Huang T S, Wang Y H, Lee S H, Lai J S
Department of Internal Medicine, College of Medicine, National Taiwan University, Taipei, Republic of China.
Am J Phys Med Rehabil. 1998 Mar-Apr;77(2):108-12.
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.
对25名脊髓损伤男性患者进行了研究，采用促肾上腺皮质激素释放激素和胰岛素诱导低血糖法评估下丘脑 - 垂体 - 肾上腺轴。25名年龄匹配的健康男性志愿者作为对照。3名脊髓损伤受试者出现高催乳素血症，3名基础促卵泡激素水平升高，1名基础促黄体生成素水平升高，4名出现低睾酮血症。脊髓损伤受试者对促肾上腺皮质激素释放激素的血浆促肾上腺皮质激素平均反应小于健康对照组，但未达到统计学显著性。脊髓损伤受试者对促肾上腺皮质激素释放激素的皮质醇反应显著低于健康对照组。然而，如果对基线值进行校正，差异就会消失。6名脊髓损伤受试者对胰岛素诱导低血糖无皮质醇反应，且他们的促肾上腺皮质激素反应极小或无反应。另外11名脊髓损伤受试者对胰岛素诱导低血糖的最大皮质醇反应低于正常下限，即0.5微摩尔/升。在这些脊髓损伤受试者中，3名在胰岛素诱导低血糖后血浆促肾上腺皮质激素升高不到50%。这些发现与脊髓损伤受试者中枢神经递质 tone 改变的观点一致，并证实了肾上腺和下丘脑之间存在传入神经通路且可能调节应激诱导的促肾上腺皮质激素分泌这一假说。长期异常的促肾上腺皮质激素分泌可能导致轻度肾上腺皮质萎缩，从而使皮质醇反应降低。
