Fallo Francesco, Della Mea Paolo, Sonino Nicoletta, Bertello Chiara, Ermani Mario, Vettor Roberto, Veglio Franco, Mulatero Paolo
Department of Medical and Surgical Sciences, University of Padova, Padova, Italy.
Am J Hypertens. 2007 Aug;20(8):855-61. doi: 10.1016/j.amjhyper.2007.03.012.
A high prevalence of metabolic syndrome has been reported in primary aldosteronism. Low levels of adiponectin, an adipokine with insulin-sensitizing properties, are considered a hallmark of the metabolic syndrome. We evaluated the relationship between adiponectin and insulin sensitivity in primary aldosteronism, with and without metabolic syndrome, compared with essential hypertension.
Forty patients with primary aldosteronism and 40 matched patients with low-renin essential hypertension (LREH) were studied. Patients with type 2 diabetes were excluded. Each group was divided into two subsets: one including patients with metabolic syndrome and one including patients without metabolic syndrome (ie, hypertension alone or associated with another component of the syndrome).
Insulin resistance, defined by increased homeostasis model assessment (HOMA index), was higher in patients with primary aldosteronism than in those with LREH only in the absence of metabolic syndrome (P<.01), whereas in the subsets bearing the syndrome it was similar. Adiponectin levels were lower in primary aldosteronism than in patients with LREH (P<.01). Like HOMA index, the difference was maintained (P<.01) only in the subsets without metabolic syndrome. Adiponectin levels were inversely correlated with HOMA index and positively correlated with potassium levels both in primary aldosteronism (P<.001) or in LREH (P<.05) groups.
Lower adiponectin as well as lower insulin sensitivity in primary aldosteronism compared with LREH seem to result from both direct (aldosterone excess) and indirect (hypokalemia) mechanisms. Therapeutic interventions aimed at correcting both potassium and adiponectin levels by specific antihypertensive agents might improve insulin sensitivity, providing better cardiovascular protection in primary aldosteronism.
原发性醛固酮增多症患者中代谢综合征的患病率较高。脂联素是一种具有胰岛素增敏特性的脂肪因子，其水平降低被认为是代谢综合征的一个标志。我们评估了原发性醛固酮增多症患者（无论有无代谢综合征）脂联素与胰岛素敏感性之间的关系，并与原发性高血压进行比较。
研究了40例原发性醛固酮增多症患者和40例匹配的低肾素原发性高血压（LREH）患者。排除2型糖尿病患者。每组分为两个亚组：一个亚组包括代谢综合征患者，另一个亚组包括无代谢综合征患者（即单纯高血压或合并综合征的其他组分）。
仅在无代谢综合征的情况下，原发性醛固酮增多症患者的胰岛素抵抗（通过稳态模型评估（HOMA指数）升高来定义）高于LREH患者（P<0.01），而在有该综合征的亚组中两者相似。原发性醛固酮增多症患者的脂联素水平低于LREH患者（P<0.01）。与HOMA指数一样，仅在无代谢综合征的亚组中差异仍然存在（P<0.01）。在原发性醛固酮增多症组（P<0.001）或LREH组（P<0.05）中，脂联素水平与HOMA指数呈负相关，与血钾水平呈正相关。
与LREH相比，原发性醛固酮增多症患者较低的脂联素水平以及较低的胰岛素敏感性似乎是由直接（醛固酮过多）和间接（低钾血症）机制共同导致的。通过特定降压药物纠正血钾和脂联素水平的治疗干预可能会改善胰岛素敏感性，为原发性醛固酮增多症提供更好的心血管保护。
