顽固性高血压应警惕原发性醛固酮增多症

原发性醛固酮增多症 (原醛 )由Ｃｏｎｎ(196 4)首次报道 ,由于肾皮质产生肿瘤或增生使醛固酮分泌过多 ,前者可经手术切除 ,后者不适于手术 ,对一般降压药物又疗效欠佳 ,对醛固酮拮抗剂 (安替舒通 )疗效好。不久前认为原醛是少见病 ,占高血压人群少于 1%,只有在高血压合并低血钾 (需除外利尿剂所致 )时才考虑进一步检查。近年来改变筛选方法 (ＡＲＲ)以后才逐渐认识到原醛比以前多见 ,患病率占高血压人群 10 %以上[1] 。Ｈｉｒａｍａｔｓｕ等[2 ] (1981)首次以ＡＲＲ(醛固酮、肾素ＰＲＡ比值 )简易方法筛选原醛 ,从 34 8例原发性高血压病人中…     

原发性醛固酮增多症与高血压

原发性醛固酮增多症(简称原醛症)以高血压、低血钾和低钾碱中毒为主要临床表现,多见于成人。原醛症是一种可以治愈的继发性高血压病,但如病程过久可造成心、肾、脑损害,并可因严重的低血钾而危及病人的生命。因此,早期诊断、正确处理甚为重要。因本症有高血压、低血钾和低钾碱中毒,故病     

原发性醛固酮增多症

肾上腺皮质球状带病变,分泌过量醛固酮,使人体产生一系列内分泌代谢紊乱,临床上表现为特征性高血压和低血钾的征候群,称为原发性醛固酮增多症(简称原醛症)。     

原发性醛固酮增多症

原发性醛固酮增多症(原醛症)是继发性高血压的常见病因之一,部分患者亦可伴有低血钾,醛固酮瘤及特发性醛固酮增多症是其主要的病理亚型。原醛症的诊断包括筛查、确诊及分型诊断3个步骤,传统影像学结合体位刺激的方法进行分型诊断,假阳性及假阴性率均较高,肾上腺静脉插管采血可作为影像学检查的补充。醛固酮瘤及原发性肾上腺增生患者应予手术治疗,特发性醛固酮增多症患者多采用药物治疗,螺内酯是其首选药物。     

原发性醛固酮增多症

原发性醛固酮增多症(简称原醛)典型临床表现为"高血压、低血钾",有学者推测高达20%的高血压可能为原醛.我国是高血压大国,保守估计高血压人群在1亿人以上,但原醛在我国的发现率仍很低,其中很大一部分原因在于我们对于原醛的认识不够.     

原发性醛固酮增多症

原发性醛固酮增多症(primary aldosteronism,简称原醛)是指由于肾上腺皮质自主性醛固酮分泌增多而导致以高血压、低血浆肾素活性(PRA)、高醛固酮血症和低钾血症为特征的临床综合征,是继发性高血压常见病因之一。原醛最常见的病因是特发性醛固酮增多症和肾上腺腺瘤,分别占65%和3     

原发性醛固酮增多症高血压患者临床特征分析

目的:分析近两年中国医学科学院阜外医院确诊为原发性醛固酮增多症(PA)的高血压患者的临床特征。方法:回顾性收集2016-01至2017-12期间中国医学科学院阜外医院高血压病房收治的4 782例高血压患者资料,将其中的PA患者与原发性高血压(PH)患者根据年龄、性别1:2匹配后比较其临床特征,并比较血钾正常和低钾血症(3.5 mmol/L)PA患者的临床特征。结果:247例(5.2%)患者确诊为PA,其中位年龄48.8(16.6)岁,男性148例(59.9%),143例(57.9%)有低钾血症。与PH患者相比,PA患者收缩压较高[150(24)mm Hg vs 145(27)mm Hg,1 mm Hg=0.133 k Pa],左心室质量指数(LVMI)较高[83.4(36.6)g/m~2 vs 75.7(26.2)g/m~2],尿微量白蛋白/肌酐较高[24.1(41.1)mg/g vs 10.5(22.1)mg/g],合并冠心病(12.6%vs 7.7%)和外周动脉疾病(11.7%vs 4.7%)者比例较高,但低密度脂蛋白胆固醇[2.6(1.0)mmol/L vs 2.9(1.1)mmol/L]、总胆固醇[4.4(1.2)mmol/L vs 4.6(1.3)mmol/L]和糖化血红蛋白水平[5.4(0.6)%vs 5.6(0.6)%]较低,差异均有统计学意义(P均0.05)。与血钾正常的PA患者相比,低钾血症PA患者年龄较小[45.9(16.8)岁vs51.3(14.3)岁],但舒张压[95(26)mm Hg vs 90(20)mm Hg]、尿微量白蛋白/肌酐[28.5(40.6)mg/g vs 20.5(32.8)mg/g]和LVMI [86.5(34.8)g/m2 vs 77.9(31.8)g/m~2]较高,差异均有统计学意义(P均0.05)。结论:与PH患者相比,PA患者靶器官损害重,合并心血管病比例高。有低钾血症的PA患者年龄较小,但舒张压较高且靶器官损害较重。     

