Azar S T, Melby J C
Evans Memorial Department of Clinical Research, Boston University Medical Center, Massachusetts 02118.
Am J Med Sci. 1993 May;305(5):321-5. doi: 10.1097/00000441-199305000-00012.
Patients with acquired immune deficiency syndrome (AIDS) are reported to have increased basal cortisol and reduced stimulated cortisol release, but the dysfunction in the hypothalamic-pituitary-adrenal (HPA) axis is not yet understood in patients with human immunodeficiency virus (HIV) infection during the advanced stage of disease that precedes the development of AIDS. To understand the status of the HPA axis during this phase of HIV infection, 25 non-AIDS ambulatory patients with advanced HIV infection and without evidence of adrenal or pituitary insufficiency were studied. Ovine corticotropin-releasing hormone was administered (1 microgram/kg BW) intravenously and plasma cortisol and adrenocorticotropin (ACTH) were measured over the following 120 minutes. Based on a standard response curve, obtained from CRH testing of 10 HIV negative volunteers with no HPA abnormalities, 13 patients were found to have normal response (group 1), 6 patients had reduced ACTH and cortisol response (group 2) and 6 patients had normal ACTH with reduced cortisol response (group 3). Basal cortisol and basal ACTH were comparable for control subjects and groups 1, 2, and 3. This suggests that, in advanced non-AIDS HIV patients with no clinical evidence of pituitary or adrenal disease, about 25% (group 2) have reduced pituitary reserve with high basal ACTH and cortisol, and about 25% (group 3) have reduced adrenal reserve with high basal cortisol and inappropriately normal basal ACTH, whereas about 50% (group 1) maintain normal HPA axis activity with increased basal cortisol secretion. The exact physiopathologic mechanism is not yet known, but an enhanced CRH production by the hypothalamus may explain the alterations in the HPA axis in advanced HIV disease.
据报道，获得性免疫缺陷综合征（AIDS）患者的基础皮质醇水平升高，刺激后的皮质醇释放减少，但在人类免疫缺陷病毒（HIV）感染且处于AIDS发生前疾病晚期阶段的患者中，下丘脑-垂体-肾上腺（HPA）轴功能障碍尚未明确。为了解HIV感染此阶段HPA轴的状态，对25例非AIDS门诊患者进行了研究，这些患者处于HIV感染晚期，且无肾上腺或垂体功能不全的证据。静脉注射羊促肾上腺皮质激素释放激素（1微克/千克体重），并在随后的120分钟内测量血浆皮质醇和促肾上腺皮质激素（ACTH）。根据对10名无HPA异常的HIV阴性志愿者进行CRH测试获得的标准反应曲线，发现13例患者反应正常（第1组），6例患者的ACTH和皮质醇反应降低（第2组），6例患者的ACTH正常但皮质醇反应降低（第3组）。对照组与第1、2、3组的基础皮质醇和基础ACTH水平相当。这表明，在无垂体或肾上腺疾病临床证据的晚期非AIDS HIV患者中，约25%（第2组）的垂体储备降低，基础ACTH和皮质醇水平升高；约25%（第3组）的肾上腺储备降低，基础皮质醇水平升高且基础ACTH水平异常正常；而约50%（第1组）的HPA轴活动正常，但基础皮质醇分泌增加。确切的生理病理机制尚不清楚，但下丘脑促肾上腺皮质激素释放激素分泌增加可能解释了晚期HIV疾病中HPA轴的改变。
