原发性醛固酮增多症高血压患者临床特征分析
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摘要
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。
Objectives: To analyze the clinical features of hypertensive patients with primary aldosteronism(PA) diagnosed in Fuwai Hospital in recent two years. Methods: From January 2016 to December 2017, 4 782 patients with hypertension were admitted to the hypertension department of Fuwai Hospital. Patients with PA were matched 1:2 with patients with primary hypertension(PH) according to age and sex to make comparisons, and patients with PA were divided into two groups according to with or without hypokalemia(< 3.5 mmol/L) to make comparisons. Results: 247(5.2%) patients were diagnosed with PA. The median age of PA patients was 48.8(16.6) years old, of whom 148(59.9%) were male and 143(57.9%) had hypokalemia. Systolic blood pressure(150[24] mm Hg vs 145[27] mm Hg), left ventricular mass index(LVMI)(83.4[36.6] g/m2 vs 75.7[26.2] g/m2), urinary albumin-creatinin ration(24.1[41.1] mg/g vs 10.5[22.1] mg/g), incidence of coronary heart disease(12.6% vs 7.7%) and peripheral artery disease(11.7% vs 4.7%) in PA patients were significantly greater than those in PH patients(all P < 0.05); while LDL cholesterol(2.6[1.0] mmol/L vs 2.9[1.1] mmol/L), total cholesterol(4.4[1.2] mmol/L vs 4.6[1.3] mmol/L)and glycosylated hemoglobin(5.4[0.6] % vs 5.6[0.6] %) inPA patients were significantly lower than those in PH patients(all P<0.05). Compared with PA patients without hypokalemia, PA patients with hypokalemia had higher diastolic blood pressure(95[26] mm Hg vs 90[20] mm Hg), urinary albumin-creatinin ration(28.5[40.6] mg/g vs 20.5[32.8] mg/g) and LVMI(86.5[34.8] g/m~2 vs 77.9[31.8] g/m~2) although they were younger(45.9[16.8] years old vs 51.3[14.3] years old), all P<0.05. Conclusions: Compared with PH patients, PA patients had heavier target organ damage and higher incidence of cardiovascular disease. PA patients with hypokalemia were younger, but they had higher diastolic blood pressure and heavier target organ damage.
Objectives: To analyze the clinical features of hypertensive patients with primary aldosteronism(PA) diagnosed in Fuwai Hospital in recent two years. Methods: From January 2016 to December 2017, 4 782 patients with hypertension were admitted to the hypertension department of Fuwai Hospital. Patients with PA were matched 1:2 with patients with primary hypertension(PH) according to age and sex to make comparisons, and patients with PA were divided into two groups according to with or without hypokalemia(< 3.5 mmol/L) to make comparisons. Results: 247(5.2%) patients were diagnosed with PA. The median age of PA patients was 48.8(16.6) years old, of whom 148(59.9%) were male and 143(57.9%) had hypokalemia. Systolic blood pressure(150[24] mm Hg vs 145[27] mm Hg), left ventricular mass index(LVMI)(83.4[36.6] g/m2 vs 75.7[26.2] g/m2), urinary albumin-creatinin ration(24.1[41.1] mg/g vs 10.5[22.1] mg/g), incidence of coronary heart disease(12.6% vs 7.7%) and peripheral artery disease(11.7% vs 4.7%) in PA patients were significantly greater than those in PH patients(all P < 0.05); while LDL cholesterol(2.6[1.0] mmol/L vs 2.9[1.1] mmol/L), total cholesterol(4.4[1.2] mmol/L vs 4.6[1.3] mmol/L)and glycosylated hemoglobin(5.4[0.6] % vs 5.6[0.6] %) inPA patients were significantly lower than those in PH patients(all P<0.05). Compared with PA patients without hypokalemia, PA patients with hypokalemia had higher diastolic blood pressure(95[26] mm Hg vs 90[20] mm Hg), urinary albumin-creatinin ration(28.5[40.6] mg/g vs 20.5[32.8] mg/g) and LVMI(86.5[34.8] g/m~2 vs 77.9[31.8] g/m~2) although they were younger(45.9[16.8] years old vs 51.3[14.3] years old), all P<0.05. Conclusions: Compared with PH patients, PA patients had heavier target organ damage and higher incidence of cardiovascular disease. PA patients with hypokalemia were younger, but they had higher diastolic blood pressure and heavier target organ damage.
引文
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[13]Gordon RD, Stowasser M, Rutherford JC. Primary aldosteronism:are we diagnosing and operating on too few patients?[J]. World J Surg,2001, 25(7):941-947.
