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Clinical Characteristics of Aldosterone Producing Adenoma and Idiopathic Hyperaldosteronism with Obstructive Sleep Apnea Hypopnea Syndrome

  • Objective To investigate the clinical characteristics of aldosterone producing adenoma (APA) and idiopathic hyperaldosteronism (IHA) complicated with obstructive sleep apnea hypopnea syndrome (OSAHS) and the effect of OSAHS on renin-angiotensin-aldosterone system (RAAS) in APA and IHA patients. Methods The clinical data of 127 patients with primary aldosteronism (PA) diagnosed from May 2010 to Aug. 2019 were retrospectively analyzed. There were 70 cases of APA, 53 cases of IHA. Another 4 cases were primary adrenal hyperplasia (PAH), so not included into further analysis. According to the results of polysomnography, the 123 patients of APA or IHA were divided into OSAHS group (96 cases) and non-OSAHS group (27 cases ). The patients with OSAHS were divided into mild, moderate and severe subgroups based on apnea hypopnea index (AHI).The clinical characteristics, biochemical parameters, plasma renin activity, aldosterone levels, and the ratio of aldosterone to renin activity (ARR) in the patients of APA and IHA complicated with OSAHS were compared with those of the patients without OSAHS. Results There were 49 OSAHS cases (49/70, 70.0%) in APA patients. and 47 OSAHS cases (47/53, 88.7%) in IHA patients. The age, male ratio, body mass index (BMI), waist circumference, triglyceride, blood uric acid, and blood creatinine in APA patients with OSAHS were higher than those in APA patients without OSAHS (P<0.05), while high-density lipoprotein and estimated glomerular filtration rate (eGFR) were lower (P<0.05). Compared to the patients without OSAHS, IHA-OSAHS patients had higher BMI and waist circumference (P<0.05). Moderate/severe OSAHS-APA patients exhibited higher plasma renin activity levels and lower ARR values than the APA patients with no/mild OSAHS (P<0.05). There were no significant differences in plasma renin activity, aldosterone levels, and ARR values between moderate/severe OSAHS-IHA group and no/mild OSAHS-IHA group. Conclusion The prevalence of OSAHS is significantly higher in the patients with PA than normal population, and OSAHS may aggravate glycose, lipid and uric acid metabolism in PA patients. Moderate/severe OSAHS can increase renin levels and decrease ARR values in APA patients, but has no significant effect on RAAS in IHA patients.
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    [4] 张福春, 严治涛, 杨晶晶, 等. 原发性醛固酮增多症与睡眠呼吸暂停关系的研究现状. 现代生物医学进展,2010,10(4): 794–796.
    [5] 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. 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
    [6] FUNDER J W, CAREY R M, MANTERO F, et al. The management of primary aldosteronism: case detection, diagnosis, andtreatment: an endocrine society clinical practice guideline. J Clin Endocrinol Metab,2016,101(5): 1889–1916. doi: 10.1210/jc.2015-4061
    [7] 中华医学会呼吸病学分会睡眠呼吸障碍学组. 阻塞性睡眠呼吸暂停低通气综合征诊治指南(2011年修订版). 中华结核和呼吸杂志,2012,35(1): 9–12. doi: 10.3760/cma.j.issn.1001-0939.2012.01.007
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    [9] MULATERO P, STOWASSER M, LOH K C, et al. Increased diagnosis of primary aldosteronism, including surgically correctable forms, in centers from five continents. J Clin Endocrinol Metab,2004,89(3): 1045–1050. doi: 10.1210/jc.2003-031337
    [10] STOWASSER M, GORDON R D, GUNASEKERA T G, et al. High rate of detection of primary aldosteronism, including surgically treatable forms, after 'non-selective' screening of hypertensive patients. J Hypertens,2003,21(11): 2149–2157. doi: 10.1097/00004872-200311000-00025
    [11] PEDROSA R P, DRAGER L F, GONZAGA C C, et al. Obstructive sleep apnea: the most common secondary cause of hypertension associated with resistant hypertension. Hypertension,2011,58(5): 811–817. doi: 10.1161/HYPERTENSIONAHA.111.179788
    [12] CALHOUN D A, NISHIZAKA M K, ZAMAN M A, et al. Hyperaldosteronism among black and white subjects with resistant hypertension. Hypertension,2002,40(6): 892–896. doi: 10.1161/01.HYP.0000040261.30455.B6
    [13] PIADITIS G, MARKOU A, PAPANASTASIOU L, et al. Progress in primary aldosteronism: a review of the prevalence of primary aldosteronism in pre-hypertension and hypertension. Eur J Endocrinol,2015,172(5): 191–203. doi: 10.1530/EJE-14-0537
    [14] LOH K C, KOAY E S, KHAW M C, et al. Prevalence of primary aldosteronism among Asian hypertensive patients in Singapore. J Clin Endocrinol Metab,2000,85(5): 2854–2859.
    [15] SANG X, JIANG Y, WANG W, et al. Prevalence of and risk factors for primary aldosteronism among patients with resistant hypertension in China. J Hypertens,2013,31(7): 1465–1471. doi: 10.1097/HJH.0b013e328360ddf6
    [16] OHNO Y, SONE M, INAGAKI N, et al. Obesity as a key factor underlying idiopathic hyperaldosteronism. J Clin Endocrinol Metab,2018,103(12): 4456–4464. doi: 10.1210/jc.2018-00866
    [17] 李南方, 史超, 李娟, 等. 阻塞性睡眠呼吸暂停低通气综合征降低原发性醛固酮增多症患者的醛固酮肾素活性比值. 中华高血压杂志,2014,22(3): 242–245.
    [18] LI M, GE Q, SHENG C S, et al. Clinical characteristics of snoring patients with primary aldosteronism and obstructive sleep apnea-hypopnea syndrome. J Hum Hypertens,2019,33(9): 693–700. doi: 10.1038/s41371-019-0208-9
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Clinical Characteristics of Aldosterone Producing Adenoma and Idiopathic Hyperaldosteronism with Obstructive Sleep Apnea Hypopnea Syndrome

