血浆醛固酮浓度/血浆肾素活性比值对原发性醛固酮增多症的诊断价值

目的探讨血浆醛固酮浓度/血浆肾素活性比值(ARR)对原发性醛固酮增多症的鉴别诊断价值。方法随机选取2017年1月至2018年12月85例原发性醛固酮增多症患者作为研究组,另选取我院同期收治的85例原发性高血压患者作为对照组,两组患者均予以血浆醛固酮浓度、血浆肾素活性检测,记录两组上述指标检测结果、计算各组血浆醛固酮浓度/血浆肾素活性比值。结果研究组血浆醛固酮浓度、血浆醛固酮浓度/血浆肾素活性比值显著高于对照组,研究组血浆肾素活性显著低于对照组,差异有统计学意义(P0.05)。结论应用血浆醛固酮浓度/血浆肾素活性比值可为鉴别诊断原发性醛固酮增多症、原发性高血压提供有力依据,提高原发性醛固酮增多症诊断准确率。     

原发性醛固酮增多症诊治分析

目的 探讨原发性醛固酮增多症的诊断及治疗.方法 回顾性分析68例原发性醛固酮增多症患者的临床资料.结果 全部患者均有不同程度的低血钾,卧、立位血浆醛固酮平均值分别为(682±332)pmol/L、(881±406)pmol/L,29例患者尿醛固酮值升高,其中48例立位的醛固酮/肾素活性比值≥50.通过影像学检查62例为原发性醛固酮增多症腺瘤型,其余6例为双侧肾上腺增生;32例予以手术治疗,24例予以口服安体舒通治疗,经治疗后56例患者血压及血钾均有不同程度的恢复.结论 原发性醛固酮增多症主要通过影像学检查定位,血、尿醛固酮测定定性诊断.肾上腺腺瘤切除仍是当前的首选治疗方法,安体舒通也是重要的治疗手段.     

原发性醛固酮增多症的临床特点

目的了解原发性醛固酮增多症(原醛症)的常见症状和早期症状,比较病理为肾上腺皮质腺瘤和增生的原醛症的临床表现的不同.方法回顾性调查原醛症患者的临床资料,选择标准为血浆醛固酮水平增高和手术病理证实为肾上腺皮质腺瘤或皮质增生的患者共90例.结果原醛症患者临床常见症状依次为高血压(100%)、口渴多尿(26.6%)、四肢乏力(23.3%)、四肢麻木(15.5%)、四肢抽搐(4.4%);早期表现为高血压,高血压至确诊时病程为(5±7)年,最高血压为(191±25)/(116±15) mm Hg,平均血压为(154±16)/(97±10) mm Hg,左心室肥厚的频率为43.5%;94.4%的患者存在低血钾;低肾素活性血症卧位发生率70.3%,立位发生率为94.3%;血浆醛固酮/血浆肾素活性比值以25/1为截取点,立位及卧位的阳性率均为72.4%,以50/1为截取点,敏感性明显下降;腺瘤组平均血压明显高于增生组[(157±17)/(99±10) mm Hg )vs(148±13)/(92±10) mm Hg];低钾血症发生率在腺瘤组更易发生(98.5% vs 84.0%);腺瘤组血浆醛固酮水平亦较增生组明显增高(P<0.05).结论原醛症的患者临床上常见症状依次为高血压、口渴多尿、四肢乏力、四肢麻木、四肢抽搐等,早期表现为高血压,且往往是在高血压多年后才因出现低血钾而确诊,部分患者可无低血钾;高血压的特点为重度高血压,药物对其有一定效果,但不能达标,易发生高血压的并发症;低肾素血症和血浆醛固酮/血浆肾素活性的比值对诊断原醛症有一定意义,但也会漏掉一部分患者;在临床表现和实验室检查上肾上腺皮质腺瘤严重程度高于肾上腺皮质增生的患者.     

原发性醛固酮增多症合并亚临床型皮质醇增多症临床特点及其发病机制探讨

目的探讨原发性醛固酮增多症合并亚临床型皮质醇增多症（即醛固酮/皮质醇共分泌瘤）的临床特点及其可能的发病机制,提高醛固酮/皮质醇共分泌瘤的诊治水平。方法回顾分析13例临床诊断为原发性醛固酮增多症（其中单纯性醛固酮腺瘤8例,合并亚临床型皮质醇增多症5例）的临床资料。通过免疫组化及RT-PCR检测腺瘤及瘤旁组织类固醇合成限速酶编码基因（CYP11B1和CYP11B2）的表达情况。结果醛固酮/皮质醇共分泌瘤的最大直径[（3.48±1.51）cm]大于单纯醛固酮腺瘤[（1.61±0.36）cm],差异具有统计学意义（t=-3.412,P=0.006）;醛固酮/皮质醇共分泌瘤患者血钾水平[（4.00±0.29）mmol/L]高于单纯醛固酮腺瘤[（3.15±0.72）mmol/L],差异具有统计学意义（t=-2.460,P=0.032）。结论原发性醛固酮增多症合并亚临床型皮质醇增多症并不少见,其具有独特的临床特点。     

