Haase Matthias, Dringenberg Till, Allelein Stephanie, Willenberg Holger S, Schott Matthias
Division for Specific Endocrinology, Medical Faculty, University of Duesseldorf, Duesseldorf, Germany.
Division of Endocrinology and Metabolism, Rostock University Medical Center, Rostock, Germany.
Horm Metab Res. 2017 Oct;49(10):748-754. doi: 10.1055/s-0043-117179. Epub 2017 Aug 24.
Catecholamines stimulate renin-secretion in the juxtaglomerular cells of the kidney and a number of case reports suggest an association between pheochromocytoma and activation of the RAAS. Therefore, it could be asked whether patients suffering from pheochromocytoma with high concentrations of circulating catecholamines present with oversecretion of renin and aldosterone. We identified twelve patients with excessive catecholamine secretion due to pheochromocytoma and compared them to a group of twelve patients with essential hypertension (EH) with regard to the activation of the renin-angiotensin-aldosterone-system (RAAS). The PubMed database was screened for studies that investigate the association between pheochromocytoma and activation of the RAAS. The plasma concentrations of metanephrines (19.9-fold) and normetanephrines (29.5-fold) were significantly higher in the pheochromocytoma group than in the EH group. Renin and aldosterone levels were 1.3-fold and 1.6-fold higher, respectively, as compared to the EH group, whereas the differences were not statistically significant. There was no significant correlation between plasma metanephrine or normetanephrine levels and the plasma renin concentration (r=0.077, r=0.049, respectively) in our patients. The data from our institution and from review of literature suggest that an association between pheochromocytoma in the context of high plasma catecholamine levels and activation of the RAAS is present. However, results have not been consistent. Thus, other causes of RAAS-activation should be considered also in the presence of pheochromocytoma or reinvestigation for aldosteronism should be offered to such patients after removal of the catecholamine-producing tumour.
儿茶酚胺可刺激肾脏球旁细胞分泌肾素，一些病例报告提示嗜铬细胞瘤与肾素 - 血管紧张素 - 醛固酮系统（RAAS）激活之间存在关联。因此，可能会有人问，患有嗜铬细胞瘤且循环儿茶酚胺浓度高的患者是否存在肾素和醛固酮分泌过多的情况。我们确定了12例因嗜铬细胞瘤导致儿茶酚胺分泌过多的患者，并将他们与12例原发性高血压（EH）患者在肾素 - 血管紧张素 - 醛固酮系统（RAAS）激活方面进行比较。在PubMed数据库中筛选了研究嗜铬细胞瘤与RAAS激活之间关联的研究。嗜铬细胞瘤组的间甲肾上腺素（19.9倍）和去甲间甲肾上腺素（29.5倍）血浆浓度显著高于EH组。与EH组相比，肾素和醛固酮水平分别高出1.3倍和1.6倍，但差异无统计学意义。在我们的患者中，血浆间甲肾上腺素或去甲间甲肾上腺素水平与血浆肾素浓度之间无显著相关性（r分别为0.077和0.049）。我们机构的数据以及文献综述表明，在高血浆儿茶酚胺水平情况下，嗜铬细胞瘤与RAAS激活之间存在关联。然而，结果并不一致。因此，在存在嗜铬细胞瘤的情况下，也应考虑RAAS激活的其他原因，或者在切除产生儿茶酚胺的肿瘤后，应为这类患者重新进行醛固酮增多症的检查。