    Corresponding author: CHEN Tao, dr.chentao@qq.com
  • 1. Adrenal Center, Department of Endocrinology and Metabolism, West China Hospital, Sichuan University, Chengdu 610041, China
  • 2. Department of Endocrinology and Metabolism, the Sixth People's Hospital, Chongqing 400060, China

doi: 10.12182/20200560602

Abstract:  Objective To investigate the clinical characteristics of aldosterone producing adenoma (APA) and idiopathic hyperaldosteronism (IHA) complicated with obstructive sleep apnea hypopnea syndrome (OSAHS) and the effect of OSAHS on renin-angiotensin-aldosterone system (RAAS) in APA and IHA patients. Methods The clinical data of 127 patients with primary aldosteronism (PA) diagnosed from May 2010 to Aug. 2019 were retrospectively analyzed. There were 70 cases of APA, 53 cases of IHA. Another 4 cases were primary adrenal hyperplasia (PAH), so not included into further analysis. According to the results of polysomnography, the 123 patients of APA or IHA were divided into OSAHS group (96 cases) and non-OSAHS group (27 cases ). The patients with OSAHS were divided into mild, moderate and severe subgroups based on apnea hypopnea index (AHI).The clinical characteristics, biochemical parameters, plasma renin activity, aldosterone levels, and the ratio of aldosterone to renin activity (ARR) in the patients of APA and IHA complicated with OSAHS were compared with those of the patients without OSAHS. Results There were 49 OSAHS cases (49/70, 70.0%) in APA patients. and 47 OSAHS cases (47/53, 88.7%) in IHA patients. The age, male ratio, body mass index (BMI), waist circumference, triglyceride, blood uric acid, and blood creatinine in APA patients with OSAHS were higher than those in APA patients without OSAHS (P<0.05), while high-density lipoprotein and estimated glomerular filtration rate (eGFR) were lower (P<0.05). Compared to the patients without OSAHS, IHA-OSAHS patients had higher BMI and waist circumference (P<0.05). Moderate/severe OSAHS-APA patients exhibited higher plasma renin activity levels and lower ARR values than the APA patients with no/mild OSAHS (P<0.05). There were no significant differences in plasma renin activity, aldosterone levels, and ARR values between moderate/severe OSAHS-IHA group and no/mild OSAHS-IHA group. Conclusion The prevalence of OSAHS is significantly higher in the patients with PA than normal population, and OSAHS may aggravate glycose, lipid and uric acid metabolism in PA patients. Moderate/severe OSAHS can increase renin levels and decrease ARR values in APA patients, but has no significant effect on RAAS in IHA patients.