以低钾周期性麻痹就诊的原发性醛固酮增多症1例

正原发性醛固酮增多症(以下简称原醛症)是由于肾上腺皮质增生或肿瘤而自主分泌过多醛固酮,临床表现为患者有高血压、钠潴留,因排钾增多而导致低钾血症。由于人们对其认识不足,常造成误诊和漏诊。原醛症过去认为是一种少见病,近年来利用血浆醛固酮与血浆肾素活性比值(ARR)从高血压人群中筛选原醛症,其发病率为5%~15%,是一种常见的继发性高血压~[1]。本科室2015年5月收治1例原醛症,表现为严     

原发性醛固酮增多症中肾上腺腺瘤与特醛术前鉴别诊断方法评价

目的 :对临床应用的原发性醛固酮增多症中肾上腺腺瘤和特醛术前鉴别诊断方法进行评价。方法 :在近 5年来临床确诊的 16 0例原醛症患者中进行体位激发试验、影像学检查 ,结果与肾上腺静脉插管采血及术后病理结果进行统计分析。结果 :①腺瘤患者血尿醛固酮、尿 pH高于特醛组 ,而血钾、血浆肾素活性则低。② 18例腺瘤及 2 6例特醛体位激发试验结果 :腺瘤患者中激发后血醛固酮较试验前上升者有 9例 ,下降者 9例 ;2 6例特醛患者激发后血醛固酮较基础值均升高。③ 9例腺瘤及 19例特醛行肾上腺静脉插管检查 ,符合率达 10 0 %。结论 :腺瘤患者生化异常程度较特醛患者明显。体位激发试验在腺瘤及特醛中有部分重叠 ,体位激发后血醛固酮升高者不能排除腺瘤 ,而血醛固酮下降者可确诊腺瘤。肾上腺静脉插管检查的准确率高 ,对于影像学未能发现明显占位性病变者须进行该检查以明确诊断。     

特发性醛固酮增多症的诊治进展

原发性醛固酮增多症（primary aldosteronism,PA）是指肾上腺腺瘤、肾上腺皮质增生等多种病理改变造成的高血压伴有低钾血症、低血浆肾素活性（plasma rennin activity,PRA）、     

原发性醛固酮增多症的超声显像诊断及其病理基础

目的 :探讨原发性醛固酮增多症 (原醛症 )的声像图表现与病理学的关系。方法 :报告经超声显像诊断并由手术和病理证实的 47例原醛症 ,将不同病因原醛症的声像图表现与其病理改变进行对照分析。结果 :47例原醛症中 ,皮质腺瘤 3 8例 ,皮质增生 9例 ,超声显像诊断符合率为 91.5% (43 / 47)。结论 :由于原醛症的病因和病理改变不同 ,其声像图表现各异。超声显像对原醛症的诊断有重要的临床应用价值。但应指出 ,对肾上腺皮质结节样增生与皮质腺瘤的超声显像鉴别诊断的准确性 ,尚应进一步提高     

原发性醛固酮增多症八例误诊分析

原发性醛固酮增多症主要是由于肾上腺皮质腺瘤或增生导致醛固酮分泌过多所产生的症候群 ,临床屡见误诊。我院 1990年 1月～ 2 0 0 3年 12月共收治该病 17例 ,误诊 8例 ,误诊率 4 7 1%。现分析如下。1　临床资料1 1　一般资料　本组男 3例 ,女 5例 ;年龄 2 3～ 5 8岁 ;病程 2个月～ 16年不等 ,其中 5年以下 3例 ,5～10年 4例 ,最长 1例达 16年。1 2　临床表现　症状 :头痛、头晕 7例 ,周期性发作肌无力 4例 ,多饮、多尿、夜尿增多 1例。体征 :血压升高7例 ,其中 6例血压波动在 170 / 98mmHg左右 ,1例高达 2 10 / 12 8mmHg ;下肢水肿 1例 ,四…     