原发性高血压还是特发性醛固酮增多症?

1 病例资料 患者,男性,汉族,52岁,因“发现血压升高10余年,视物模糊1周”由门诊收住院.患者于10多年前体检时发现血压升高,约为170/80 mm Hg（1 mm Hg=0.133 kPa）,开始口服洛汀新（10 mg,Qd）降压治疗,自述血压控制尚可,在：130～140/95 mm Hg.3年后血压逐渐控制欠佳,波动于140～160/90～100 mm Hg,降压方案改为洛汀新20 mg/d,血压仍有波动.约5年后患者间歇头晕、头胀发作,自测血压波动于140～170/80～100 mm Hg.门诊复诊后降压方案改为洛汀新20 mg/d＋络活喜5 mg/d,此后一直按此降压方案降压治疗,期间血压波动于130～180/70～95 mm Hg.2012年2月1日突发右眼视物模糊,于外院行眼底镜检查提示：右眼底出血,给予治疗（不详）后,视物模糊较前稍好.     

原发性醛固酮增多症与原发性高血压代谢异常的比较

目的 探讨原发性醛固酮增多症的代谢异常.方法 入选已确诊的原发性醛固酮增多症(原醛)患者220例(男117例,女103例)与性别、年龄及高血压病程相匹配的同期住院原发性高血压(EH)患者200例(男104例,女96例).记录入选者一般临床资料和生化指标,在两组间行代谢综合征患病率及两组代谢异常特点比较.结果 (1)原醛组代谢综合征患病率显著高于同期住院EH组(47.3％对31.5％,P=0.009).(2)原醛患者整体血压水平显著高于EH患者[24 h平均收缩压(150.67±15.45)mm Hg对(145.69±17.13)mm Hg,P=0.042;24 h平均舒张压(93.03±10.51)mm Hg对(85.83±14.44)mm Hg,P=0.037],且原醛组以2、3级高血压为主.(3)原醛患者腹型肥胖和胰岛素抵抗发生率显著高于EH患者[86.8％(191/220)对78.5％(157/200),P=0.024;胰岛素抵抗指数42.42±16.11对49.58±22.43,P=0.008].结论 原醛以腹型肥胖、中重度高血压及严重的胰岛素抵抗为主要特征,直接导致其代谢综合征患病率显著高于EH患者.     

原发性醛固酮增多症肾损害

病例摘要 病史患者女性,27岁,因"血压升高、低血钾9年,肾功能不全、蛋白尿5年"于2004-04-28入院.     

Prevalence of primary aldosteronism among Asian hypertensive patients in Singapore

Recent studies using the ratio of plasma aldosterone concentration (PAC) to PRA as the screening test for primary aldosteronism in hypertensive populations suggested that the prevalence may be as high as 5-15%, with well over half of the subjects having normal serum potassium concentrations. Despite an increasing clinical awareness of this entity, many clinicians are reluctant to consider routine screening for primary aldosteronism in essential hypertensive patients because there are few community-based prevalence studies of primary aldosteronism in different populations. Furthermore, genetic and environmental differences may affect the prevalence and presentation of primary aldosteronism in distinct populations. This study was designed to determine the prevalence of primary aldosteronism in the predominantly Chinese population in Singapore. Three hundred and fifty unselected adult hypertensive patients attending two primary care clinics had random ambulatory measurements for PAC (nanograms per dL) and PRA (nanograms per mL/h). Serum urea, creatinine, and electrolyte measurements were obtained simultaneously. Subjects with renal insufficiency (serum creatinine, >140 micromol/L) and those treated with glucocorticoids or spironolactone were excluded. Screening was considered positive if the PAC: PRA ratio was more than 20 and the PAC was more than 15 ng/dL (>416 pmol/L). Primary aldosteronism was confirmed with the determination of PAC after 2 L saline administered iv over 4 h. Adrenal computed tomographic (CT) scans were performed in biochemically confirmed cases of primary aldosteronism. Further localization with adrenal vein sampling was carried out in selected patients with equivocal findings on adrenal CT scan. Sixty-three (18%) of the 350 hypertensive patients (215 women and 135 men; age range, 23-75 yr) were screened positive for primary aldosteronism. Only 13 of these 63 subjects (21%) were hypokalemic (serum potassium, <3.5 mmol/L). Confirmatory studies were carried out in 56 (89%) of the subjects with a positive PAC:PRA ratio. Using a PAC above 10 ng/dL (>277 pmol/L) after saline infusion as the diagnostic cut-off, 16 of the 56 patients had biochemically confirmed primary aldosteronism. Hypokalemia was found in 6 of the 16 patients (37.5%) with primary aldosteronism. Subtype evaluation with adrenal CT scan and adrenal vein sampling indicated that half of the patients with primary aldosteronism may have had potentially curable unilateral adrenal adenoma. Our data suggest that primary aldosteronism occurs in at least 5% of the adult Asian hypertensive population, and approximately half of these individuals may have potentially curable, unilateral, aldosterone-producing adrenal adenoma. Our findings also confirm the poor predictive value of hypokalemia in both the diagnosis and the exclusion of primary aldosteronism.     

住院老年高血压患者中原发性醛固酮增多症的检出率

目的探讨住院老年高血压患者中原发性醛固酮增多症(PA)的检出率。方法选择2012年1月²013年5月入住本院内科的老年高血压患者242例,均接受PA及其他相关检查,排除其他继发性高血压,并分为PA组43例和原发性高血压(EH)组199例。2组检查项目包括地塞米松抑制试验;立位和卧位试验;卡托普利试验;静脉高钠试验;血钾测定,肾上腺及(或)垂体CT扫描,主要指标为血、尿皮质醇、血浆醛固酮、肾素活性及醛固酮与肾素活性比值(ARR),全部手术患者均在术前行垂体CT扫描。比较2组相关指标。结果与EH组比较,PA组患者血浆醛固酮水平在立位[796.44(517.48,899.13)ng/L vs 489.36(431.47,586.32)ng/L]、卧位[(688.20±81.96)ng/L vs(417.63±106.25)ng/L]和服用卡托普利前、后均显著升高[(655.15±109.33)ng/L vs(411.24±114.21)ng/L,(599.64±101.34)ng/L vs(317.65±94.52)ng/L,P<0.05,P<0.01],立位、卧位状态及服用卡托普利前ARR均显著升高(P<0.05),立位状态及服用卡托普利前肾素活性均显著下降(P<0.05,P<0.01)。结论在本院同期住院的老年高血压患者中,PA的检出率较高。     

在高血压患者中筛选原发性醛固酮增多症国人血浆醛固酮/肾素活性比值标准的探讨

目的血浆醛固酮/血浆肾素活性比值(ARR)测定是目前从高血压患者中检出原发性醛固酮增多症(原醛)患者最常用和有效的筛选方法。ARR 值在不同人种中有很大差别,测定条件对其结果影响较大。本研究在严格控制药物、体位等条件下,建立中国人筛选原醛 ARR 值。方法根据肾上腺增强 CT 检查结果,将110例高血压患者分为原发性高血压组(65例)和肾上腺腺瘤/增生组(45例)。停用对肾素和醛固酮分泌有影响的降压药物至少2周,利尿剂包括螺内酯停用4周。对于不宜停服降压药物的患者,改服非双氢吡啶类钙拮抗剂维拉帕米缓释片(varapamil-SR)和(或)α受体阻滞剂特拉唑嗪(terazosin)。低血钾患者补钾至正常水平。采血日晨起保持立位2 h 后,于上午9～10点立位取肘静脉血测定血浆肾素活性、血浆醛固酮浓度,计算 ARR。结果 ARR 值以醛固酮 pg/ml/肾素活性 ng·ml~(-1)·h~(-1)为单位。立位 ARR 值在原发性高血压组为100.00±48.65,肾上腺腺瘤/增生组为699.33±213.33。由 ROC 曲线所得切割值为240,立位 ARR 较卧位 ARR 更有筛查价值。在肾上腺腺瘤/增生组93.3%(42/45)患者的 ARR 值高于240,原发性高血压组90.7%(59/65)患者ARR 值低于该值。取 ARR 值240为切割点,我们从近178例高血压患者中检出15例原醛患者(手术病理证实),所有15例患者 ARR 均大于240,显示极高的敏感性和特异性。结论采用本研究试验条件,中国人立位 ARR 值为240。ARR 测定是一项简便、有效的原醛筛查方法,测定时须注意体位、药物、血钾的影响。     