  • 原发性醛固酮增多症(primary aldosteronism,PA)是由于肾上腺皮质球状带病变引起醛固酮分泌异常增多,进而导致高血压、低血钾,并抑制肾素-血管紧张素-醛固酮(renin-angiotensin-aldosterone system,RAAS)系统,使血浆肾素活性降低的一类疾病。目前PA主要有5种病理类型,包括醛固酮瘤(aldosterone producing adenoma,APA)、特发性醛固酮增多症(idiopathic hyperaldosteronism,IHA)、原发性肾上腺皮质增生(primary adrenal hyperplasia,PAH)、家族性醛固酮增多症(familial hyperaldosteronism,FH)、分泌醛固酮的肾上腺皮质癌及异位醛固酮分泌瘤或癌。

    阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea hypopnea syndrome,OSAHS)是睡眠时反复出现的呼吸暂停和低通气引起间歇性低氧、血氧饱和度下降及睡眠结构紊乱的一种临床综合征,属于比较常见的睡眠呼吸疾病。PA与OSAHS都可引起继发性高血压,二者之间联系密切。据报道,难治性高血压中OSAHS的患病率达72%,而PA患者中OSAHS的患病率高达78.1%[1]。OSAHS引起血压升高的机制包括交感神经系统及RAAS激活、氧化应激、内皮损伤等[2],而PA患者的醛固酮分泌增加引起水钠潴留,导致颈部水肿,增加气道阻力及OSAHS的发生。目前研究认为醛固酮是PA与OSAHS联系的枢纽[3-4]

    APA和IHA是PA中常见的病理类型,约占PA患者的35%和60%[5],但目前尚无PA不同分型合并OSAHS的相关研究,本研究主要探索PA及其主要类型(APA和IHA)合并OSAHS的临床特征,以及OSAHS对APA、IHA患者RAAS的影响。

1.   对象和方法
  • 纳入2010年5月至2019年8月在四川大学华西医院确诊的PA患者为研究对象。PA的诊断符合2016年美国内分泌学会原发性醛固酮增多症的诊断标准[6]

  • 醛固酮与肾素活性比值(aldosterone to renin activity ratio,ARR)>30 (ng/dL)/(ng/mL·h)且卡托普利抑制试验后血醛固酮浓度下降<30%或生理盐水输注试验后血醛固酮>10 ng/dL;且行睡眠呼吸监测的患者。

  • 排除合并慢性肾脏病、肾动脉狭窄、肾素瘤、甲亢的患者。

  • APA诊断标准:①确诊PA;②分侧肾上腺静脉采血(adrenal venous sampling,AVS)提示单侧醛固酮分泌优势;③肾上腺切除术后3个月随访,患者低钾血症缓解,血压较手术前降低或恢复正常,提示手术切除成功;④临床及实验室检查提示典型的PA,同时影像学检查或手术、病理结果明确为醛固酮瘤。IHA诊断标准:①确诊PA;②AVS未提示存在单侧醛固酮分泌优势;③临床诊断PA,未做AVS,但不符合上述APA诊断标准,且排除分泌醛固酮的肾上腺皮质癌者。OSAHS诊断标准根据2011年中华医学会阻塞性睡眠呼吸暂停低通气综合征诊治指南[7]。睡眠呼吸暂停低通气指数(apnea hypopnea index,AHI)=(总呼吸暂停次数+总低通气次数)/总睡眠时间(h),OSAHS根据AHI分为轻度:AHI 5~15 次/h,中度:AHI 16~30 次/h,重度:AHI>30 次/h。

    共纳入127例符合上述纳入和排除标准的PA患者作为研究对象。PA患者根据多导睡眠监测结果将其分为PA合并OSAHS(PA-OSAHS)组和PA未合并OSAHS(PA-nonOSAHS)组。PA-OSAHS患者根据AHI,分为轻度、中度、重度OSAHS-PA亚组。

    本研究方案通过了四川大学华西医院伦理委员会的审核批准(批准号:2019年审229号)。

  • 包括血钾、24 h尿钾、空腹血糖、糖化血红蛋白、血脂、血尿酸、血肌酐、估算肾小球滤过率(eGFR)。常规血液及体液生化检测使用自动分析仪完成。

  • 测定前停用螺内酯6周以上,停用利尿剂4周以上,停用β受体阻滞剂、血管紧张素转换酶抑制剂、血管紧张素受体拮抗剂、二氢吡啶类钙拮抗剂等2周以上,如患者血压控制不佳,则使用维拉帕米或α1受体拮抗剂如特拉唑嗪等对RAAS影响较小的药物。血浆肾素活性、醛固酮采用放射免疫法测定(北方生物技术研究所提供的放免试剂盒),计算ARR值,ARR=血浆醛固酮/血浆肾素活性。

