Hood Sue, Cannon John, Foo Roger, Brown Morris
Clinical Pharmacology Unit, Addenbrooke's Hospital, Cambridge.
Clin Med (Lond). 2005 Jan-Feb;5(1):55-60. doi: 10.7861/clinmedicine.5-1-55.
Recent studies have suggested that primary hyperaldosteronism may be present in more than 10% of patients with hypertension. We aimed to estimate the prevalence in unselected patients in primary care, and investigate the influence of current drug treatment upon the aldosterone/renin ratio (ARR) and its prediction of blood pressure response to spironolactone. We measured blood pressure, plasma electrolytes, renin activity and aldosterone in 846 patients with hypertension. Spironolactone 50 mg was prescribed for one month to patients with blood pressure > or = 130/85 mmHg and ARR > or = 400. The primary outcome measure was to discover the proportion of patients with plasma aldosterone > or = 400 pmol/l and ARR > or = 800 and either an adrenal adenoma on computed tomography scan or a systolic blood pressure response to spironolactone > or = 20 mmHg. Only one patient had an adenoma, and only 16 (1.8%) had both a plasma aldosterone > or = 400 pmol/l and ARR > or = 800. By contrast, 119 patients (14.1%) had an elevated ARR but normal plasma aldosterone. In 69 patients out of the 119 who received spironolactone, blood pressure fell by 26/11 mmHg. These patients were normokalaemic but had uncontrolled hypertension despite multiple drugs. The response to spironolactone was best predicted by a low plasma renin, < or = 0.5 pmol/ml/h (<10 mU/l), despite treatment with an ACE inhibitor. We concluded that adrenal adenomas are an uncommon cause of hypertension. In the absence of hypokalaemia, a low plasma renin is a sufficient and simple way of detecting spironolactone-responders among patients with resistant hypertension. Only patients with both hypokalaemia and low plasma renin, measured while the patient is off beta blockade, require measurement of aldosterone. A plasma aldosterone >400 pmol/l together with renin activity < or = 0.5 pmol/ml/h should trigger further investigations for an adrenal adenoma.
近期研究表明,原发性醛固酮增多症可能存在于超过10%的高血压患者中。我们旨在评估初级保健中未经挑选的患者的患病率,并研究当前药物治疗对醛固酮/肾素比值(ARR)的影响及其对螺内酯血压反应的预测作用。我们测量了846例高血压患者的血压、血浆电解质、肾素活性和醛固酮。对于血压≥130/85 mmHg且ARR≥400的患者,给予50 mg螺内酯治疗1个月。主要结局指标是发现血浆醛固酮≥400 pmol/l且ARR≥800,以及计算机断层扫描显示肾上腺腺瘤或对螺内酯的收缩压反应≥20 mmHg的患者比例。只有1例患者有腺瘤,只有16例(1.8%)血浆醛固酮≥400 pmol/l且ARR≥800。相比之下,119例患者(14.1%)的ARR升高但血浆醛固酮正常。在接受螺内酯治疗的119例患者中,69例患者的血压下降了26/11 mmHg。这些患者血钾正常,但尽管使用了多种药物,高血压仍未得到控制。尽管使用了血管紧张素转换酶抑制剂治疗,但血浆肾素低(≤0.5 pmol/ml/h,即<10 mU/l)对螺内酯反应的预测效果最佳。我们得出结论,肾上腺腺瘤是高血压的一种罕见病因。在无低钾血症的情况下,血浆肾素低是在难治性高血压患者中检测螺内酯反应者的一种充分且简单的方法。只有在停用β受体阻滞剂时测量血钾低且血浆肾素低的患者才需要检测醛固酮。血浆醛固酮>400 pmol/l且肾素活性≤0.5 pmol/ml/h应引发对肾上腺腺瘤的进一步检查。