Rosas Alejandro L, Kasperlik-Zaluska Anna A, Papierska Lucyna, Bass Barbara Lee, Pacak Karel, Eisenhofer Graeme
Department of Anesthesiology, The Methodist Hospital, 6565 Fannin, MS M375, Houston, Texas 77005, USA.
Eur J Endocrinol. 2008 Mar;158(3):423-9. doi: 10.1530/EJE-07-0778.
Pheochromocytoma crisis (PC) is a rare life-threatening endocrine emergency that may present spontaneously or can be unmasked by 'triggers', including certain medications that provoke the release of catecholamines by tumors. Several isolated cases of PC have been reported after administration of exogenous glucocorticoids; evidence that these drugs cause adverse events in patients with pheochromocytoma is mainly anecdotal.
We report four cases of PC most likely induced by glucocorticoids and review seven previous reports in the literature linking steroid administration to the development of PC.
In four new cases reported here, glucocorticoid administration was associated with a fatal outcome in one case, a pheochromocytoma multisystem crisis in another, and serious hypertensive crises in two others. Two patients had incidental adrenal masses and were undergoing high-dose dexamethasone suppression tests (DST).
Exogenous glucocorticoids may unpredictably trigger PC. Pheochromocytoma should be included in the differential diagnosis of any patient who develops a hypertensive crisis, cardiac failure, tachycardia, headache, and abdominal or chest pain after receiving exogenous glucocorticoids. Glucocorticoid induced PC is frequently associated with hemorrhagic pheochromocytoma. Although exogenous glucocorticoids cause serious complications unpredictably, they should be avoided or administered only if necessary and with caution in patients with known or suspected pheochromocytoma. During the investigation of incidental adrenal masses, pheochromocytoma should ideally be ruled out before administering glucocorticoids. However, no cases have been reported with 1 mg of dexamethasone when given as a DST in patients with pheochromocytoma; larger doses, as low as 2 mg of dexamethasone, may trigger a PC. A patient with pheochromocytoma presenting as an adrenal incidentaloma may also be at risk if exposed to glucocorticoids given as pre-treatment in case of allergy to contrast media.
嗜铬细胞瘤危象（PC）是一种罕见的危及生命的内分泌急症，可自发出现或由“触发因素”引发，包括某些促使肿瘤释放儿茶酚胺的药物。已有数例在给予外源性糖皮质激素后发生PC的孤立病例报告；这些药物在嗜铬细胞瘤患者中导致不良事件的证据主要为个案报道。
我们报告了4例极有可能由糖皮质激素诱发的PC病例，并回顾了文献中之前7篇将类固醇给药与PC发生相关联的报道。
在本文报告的4例新病例中，1例糖皮质激素给药与致命结局相关，另1例与嗜铬细胞瘤多系统危象相关，还有2例与严重高血压危象相关。2例患者有肾上腺意外瘤且正在接受大剂量地塞米松抑制试验（DST）。
外源性糖皮质激素可能不可预测地触发PC。对于任何在接受外源性糖皮质激素后出现高血压危象、心力衰竭、心动过速、头痛以及腹痛或胸痛的患者，嗜铬细胞瘤均应纳入鉴别诊断。糖皮质激素诱发的PC常与出血性嗜铬细胞瘤相关。尽管外源性糖皮质激素会不可预测地导致严重并发症，但在已知或疑似嗜铬细胞瘤的患者中，应避免使用，仅在必要时谨慎使用。在对肾上腺意外瘤进行检查期间，理想情况下应在给予糖皮质激素之前排除嗜铬细胞瘤。然而，尚无嗜铬细胞瘤患者在进行DST时给予1 mg地塞米松后发生PC的病例报告；低至2 mg地塞米松的较大剂量可能会触发PC。表现为肾上腺偶发瘤的嗜铬细胞瘤患者如果在对造影剂过敏的情况下接受作为预处理给予的糖皮质激素，也可能有风险。