  • 受试者在行呼吸睡眠监测检查前24 h内禁饮酒、茶、咖啡等影响睡眠的食物,保持平时的睡眠习惯。睡眠监测采用美国Alice 6多功能多导睡眠监测系统,导联包括:脑电图、眼电图(双侧)、肌电图(下颌及胫骨前肌)、热敏与压力式口鼻气流、胸腹运动、指脉氧饱和度。睡眠主要指标包括各睡眠分期占比、入睡潜伏期、总睡眠时间、微觉醒指数、AHI、平均血氧饱和度等。

  • 计量资料首先进行正态性检验,符合正态分布资料用$\bar x$±s表示,组间比较采用t检验;非正态分布资料用中位数与四分位数间距(P25,P75)表示,组间比较采用Mann-Whitney U检验;计数资料用率或构成比表示,组间比较采用χ2检验。P<0.05为差异有统计学意义。

2.   结果
  • 共127例在四川大学华西医院确诊的PA患者纳入研究。其中APA患者70例(55.1%),IHA患者共53例(41.7%),PAH患者4例(3.2%)。PA-OSAHS组患者99例,占78.0%,PA-nonOSAHS组患者28例,占22.0%。在PA-OSAHS患者中,APA-OSAHS患者49例,占PA-OSAHS患者的49.5%(49/99),APA-OSAHS占APA患者的70.0%(49/70),其中轻度APA-OSAHS患者19例,中度15例,重度15例;IHA-OSAHS患者47例,占PA-OSAHS患者的47.5%(47/99),IHA-OSAHS占IHA患者的88.7%(47/53),其中轻度IHA-OSAHS患者14例,中度16例,重度17例;PAH-OSAHS患者3例,占PA-OSAHS患者的3.0%(3/99);在PA-nonOSAHS患者中,APA-non OSAHS患者21例,占75.0%(21/28),IHA-nonOSAHS患者6例,占21.4%(6/28),PAH-nonOSAHS患者1例,占3.6%(1/28)。

  • APA-OSAHS组与APA-nonOSAHS组比较,年龄、男性构成比、体质量指数(BMI)、腰围、三酰甘油、血尿酸、血肌酐均高于APA-nonOSAHS组,差异有统计学意义(P均<0.05);而高密度脂蛋白、eGFR低于APA-nonOSAHS组,差异有统计学意义(P<0.05);两组患者血钾、收缩压、舒张压、空腹血糖、糖化血红蛋白、总胆固醇、低密度脂蛋白差异无统计学意义,见表1

    CharacteristicAPA-OSAHS group (n=49)APA-nonOSAHS group (n=21)P
    Age/yr.49.1±9.939.4±12.00.001
    Male/case (%)30 (61.2)5 (23.8)0.004
    BMI/(kg/m2)26.4±4.122.9±3.30.001
    WC/cm92.7±9.780.3±8.00.000
    Potassium/(mmol/L)3.0±0.53.0±0.50.747
    24 h urinary K+*/(mmol/L)46.3 (29.4, 57.4)54.5 (42.4, 86.0)0.048
    SBP/mmHg176±22183±230.256
    DBP/mmHg109±15112±110.451
    Fasting glucose*/(mmol/L)4.9 (4.6, 5.3)4.6 (4.3, 5.2)0.137
    HbA1C*/%5.6 (5.3, 5.8)5.5 (5.0, 5.7)0.221
    Triglycerides*/(mmol/L)1.4 (0.9, 2.1)0.9 (0.6, 1.0)0.000
    Total cholesterol/(mmol/L)4.4±0.84.4±0.90.744
    HDL cholesterol/(mmol/L)1.2±0.41.5±0.40.002
    LDL cholesterol/(mmol/L)2.6±0.72.4±0.80.263
    Uric acid/(µmol/L)337.1±96.1273.8±71.10.009
    Plasma creatinine/(µmol/L)74.0±20.858.9±14.20.003
    eGFR/(mL/(mL·1.73 m2) )96.9±18.5111.0±16.80.008
      *Median (P25, P75); APA: Aldosterone producing adenoma; OSAHS: Obstructive sleep apnea hypopnea syndrome; BMI: Body mass index; WC: Waist circumference; SBP: Systolic blood pressure; DBP: Diastolic blood pressure; 1 mmHg=0.133 kPa; HbA1C: Glycated hemoglobin A1C; HDL: High-density lipoprotein; LDL: Low-density lipoprotein; eGFR: Estimated glomerular filtration rate