不同检查方法对特发性醛固酮增多症的诊断价值（附62例报告）

目的 :探讨不同检查方法对特发性醛固酮增多症的诊断价值。方法 :6 2例临床确诊特醛症患者中 ,11例行体位激发试验、2 6例行赛庚啶试验、11例行肾上腺静脉插管检查 ,6 2例行肾上腺B超及CT检查。结果 :① 6 2例特醛症患者中 98.39% (6 1/ 6 2 )有高血压 ,6 1.2 9% (38/ 6 2 )有低血钾 ,血醛固酮升高者为 85 .4 8% (5 3/ 6 2 ) ,尿醛固酮升高者为 6 1.2 9% (38/ 6 2 ) ;②特醛症患者肾上腺B超检查诊断符合率为 72 .5 8% (4 5 / 6 5 ) ,CT检查诊断符合率为37.10 % (2 3/ 6 2 ) ;③ 11例特醛症患者行血醛固酮动态试验 ,所有患者激发后血醛固酮较基础值均升高 ,有 8例升幅>30 % ,诊断符合率为 72 .73% (8/ 11) ;④ 2 6例特醛症患者行赛庚啶试验 ,服药后降幅 >30 %者占 6 9.2 3% (18/2 6 ) ;⑤ 11例特醛症患者行肾上腺静脉插管检查 ,所有患者分泌较高侧与对侧血醛固酮比值均 <2 .0 ,诊断符合率为10 0 % (11/ 11)。结论 :基本上所有患者都表现为高血压 ,但低血钾仅在部分患者中出现。动态试验在原醛症的分型诊断中可作为参考 ,但不宜作为鉴别腺瘤或特醛症的主要标准。影像学未能发现明显占位性病变者可进行肾上腺静脉插管检查 ,有助于明确诊断。     

Activity of [des-Aspartyl1]-Angiotensin II in Primary Aldosteronism

This study describes the effects of [des-Aspartyl(1)]-angiotensin II ([des-Asp]-AII) on blood pressure and aldosterone production in patients with primary aldosteronism due to aldosterone-producing adrenal adenoma (APA) and idiopathic adrenal hyperplasia (IHA), and in normotensive control subjects. 10 patients with primary aldosteronism, 7 with APA and 3 with IHA, and 6 normotensive control subjects were placed on a constant 150-meq sodium diet for 4 days. [des-Asp]-AII was infused for 30 min at 6, 12, and 18 pmol/kg per min. Three groups of patients were identified on the basis of aldosterone response to [des-Asp]-AII. Group I, composed of normotensive control subjects, showed incremental increases in plasma aldosterone concentration from 6+/-1 to 14+/-3 ng/100 ml (P < 0.01) with [des-Asp]-AII infusion. Group II, composed of patients with primary aldosteronism, showed incremental increases in plasma aldosterone concentration from 33+/-8 to 65+/-13 ng/100 ml (P < 0.05) with 12 pmol/kg per min of [des-Asp]-AII. Group III, also composed of patients with primary aldosteronism, showed no increase of plasma aldosterone concentration with [des-Asp]-AII. Groups I and II showed similar percentage increases in plasma aldosterone concentration (P = NS). Group III showed significantly lower aldosterone responses than group I (P < 0.01). Group II included all patients with IHA and two patients with APA. Group III included only patients with APA. The blood pressure responses to [des-Asp]-AII of subjects in group I did not differ significantly from those of groups II or III.Thus, patients with IHA and a subgroup of patients with APA showed responsiveness to [des-Asp]-AII which was limited to adrenal cortical stimulation of aldosterone biosynthesis. This suggests that adrenal responsiveness to angiotensin is a major control mechanism in some forms of primary aldosteronism. The differential adrenal responsiveness to [des-Asp]-AII in patients with APA indicates either that there are two distinct subpopulations of APA, or that alteration in tumor response to angiotensin occurs during the natural progression of the disease history.     

肾上腺增生38例临床分析

[目的]提高肾上腺增生疾病的诊治水平.[方法]以肾上腺增生为关键词,于本院病案室查询8年来病例数,并进行一般资料、起病方式、影像学、功能试验、预后等方面的统计.[结果]共有肾上腺增生病例38例（肾上腺CT平扫＋增强证实）.女性20例,男性18例,年龄44.7±16.4岁.以波动性高血压、常规药物降压效果差就诊者30例（78.9%）,左侧肾上腺增生30例（78.9%）,确诊功能性肾上腺疾病5例（16.7%）,确诊无功能性肾上腺疾病6例,余27例因未入住内分泌科及泌尿外科而未行详细专科检查.8例行手术治疗,1例拒绝手术,其余药物治疗.异位促肾上腺皮质激素综合征1例最终死亡,其余预后良好.[结论]①肾上腺增生病例大多数由高血压起病而发现,早期治疗原发疾病可以治愈高血压,因此有必要在高血压患者中进行肾上腺检查.②大部分患者未于内分泌科住院,未详细进行肾上腺检查,可能漏诊相关疾病,故需要提高各科室对肾上腺疾病的认识及诊治水平.③左侧肾上腺增生多见,与既往文献报道一致,目前关于原因研究尚少.     