Detecting and treating primary aldosteronism: primary aldosteronism.

Primary aldosteronism (PA) is the most common cause of mineralocorticoid hypertension. Different studies, using the plasma aldosterone concentration to plasma renin activity ratio (PAC/PRA) for the screening of patients with hypertension, have shown a marked increase in the detection rate of PA. Idiopathic bilateral adrenal hyperplasia (IHA) and aldosterone-producing adrenal adenoma (APA), are the leading causes of primary aldosteronism. Glucocorticoid-remediable aldosteronism (GRA), also called familial hyperaldosteronism type I, familial hyperaldosteronism type II and carcinomas are rare causes of PA. Patients with hypertension and hypokalemia, those with a family history of hypertension and stroke at an early age, or patients with medication-resistant hypertension should be screened for PA using the PAC/PRA ratio. If a high ratio is found, a sodium loading test or a captopril test is warranted to confirm the diagnosis. Adrenal gland imaging is important in subtype differentiation (APA vs IHA). Adrenal venous sampling should be used when other tests prove inconclusive. Genetic testing has facilitated detection of GRA. Surgery is considered the treatment of choice for patients with APA, while bilateral hyperplasia subtypes are treated medically. Normalization of aldosterone levels or aldosterone receptor blockade are necessary to prevent the morbidity and mortality associated with hypertension, hypokalemia, and cardiovascular damage.     

Malignant hypertension and hypertensive encephalopathy in primary aldosteronism caused by adrenal adenoma

Two cases are reported as follows: 1) 1 female patient with accelerated-malignant hypertension secondary to an aldosterone-producing adrenal adenoma; and 2) 1 female patient with adrenal adenoma, severe hypertension, and hypertensive encephalopathy. This association is a rare clinical finding, and malignant hypertension may modify the hormonal characteristic of primary aldosteronism, making its diagnosis more difficult. The diagnosis of primary aldosteronism should be considered in patients with malignant hypertension or hypertensive encephalopathy if persistent hypokalemia occurs. Identification of primary aldosteronism is of paramount importance for the patient's evolution, because the surgical treatment makes the prognosis more favorable.     

Primary aldosteronism and hypertensive disease

Recent studies in hypertensive populations that have used the serum aldosterone (SA) to plasma renin activity (PRA) ratio as a screening test have demonstrated a high prevalence of primary aldosteronism (PA). This frequency is higher than that previously described when hypokalemia was used as a screening tool. However, other factors, such as the characteristics of hypertensive disease, could also influence the prevalence of PA. We studied 609 essential hypertensive patients, classified according to the Joint National Committee VI (JNC VI), in 3 different stages depending on the severity of their hypertensive disease. We measured SA and PRA and calculated the SA-PRA ratio for all patients. An SA-PRA ratio >25 was detected in 63 of 609 patients, and the fludrocortisone test confirmed the PA diagnoses in 37 of 609 (6.1%) cases. PA prevalence according to hypertension stage was as follows: stage 1, 6 of 301 cases (1.99%); stage 2, 15 of 187 cases (8.02%); and stage 3, 16 of 121 cases (13.2%). PA patients were slightly younger than the other hypertensive patients (48.4+/-10.5 vs 53.6+/-10.2 years; P<0.05). Serum potassium levels were normal in 36 of 37 PA patients; only 1 patient had minor hypokalemia. Computed tomography scans showed bilateral adrenal enlargement in 7 and an adrenal nodule in 2 cases. In summary, we found a high frequency of PA in essential hypertensives classified in stages 2 and 3 according to the JNC VI. The low frequency of computed tomography scan abnormalities and hypokalemia suggests that the diagnosis for most PA patients corresponds to attenuated forms of the disease.