[14]Pedrosa RP, Drager LF, Gonzaga CC, et a1. Obstructive sleep apnea:the most common secondary cause of hypertension associated with resistant hypertension[J]. Hypertension, 2011, 58(5):811-817. DOI:10. 1161/HYPWETENSIONAHA. 111. 179788.
[15]Pratt-Ubunama MN, Nishizaka MK, Boedefeld RL, et a1. Plasma aldosterone is related to severity of obstructive sleep apnea in subjects with resistant hypertension[J]. Chest, 2007, 131:453-459. DOI:10.1378/chest. 06-1442.
[16]Yao X, Li N, Zhang Y, et al. Plasma aldosterone concentration is positively associated with pulse pressure in patients with primary hypertension[J]. Medicine, 2015, 94(10):e614-e617. DOI:10. 1097/MD. 0000000000000614.
[17]马轩,姚晓光,李南方,等.原发性醛固酮增多症患者中代谢综合征的患病情况[J].中华内分泌代谢杂志, 2011, 27(9):724-728.DOI:10. 3760/cma. j. issn. 1000-6699. 2011. 09. 005.
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[19]Abad-Cardie1 M,álvarez-álvarez B, Luque-Fernandez L, et a1.Hypertension caused by prim ary hyperaldosteronism:increased heart damage and cardiovascular risk[J]. Rev Esp Cardiol(Engl Ed), 2013,66(1):47-52. DOI:10. 1016/j. recesp. 2012. 07. 025.
[20]Milan A, Magnino C, Fabbri A, et al. Left heart morphology and function in primary aldosteronism[J]. High Blood Press Cardiovasc Prev,2012, 19(1):11-17. DOI:10. 2165/11593690-000000000-00000.
[21]Kato J, Etoh T, Kitamura K, et al. Atrial and brain natriuretic peptides as markers of cardiac load and volume retention in primary aldosteronism[J]. Am J Hypertens, 2005, 18(3):354-357. DOI:10.1016/j. amjhyper. 2004. 09. 016.
[22]ZhouPH,ShiL,HuW,etal.Changesofadrenomedullinand natriuretic peptides in patients with adrenal medullary hyperplasia prior to and following pharmacological therapy and adrenalectomy[J].Exp Ther Med, 2016, 12(2):864-872. DOI:10. 3892/etm. 2016. 3418.
[23]Kramers BJ, Kramers C, Lenders JW, et a1. Effects of treating primary aldosteronism on renal function[J].J Clin Hypertens(Greenwich),2017, 19:290-295. DOI:10. 1111/jch. 12914.
[24]Kuo CC, Wu VC, Tsai CW, et al. Relative kidney hyperfiltration inprimaryaldosteronism:ameta-analysis[J].JRenin AngiotensinAldosteroneSyst,2011,12(2):113-122.DOI:10.1177/1470320310391331.
[25]LinYH,WangSM,WuVC,etal.Theassociationofserum potassium level with left ventricular mass in patients with primary aldosteronism[J]. Eur J Clin Invest, 2011, 41(7):743-750. DOI:10.1111/j. 1365-2362. 2010. 02462. x.
[2]李南方,李红建,王新玲,等.原发性醛固酮增多症患者左室结构损害的研究[J].中华内分泌代谢杂志, 2012, 28(2):117-120. DOI:10. 3760/cma. j. issn. 1000-6699. 2012. 02. 006.
[3]李南方,马轩,李红健,等.原发性醛固酮增多症患者蛋白尿情况分析[J].中华高血压杂志, 2013, 21(3):249-252. DOI:10. 16439/j.cnki. 1673-7245. 2013. 03. 027.
[4]中华医学会内分泌学分会肾上腺学组.原发性醛固酮增多症诊断治疗的专家共识[J].中华内分泌代谢杂志, 2016, 32(3):188-195.DOI:10. 3760/cma. j. issn. 1000-6699. 2016. 03. 003.
[5]孙宁玲, Jaw-Wen Chen,王继光,等.亚洲高血压合并左心室肥厚诊治专家共识[J].中华高血压杂志, 2016, 24(7):619-627. DOI:10.16439/j. cnki. 1673-7245. 2016. 07. 008.
[6]Hiramatsu K, Yamada T, Yukimura Y, et al. A screening test to identify aldosterone producing adenoma by measuring plasma rennin activity. Results in hypertensive patients[J]. Arch Intern Med, 1981,141(12):1589-1593.
[7]Gordon RD, Stowasser M, Tunny TJ, et a1.High incidence of primary aldosteronism in 199 patients referred with hypertension[J]. Clin Exp Pharmacol Physiol, 1994, 21:315-318.
[8]Song Y, Yang S, He W, et al. Confirmatory tests for the diagnosis ofprimaryaldosteronism:prospectivediagnosticaccuracy study[J]. Hypertension, 2018, 71(1):118-124. DOI:10. 1161/HYPERTENSIONAHA. 117. 10197.
