title: Impaired hypothalamus-pituitary-adrenal axis in men with spinal cord injuries.
abstract: Twenty-five men with spinal cord injuries were studied for evaluation of the hypothalamus-pituitary-adrenal axis, using corticotropin-releasing hormone and insulin-induced hypoglycemia. Twenty-five age-matched healthy male volunteers served as controls. Three spinal cord-injured subjects had hyperprolactinemia, three had elevated basal follicle-stimulating hormone levels, one had an elevated basal luteinizing hormone level, and four had hypotestosteronemia. The mean plasma adrenocorticotropin response to corticotropin-releasing hormone of spinal cord-injured subjects was smaller than that of the healthy controls but did not reach a statistical significance. The cortisol response to corticotropin-releasing hormone of the spinal cord-injured subjects was significantly lower than that of healthy controls. However, the difference disappeared if a correction was made for baseline values. Six spinal cord-injured subjects did not have a cortisol response to insulin-induced hypoglycemia, and they had either a minimal or no adrenocorticotropin response. Another 11 spinal cord-injured subjects had a maximal cortisol response to insulin-induced hypoglycemia below the lowest limit of normal, i.e., 0.5 micromol/l. Among these spinal cord-injured subjects, three had a less than 50% increase of plasma adrenocorticotropin after insulin-induced hypoglycemia. These findings are consistent with the notion that spinal cord-injured subjects have an altered central neurotransmitter tone and substantiate the hypothesis that an afferent neural pathway exists between the adrenal and hypothalamus and may modulate stress-induced secretion of adrenocorticotropin. Long-term abnormal adrenocorticotropin secretion may cause mild adrenocortical atrophy and, thereby, a reduced cortisol response.
authors.affiliation: Department of Internal Medicine, College of Medicine, National Taiwan University, Taipei, Republic of China.
authors.forename: T S
authors.initials: TS
authors.lastname: Huang
authors.forename: Y H
authors.initials: YH
authors.lastname: Wang
authors.forename: S H
authors.initials: SH
authors.lastname: Lee
authors.forename: J S
authors.initials: JS
authors.lastname: Lai
mesh_terms: D000293:Adolescent; D000304:Adrenal Cortex Function Tests; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D000344:Afferent Pathways / Q000503:physiopathology; D001786:Blood Glucose / Q000032:analysis; D016022:Case-Control Studies; D005640:Follicle Stimulating Hormone / Q000097:blood; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D008875:Middle Aged; D010913:Pituitary-Adrenal System / Q000503:physiopathology*; D011388:Prolactin / Q000097:blood; D013119:Spinal Cord Injuries / Q000097:blood / Q000503:physiopathology*; D013739:Testosterone / Q000097:blood
chemical_list: D001786:Blood Glucose; D013739:Testosterone; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone