Guignat Laurence, de Bucy Charlotte, Bertherat Jérôme
Centre de référence maladies rares de la surrénale, service des maladies endocriniennes et métaboliques, hôpital Cochin, AP-HP, 75679 Paris.
Rev Prat. 2008 May 15;58(9):966-70.
Glucocorticoid treatments inhibit adrenal axis at the hypothalamo-pituitary level. This inhibition decreases ACTH plasma levels, leading to unpredictable secondary adrenal insufficiency after glucocorticoids withdrawal. Almost half of the patients will present with corticotrop axis suppression after long term glucocorticoid treatment. Glucocorticoid dose and duration of treatment might be linked to hypothalamic-pituitary-adrenal suppression; but some not yet clearly identified individual parameters are also important. After long-term glucocorticoid treatment, in order to reduce the risk of clinical sign of adrenal deficiency, the glucocorticoid dose is progressively decreased. When the daily glucocorticoid dose is tapered below 5 mg/day of equivalent prednisone, a hydrocortisone substitutive treatment can be started. Before discontinuation of the treatment the full recovery of the corticotrop axis could be assayed by corticotropin stimulation test.
糖皮质激素治疗在丘脑 - 垂体水平抑制肾上腺轴。这种抑制会降低促肾上腺皮质激素(ACTH)的血浆水平,导致停用糖皮质激素后出现不可预测的继发性肾上腺功能不全。几乎一半的患者在长期接受糖皮质激素治疗后会出现促肾上腺皮质激素轴抑制。糖皮质激素的剂量和治疗持续时间可能与下丘脑 - 垂体 - 肾上腺抑制有关;但一些尚未明确识别的个体参数也很重要。长期糖皮质激素治疗后,为降低肾上腺功能不全临床症状的风险,需逐渐减少糖皮质激素剂量。当每日糖皮质激素剂量逐渐减至低于相当于5毫克/天的泼尼松时,可开始氢化可的松替代治疗。在停止治疗前,可通过促肾上腺皮质激素刺激试验检测促肾上腺皮质激素轴的完全恢复情况。