Soest R, Müller-Lissner S
Innere Abteilung des Krankenhauses Weissensee, Berlin.
Dtsch Med Wochenschr. 1996 Mar 29;121(13):406-8. doi: 10.1055/s-2008-1043019.
For 4 months a 37-year-old woman had been treated for Hashimoto thyroiditis with L-thyroxine, at first 25, then 50 micrograms. From the moment the higher dose had been started she experienced weakness, dizzy spells, nausea, vomiting, weight loss and hyperpigmentation. Her blood pressure was reduced to about 80/60 mm Hg.
The cortisol level was 5.4 nmol/l. When adrenocorticotrophic hormone was administered the cortisol level rose inadequately. Serum ACTH was raised to 3993 pg/ml.
When hydrocortisone was administered (10 mg in the morning plus 5 mg three times daily) her condition immediately improved and L-thyroxine (50 micrograms/d) was now well tolerated.
Substitution with thyroid hormone causes an increased cortisol breakdown in the liver. It is likely that this will have accentuated the previously latent cortisol deficiency resulting from adrenal cortical insufficiency (caused by an autoimmune mechanism) thus producing typical addisonian signs.
一名37岁女性因桥本甲状腺炎接受左甲状腺素治疗4个月,起初剂量为25微克,之后为50微克。自开始使用较高剂量起,她出现乏力、头晕、恶心、呕吐、体重减轻及色素沉着。她的血压降至约80/60毫米汞柱。
皮质醇水平为5.4纳摩尔/升。给予促肾上腺皮质激素后,皮质醇水平升高不足。血清促肾上腺皮质激素升高至3993皮克/毫升。
给予氢化可的松(上午10毫克,每日三次,每次5毫克)后,她的病情立即改善,且现在能很好地耐受左甲状腺素(50微克/天)。
甲状腺激素替代治疗会导致肝脏中皮质醇分解增加。这可能加剧了先前因肾上腺皮质功能不全(由自身免疫机制引起)导致的潜在皮质醇缺乏,从而产生典型的艾迪生病体征。