Department of Medical and Surgical Sciences, University of Padova, Padova, Italy.
J Hypertens. 2011 Sep;29(9):1773-7. doi: 10.1097/HJH.0b013e32834937f3.
Primary aldosteronism is the most frequent cause of secondary hypertension and is responsible for an increased risk of cardiometabolic complications. A concomitant subtle cortisol hyperproduction could enhance cardiovascular risk. We prospectively estimated the occurrence of subclinical hypercortisolism in primary aldosteronism patients.
In a large population of hypertensive patients without clinical signs of hypercortisolism, 76 consecutive patients with primary aldosteronism were investigated. Differential diagnosis between unilateral and bilateral aldosterone hypersecretion was made by computed tomography/MRI and/or adrenal venous sampling (AVS). Subclinical hypercortisolism was defined as failure to suppress plasma cortisol to less than 50 nmol/l after 1 mg-overnight dexamethasone, used as screening test, and at least one of two other abnormal hormonal parameters, that is, adrenocorticotrophin (ACTH) less than 2 pmol/l and urinary cortisol more than 694 nmol/24 h.
Three out of 76 patients had postdexamethasone plasma cortisol more than 50 nmol/l. Only one also showed low-normal ACTH and mildly elevated urinary cortisol. The patient had a right 4 cm adrenal mass. Laparoscopic adrenalectomy was followed by short-term steroid replacement to prevent adrenal insufficiency. In-situ hybridization showed CYP11B1 expression exclusively in tumoral tissue, whereas CYP11B2 was expressed only in a peritumoral region composed of zona glomerulosa-like cells, suggesting the co-existence of a cortisol-producing adenoma and an aldosterone-producing hyperplasia in the same adrenal. The restoration of hormone abnormalities to normal levels was confirmed at 12 months of follow-up.
Concurrent aldosterone and subclinical cortisol hypersecretion seems to be a rare event in primary aldosteronism patients; however, its detection by appropriate testing is important to avoid AVS misinterpretation.
原发性醛固酮增多症是继发性高血压最常见的病因，可导致代谢心血管并发症风险增加。同时存在轻微的皮质醇过度生成可能会增加心血管风险。我们前瞻性地评估了原发性醛固酮增多症患者亚临床性皮质醇增多症的发生情况。
在没有皮质醇增多症临床迹象的高血压患者的大人群中，我们调查了 76 例连续的原发性醛固酮增多症患者。单侧和双侧醛固酮分泌过多的鉴别诊断通过计算机断层扫描/磁共振成像和/或肾上腺静脉采样（AVS）进行。亚临床性皮质醇增多症的定义为使用 1 mg 地塞米松进行 overnight 筛查后，血浆皮质醇未能抑制到 50 nmol/l 以下，并且至少存在两个其他异常激素参数之一，即促肾上腺皮质激素（ACTH）<2 pmol/l 和尿皮质醇>694 nmol/24 h。
76 例患者中有 3 例在使用地塞米松后血浆皮质醇>50 nmol/l。只有 1 例患者同时显示 ACTH 水平正常低值和轻度升高的尿皮质醇。该患者右侧有一个 4 cm 的肾上腺肿块。腹腔镜肾上腺切除术随后进行短期类固醇替代治疗以预防肾上腺功能不全。原位杂交显示 CYP11B1 仅在肿瘤组织中表达，而 CYP11B2 仅在由类似于球状带样细胞的肿瘤周围区域表达，提示在同一肾上腺中存在皮质醇产生腺瘤和醛固酮产生增生共存。在 12 个月的随访中，激素异常恢复到正常水平。
在原发性醛固酮增多症患者中，同时存在醛固酮和亚临床性皮质醇过度分泌似乎是一种罕见事件；然而，通过适当的检测发现它非常重要，以避免对 AVS 的错误解释。