[9]Mosso L, Carvajal C, Gonzulez A, et al. Primary aldosteronism and hypertensive disease[J]. Hypertension, 2003, 42(2):161-165. DOI:10.1161/01. HYP. 25750. 11.
[10]CalhounDA.Isthereanunrecognizedepidemicofprimary aldosteronism? Pro.[J]. Hypertension, 2007, 50(3):447-453. DOI:10.1161/HYPERTENSIONAHA. 106. 086116.
[11]Mulatero P, Stowasser M, Loh KC, et al. Increased diagnosis of primary aldosteronism, including surgically correctable forms, in centers from five continents[J]. J Clin Endocrinol Metab, 2004, 89(3):1045-1050.DOI:10. 1210/jc. 2003-031337.
[12]Rossi GP, Bernini G, Caliumi C, et al. A prospective study of the prevalence of primary aldosteronism in 1, 125 hypertensive patients[J].J Am Coll Cardiol, 2006, 48(11):2293-2300. DOI:10. 1016/j. jacc.2006. 07. 059.
[13]Gordon RD, Stowasser M, Rutherford JC. Primary aldosteronism:are we diagnosing and operating on too few patients?[J]. World J Surg,2001, 25(7):941-947.
[14]Pedrosa RP, Drager LF, Gonzaga CC, et a1. Obstructive sleep apnea:the most common secondary cause of hypertension associated with resistant hypertension[J]. Hypertension, 2011, 58(5):811-817. DOI:10. 1161/HYPWETENSIONAHA. 111. 179788.
[15]Pratt-Ubunama MN, Nishizaka MK, Boedefeld RL, et a1. Plasma aldosterone is related to severity of obstructive sleep apnea in subjects with resistant hypertension[J]. Chest, 2007, 131:453-459. DOI:10.1378/chest. 06-1442.
[16]Yao X, Li N, Zhang Y, et al. Plasma aldosterone concentration is positively associated with pulse pressure in patients with primary hypertension[J]. Medicine, 2015, 94(10):e614-e617. DOI:10. 1097/MD. 0000000000000614.
[17]马轩,姚晓光,李南方,等.原发性醛固酮增多症患者中代谢综合征的患病情况[J].中华内分泌代谢杂志, 2011, 27(9):724-728.DOI:10. 3760/cma. j. issn. 1000-6699. 2011. 09. 005.
[18]Aronova A, Fahey TJ III, Zarnegar R. Management of hypertension in primary aldosteronism[J]. World J Cardiol, 2014, 6(5):227-233. DOI:10. 4330/wjc. v6. i5. 227.
[19]Abad-Cardie1 M,álvarez-álvarez B, Luque-Fernandez L, et a1.Hypertension caused by prim ary hyperaldosteronism:increased heart damage and cardiovascular risk[J]. Rev Esp Cardiol(Engl Ed), 2013,66(1):47-52. DOI:10. 1016/j. recesp. 2012. 07. 025.
[20]Milan A, Magnino C, Fabbri A, et al. Left heart morphology and function in primary aldosteronism[J]. High Blood Press Cardiovasc Prev,2012, 19(1):11-17. DOI:10. 2165/11593690-000000000-00000.
[21]Kato J, Etoh T, Kitamura K, et al. Atrial and brain natriuretic peptides as markers of cardiac load and volume retention in primary aldosteronism[J]. Am J Hypertens, 2005, 18(3):354-357. DOI:10.1016/j. amjhyper. 2004. 09. 016.
[22]ZhouPH,ShiL,HuW,etal.Changesofadrenomedullinand natriuretic peptides in patients with adrenal medullary hyperplasia prior to and following pharmacological therapy and adrenalectomy[J].Exp Ther Med, 2016, 12(2):864-872. DOI:10. 3892/etm. 2016. 3418.
[23]Kramers BJ, Kramers C, Lenders JW, et a1. Effects of treating primary aldosteronism on renal function[J].J Clin Hypertens(Greenwich),2017, 19:290-295. DOI:10. 1111/jch. 12914.
[24]Kuo CC, Wu VC, Tsai CW, et al. Relative kidney hyperfiltration inprimaryaldosteronism:ameta-analysis[J].JRenin AngiotensinAldosteroneSyst,2011,12(2):113-122.DOI:10.1177/1470320310391331.
[25]LinYH,WangSM,WuVC,etal.Theassociationofserum potassium level with left ventricular mass in patients with primary aldosteronism[J]. Eur J Clin Invest, 2011, 41(7):743-750. DOI:10.1111/j. 1365-2362. 2010. 02462. x.