Transient hypogonadotrophic hypogonadism after head trauma: effects on steroid precursors and correlation with sympathetic nervous system activity.
Transient hypogonadotrophic hypogonadism commonly occurs after major medical insults. Because data on testosterone precursors are sparse and because little is known about the aetiology of these changes, we studied the interactions of traumatic brain injury with gonadal steroidogenesis and with sympathetic nervous system activation. Patients were divided into two groups based upon the severity of neurological dysfunction using the Glasgow Coma Score (GCS); Group 1 less than 8, Group 2 greater than or equal to 8. Group 1 was further divided into those patients treated (Group 1b) and those not treated with dexamethasone (Group 1a). Plasma levels of testosterone, androstenedione, 17-hydroxyprogesterone, DHEA sulphate, cortisol, LH, FSH, and the catecholamines noradrenaline (NE), adrenaline (EPI) and dopamine were measured in 31 acutely brain injured men, aged 18-95, shortly after their accident and 4 days later. In all patients, NE and EPI were elevated on admission (NE: 841 +/- 105 (SEM) pg/ml; EPI: 191 +/- 32 pg/ml and there were highly significant inverse correlations between admission NE (r = -0.52, P less than 0.003) and EPI (r = 0.44, P less than 0.02) levels and day 4 testosterone concentrations. Testosterone fell 53% (P less than 0.001) in 13 Group 1a men, but only 25% (P = NS) in the less severely injured. Similar reductions occurred in cortisol and the steroid precursors. However, only testosterone, 17-hydroxyprogesterone, and DHEA sulphate levels were significantly lower than normal on day 4. LH and FSH levels were also significantly reduced from elevated admission levels. In the eight men treated with dexamethasone (8-40 mg/ml) (Group 1b), the decrease in testosterone, LH and FSH concentrations were similar to those present in Group 1a. Thus, severe traumatic brain injury leads to hypogonadotrophic hypogonadism which affects testosterone and its precursors. The magnitude of the hormonal dysfunction is dependent upon the severity of the neurological insult. Finally, the decrease in testosterone is significantly correlated with admission catecholamine levels, which may suggest a role for the sympathetic nervous system (SNS) in mediating this response in men.
D000293:Adolescent; D000328:Adult; D000368:Aged; D002395:Catecholamines / Q000097:blood; D006259:Craniocerebral Trauma / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D003907:Dexamethasone / Q000627:therapeutic use; D005640:Follicle Stimulating Hormone / Q000097:blood; D006728:Hormones / Q000097:blood*; D006801:Humans; D007006:Hypogonadism / Q000188:drug therapy / Q000209:etiology*; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D008875:Middle Aged; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D013739:Testosterone / Q000097:blood
D002395:Catecholamines; D006728:Hormones; D013739:Testosterone; D003907:Dexamethasone; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone