBJECTIVE: To investigate the prevalence, risk factors, and etiology of T deficiency (hypogonadism) in otherwise-healthy men with chronic, motor complete SCI. DESIGN: Secondary cross-sectional analysis. SETTING: Rehabilitation research centers in Washington, DC, and Miami, Florida. PARTICIPANTS: Men (n = 58) aged 18-45 years with chronic (≥1 year), motor complete SCI without comorbidities or use of testosterone therapy. METHODS: Plasma concentrations of hormones were measured with standardized assays. Body composition was assessed with dual-energy x-ray absorptiometry scan. MAIN OUTCOME MEASUREMENTS: Serum total T and calculated free T. RESULTS: T deficiency was more common in men after SCI than in a matched cohort of similarly-aged men without SCI (25%, SCI versus 6.7%, non-SCI, P < .001). The risk of hypogonadism appeared to be increased in men with more extensive injury and with higher percent body fat. The majority of men with SCI with low T had low serum LH levels, suggesting that central suppression of the hypothalamic-pituitary-gonadal axis may be the most common etiology of hypogonadism after SCI. CONCLUSIONS: Hypogonadism is more common in young men with SCI than in similarly aged men without SCI, suggesting that SCI should be identified as a risk factor for T deficiency and that routine screening for hypogonadism should be performed in the SCI population. LEVEL OF EVIDENCE: II.
BACKGROUND:Spinal cord injury (SCI) triggers an "accelerated aging" process that may include development of hypogonadism, even among younger men with SCI; however, few studies have investigated the prevalence or etiology of hypogonadism in men with SCI. Young men with SCI also are at increased risk for developing metabolic dysfunction after injury, which may be exacerbated by concomitant testosterone(T) deficiency, thus identifying the prevalence and risk factors for T deficiency in men with SCI is important for their long-term health. OBJECTIVE: To investigate the prevalence, risk factors, and etiology of T deficiency (hypogonadism) in otherwise-healthy men with chronic, motor complete SCI. DESIGN: Secondary cross-sectional analysis. SETTING: Rehabilitation research centers in Washington, DC, and Miami, Florida. PARTICIPANTS: Men (n = 58) aged 18-45 years with chronic (≥1 year), motor complete SCI without comorbidities or use of testosterone therapy. METHODS: Plasma concentrations of hormones were measured with standardized assays. Body composition was assessed with dual-energy x-ray absorptiometry scan. MAIN OUTCOME MEASUREMENTS: Serum total T and calculated free T. RESULTS:T deficiency was more common in men after SCI than in a matched cohort of similarly-aged men without SCI (25%, SCI versus 6.7%, non-SCI, P < .001). The risk of hypogonadism appeared to be increased in men with more extensive injury and with higher percent body fat. The majority of men with SCI with low T had low serum LH levels, suggesting that central suppression of the hypothalamic-pituitary-gonadal axis may be the most common etiology of hypogonadism after SCI. CONCLUSIONS:Hypogonadism is more common in young men with SCI than in similarly aged men without SCI, suggesting that SCI should be identified as a risk factor for T deficiency and that routine screening for hypogonadism should be performed in the SCI population. LEVEL OF EVIDENCE: II.
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