    Table 1.  Clinical characteristics of the APA with OSAHS and APA without OSAHS patients

    与IHA-nonOSAHS组比较,IHA-OSAHS组BMI和腰围较高(P<0.05);而其他指标差异均无统计学意义,见表2

    CharacteristicIHA-OSAHS group (n=47)IHA-nonOSAHS group (n=6)P
    Age/yr.51.7±10.651.2±10.30.900
    Male/case (%)26 (55.3)3 (50.0)0.805
    BMI/(kg/m2)26.6±3.722.6±3.30.014
    WC/cm93.9±10.179.2±9.30.004
    Potassium/(mmol/L)3.3±0.43.1±0.50.321
    24 h urinary K+/(mmol/L)46.8±15.931.9±12.10.052
    SBP/mmHg170±23175±250.600
    DBP/mmHg105±15108±150.676
    Fasting glucose*/(mmol/L)5.1 (4.7, 5.8)4.7 (4.4, 5.6)0.197
    HbA1C*/%6.0 (5.3, 6.5)6.0 (5.3, 6.4)0.891
    Triglycerides*/(mmol/L)1.6 (1.2, 2.0)1.4 (0.8, 2.1)0.246
    Total cholesterol/(mmol/L)4.5±1.14.5±0.60.923
    HDL cholesterol/(mmol/L)1.2±0.31.3±0.10.437
    LDL cholesterol/(mmol/L)2.7±0.92.6±0.60.734
    Uric acid/(µmol/L)373.7±85.0348.3±96.80.501
    Plasma creatinine/(µmol/L)71.0±18.478.5±28.30.378
    eGFR/(mL/(mL·1.73 m2) )98.9±19.096.4±24.20.787
    IHA:Idiopathic hyperaldosteronism; *, OSAHS, BMI, WC, SBP, DBP, HbA1C, HDL, LDL and eGFR note the same as table 1

    Table 2.  Clinical characteristics of the IHA with OSAHS and IHA without OSAHS patients

  • 中、重度OSAHS-APA患者与无或轻度OSAHS-APA患者比较,血浆肾素活性水平升高,ARR值降低,差异有统计学意义(P<0.05);而血浆醛固酮水平无明显差异,见表3;中、重度OSAHS-IHA组与无或轻度OSAHS-IHA组比较,血浆肾素活性、醛固酮水平及ARR值均无统计学差异,见表4

    ItemNo/mild OSAHS-APA group (n=40)Moderate/severe OSAHS-APA group (n=30)P
    Supine PRA/(ng/mL·h)0.09 (0.05, 0.14)0.14 (0.06, 0.41)0.021
    Supine PAC/(ng/dL)25.6 (21.4, 36.8)26.2 (23.8, 33.1)0.809
    Supine ARR/((ng/dL):(ng/mL·h))355.3 (178.9, 512.2)184.1 (72.1, 448.9)0.039
    Upright PRA/(ng/mL·h)0.13 (0.06, 0.44)0.40 (0.12, 0.88)0.032
    Upright PAC/(ng/dL)32.4 (24.1, 40.0)29.1 (22.7, 35.0)0.352
    Upright ARR/((ng/dL):(ng/mL·h))290.8 (143.1, 541.4)93.2 (34.1, 275.8)0.021
     Values are indicated as median (P25, P75); PRA: Plasma renin activity; PAC: Plasma aldosterone concentration; ARR: Aldosterone to renin activity ratio; 1 ng/dL=27.7 pmol/L

    Table 3.  Comparison of renin-angiotensin-aldosterone system (RAAS) between the moderate/severe OSAHS with APA group and no/mild OSAHS with APA group

    ItemNo/mild OSAHS-IHA group (n=20)Moderate/severe OSAHS-IHA group (n=33)P
    Supine PRA/(ng/mL·h)0.16 (0.08, 0.27)0.16 (0.07, 0.25)0.559
    Supine PAC/(ng/dL)18.5 (14.6, 22.1)22.4 (17.8, 24.1)0.072
    Supine ARR/((ng/dL):(ng/mL·h))116.8 (74.4, 254.3)182.6 (97.4, 295.3)0.178
    Upright PRA/(ng/mL·h)0.29 (0.24, 0.59)0.29 (0.12, 0.51)0.493
    Upright PAC/(ng/dL)23.0 (19.9, 29.7)25.5 (22.9, 34.7)0.243
    Upright ARR/((ng/dL):(ng/mL·h))72.7 (48.8, 111.9)87.0 (56.7, 234.8)0.183
    Values are indicated as median (P25,P75); OSAHS notes the same as table 1; IHA notes the same as table 2; PRA, PAC, ARR note the same as table 3

