Division of Endocrinology and Metabolism, School of Medicine, Dokuz Eylul University, Inciralti, 35340, Izmir, Turkey.
J Endocrinol Invest. 2011 Apr;34(4):265-70. doi: 10.1007/BF03347083. Epub 2010 Jun 4.
Subtle changes in hypothalamic- pituitary-adrenal (HPA) axis of subjects with nonfunctioning adrenal adenoma may be associated with endothelial alterations. We sought to investigate endothelial function, visceral adiposity and osteoprotegerin (OPG) and interleukin- 18 (IL-18) levels in subjects with non-functioning adrenal adenomas.
The adenoma group included 40 subjects without clinical and subclinical findings of hypercortisolism or other adrenal gland disorders. Twenty-two body mass index-matched controls were also enroled. The patients and control subjects underwent hormonal evaluation and assessment of anthropometric and metabolic parameters. Endothelial function was assessed with flowmediated dilatation (FMD) of the brachial artery and intima media thickness (IMT) of common carotid arteries. Visceral adipose tissue area was measured by computed tomography. Plasma OPG and serum IL-18 levels were also measured.
When compared with healthy controls, the adenoma group had elevated systolic blood pressure, post-dexamethasone suppression test cortisol and reduced DHEAS. Visceral adipose tissue area and IMT of common carotid arteries were comparable. In the adenoma group, FMD of the brachial artery was significantly impaired and IL-18 level was significantly elevated. Visceral adipose tissue area was independently related with FMD. Homeostasis model assessment (HOMA) was the independent factor associated with visceral adipose tissue area. Cortisol, DHEAS and visceral adipose tissue area were independently associated with HOMA.
We achieved evidence that could be attributable to endothelial alterations in subjects with non-functioning adrenal adenomas. Impaired FMD appeared to be a consequence of subtle changes in HPA axis in terms of elevated cortisol and reduced DHEAS as these conditions were known to disturb endothelial-dependent vasodilatation.
无功能性肾上腺腺瘤患者的下丘脑-垂体-肾上腺(HPA)轴的细微变化可能与血管内皮改变有关。我们旨在研究无功能性肾上腺腺瘤患者的血管内皮功能、内脏脂肪和骨保护素(OPG)及白介素-18(IL-18)水平。
腺瘤组包括 40 例无临床和亚临床皮质醇增多症或其他肾上腺疾病表现的患者。还招募了 22 名体重指数匹配的对照组。患者和对照组均进行了激素评估,并评估了人体测量和代谢参数。通过肱动脉血流介导的舒张(FMD)和颈总动脉内膜中层厚度(IMT)评估内皮功能。通过计算机断层扫描测量内脏脂肪组织面积。还测量了血浆 OPG 和血清 IL-18 水平。
与健康对照组相比,腺瘤组的收缩压、地塞米松抑制后皮质醇和 DHEAS 降低。颈总动脉 IMT 与内脏脂肪组织面积相当。在腺瘤组,肱动脉 FMD 显著受损,IL-18 水平显著升高。内脏脂肪组织面积与 FMD 独立相关。稳态模型评估(HOMA)是与内脏脂肪组织面积相关的独立因素。皮质醇、DHEAS 和内脏脂肪组织面积与 HOMA 独立相关。
我们有证据表明,无功能性肾上腺腺瘤患者存在内皮改变。FMD 受损可能是由于 HPA 轴中皮质醇升高和 DHEAS 降低导致的细微变化,因为这些情况已知会干扰内皮依赖性血管舒张。