    Table 4.  Comparison of renin-angiotensin-aldosterone system (RAAS) between the moderate/severe OSAHS with IHA group and no/mild OSAHS with IHA group

3.   讨论
  • 近年来,流行病学的数据提示PA合并OSAHS的患病率很高。在合并OSAHS的高血压患者中,PA的患病率约为20.9%~36%[8-13],显著高于普通高血压人群(为5%)及难治性高血压患者(7.1%)[14-15]。因此,2016年美国内分泌学会及中华医学会指南均建议高血压合并OSAHS的患者应该进行PA的筛查[5-6]

    本研究结果发现,在PA患者中,合并OSAHS的患者占78.0%,该研究结果与RESIST-POL研究中PA患者OSAHS的患病率基本一致(78.1%)[1],说明在PA患者中,OSAHS的患病率明显高于正常人群,且与APA患者相比,IHA患者更容易合并出现OSAHS(88.7%)。

    在难治性高血压患者中PA、OSAHS、代谢综合征(metabolic syndrome,MS)三者之间关系密切,提示三者之间可能存在共同的病理生理机制。肥胖是高血压、OSAHS、MS的独立危险因素,PA-OSAHS患者BMI、腰围明显大于PA-nonOSAHS患者。OHNO等报道脂肪细胞因子可以促进肾上腺皮质细胞分泌醛固酮,刺激醛固酮分泌的因子包括CTRP1,瘦素和抵抗素[16],提示这些因素可能在PA尤其是IHA的发病机制中发挥了重要作用。

    与APA-nonOSAHS相比,APA-OSAHS组的患者三酰甘油、空腹血糖、血尿酸均高于APA患者,而低密度脂蛋白低于APA患者,IHA-OSAHS的患者糖脂代谢及尿酸代谢异常较IHA患者更加明显,这些可能是PA患者更易并发心脑血管终点事件的贡献因素。

    OSAHS对PA患者RAAS的影响尚不明确。目前的研究认为OSAHS可以使PA患者血浆肾素活性水平升高,ARR值降低,但对血浆醛固酮水平的影响目前的研究结果并不一致[17-18]。APA和IHA是PA的两种不同的病理类型,OSAHS对二者RAAS的影响可能不同。本研究发现,中重度OSAHS使APA患者血浆肾素活性水平升高,ARR值降低,血浆醛固酮水平无明显变化。而OSAHS对IHA患者RAAS影响不显著,中重度OSAHS合并IHA组与轻度或无OSAHS合并IHA组比较,血浆肾素活性、醛固酮水平及ARR值均无明显差异。这说明OSAHS与APA和IHA的关系可能不一样,APA可因缺氧、交感神经激活等导致肾素活性升高,而OSAHS及相关危险因素(如肥胖)可能是IHA的危险因素、参与了IHA的发生。确切的机制尚需进一步研究。本研究中,IHA-nonOSAHS的患者非常少见,一方面说明IHA多合并OSAHS,另一方面,限制了本研究对OSAHS与IHA患者RAAS的分析,后续需进一步扩大样本量进行研究。

    本研究与其他文献报道的优势在于:所有PA患者均进行了确诊试验,所有阻塞性睡眠呼吸暂停低通气综合征患者均由多导睡眠监测确诊,且对PA的两种常见病理类型分别进行分析。本研究存在的不足:未对APA术后及IHA药物治疗后病人进行睡眠监测,将来可以对APA术后及IHA治疗后病人进行随访监测,进一步探讨APA、IHA与OSAHS之间的关系。本研究样本量较小,有待进行大规模、多中心的相关研究进一步验证结果。

    综上所述,在PA患者中,OSAHS的患病率显著高于正常人群,且IHA患者较APA患者更容易合并出现OSAHS,OSAHS会加重APA及IHA患者的糖脂代谢及尿酸代谢异常,因此临床医师除了要对高血压合并OSAHS患者进行PA的筛查外,还应对PA患者进行OSAHS的筛查。

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