Plasma Progesterone and 17-hydroxyprogesterone in normal men and children with congenital adrenal hyperplasia

Plasma 17-hydroxyprogesterone (17-OHP) concentrations in normal men averaged 0.094 mug/100 ml. Studies using suppressive doses of androgens and glucocorticoids showed that 90% of the 17-OHP originated from the Leydig cell. The 17-OHP production rate was 1.8 mg/24 hr. Plasma 17-OHP has a marked circadian variation, the 8 p.m. values being only 40% of the 8 a.m. values. Plasma luteinizing hormone measured in the same samples did not vary.The adrenal cortex has the capacity to synthesize and secrete 17-OHP and progesterone since adrenocorticotrophic hormone (ACTH) caused a fourfold increase in these plasma steroids. In children with congenital adrenal hyperplasia, plasma 17-OHP levels were 50-200 times those of normal men and plasma progesterone was increased 6- to 10-fold over normal men.     

Multiple plasma steroid responses to graded ACTH infusions in patients with primary aldosteronism

We measured the simultaneous responses of eight plasma steroids to the infusion of alpha 1-24 ACTH at incremental rates of 12.5 to 200 mlU/30 min in seven patients with primary aldosteronism (five with adenomas, two with adrenal hyperplasia) and in 10 normal controls studied on regular sodium intakes and while supine. Patients with primary aldosteronism from adenomas had relatively higher concentrations (p less than 0.05) of aldosterone, 18 OH-B, corticosterone, and DOC than the two with hyperplasia and, save corticosterone, above the range of the normal controls. We found inconsistent differences in plasma progesterone, 17-hydroxyprogesterone, deoxycortisol, and cortisol. These findings suggest that the intermediate steps in aldosterone biosynthesis are hypersensitive to physiologic amounts of ACTH in patients with aldosterone-producing adenomas. Plasma levels of steroids distal to progesterone, i.e., DOC, corticosterone, 18 OH-B, and aldosterone, are relatively higher after small amounts of ACTH in patients with adenomas than in normal subjects or those with adrenal hyperplasia.     

Detection of primary aldosteronism using the captopril test

In order to evaluate whether changes in the plasma concentration of aldosterone (PA) following the administration of captopril, an inhibitor of angiotensin-converting enzyme, will establish the diagnosis of primary aldosteronism we have used this test in 9 healthy subjects and in 22 patients with various forms of hypertension, including 5 patients with primary aldosteronism due to idiopathic adrenal hyperplasia (n = 4) or aldosterone-producing adenoma (n = 1). The response of PA to captopril (25 mg orally) was investigated on an outpatient basis, following a rest period of 120 minutes in the supine position. In healthy subjects PA decreased from a mean basal value of 11.5 +/- 5.9 ng/dl to less than 6.4 ng/dl (4.9 +/- 1.4 ng/dl [p less than 0.01]). Similarly, captopril induced a fall in PA concentration to less than 6.4 ng/dl in patients with essential hypertension, with renal artery stenosis or with an afunctional kidney. Post-captopril concentrations of plasma aldosterone were about twice the normal level in 3 of 4 patients with idiopathic adrenal hyperplasia and about four-fold raised above normal in the patient with an aldosterone-producing adenoma. In spite of a false-negative result in one patient with idiopathic adrenal hyperplasia, the administration of captopril appears to be of use in recognizing patients with primary aldosteronism on an outpatient basis.     

Primary hyperaldosteronism-evaluation of procedures for diagnosis and localization

We have reviewed the clinical, investigative and pathologicalfindings in 16 patients with primary hyperaldosteronism, 6 withidiopathic adrenal hyperplasia and 10 with an aldosterone-producingadenoma. The ratio of serum aldosterone to plasma renin activitywas >1 1400 pmol/µg/l/h in all patients when measuredsupine on a normal salt diet, negating the need for salt loadingto confirm primary hyperaldosteronism. Postural changes in serumaldosterone confirmed the presence of an aldosterone-producingadenoma in all but one patient when results on normal and highsalt intakes were reviewed together. Nevertheless, the needfor salt loading for discrimination is questioned, as the combinationof postural changes in serum aldosterone on normal saltintake combined with CT confirmed and localized all aldosterone-producingadenomas. Urinary aldosterone measurements were of little value.Localizing procedures consisting of CT and isotopic scanningusing ⁷⁵Se-selenomethyl-cholesterol proved most useful; adrenalvenous sampling yielded less useful information. The lattermay be due to the high predominance of patients (8) showinga background of micronodular hyperplasia with a dominant aldosterone-producingtumour. Only three of these patients have remained normotensiveand normokalaemic on no medication. The presence of micronodularbackground suggests the need for life-long monitoring of suchpatients.     

125I radioimmunoassay for 17 alpha-hydroxyprogesterone in plasma, for diagnosing and managing congenital adrenal hyperplasia

This rapid, inexpensive, and sensitive radioimmunoassay (RIA) for plasma 17 alpha-hydroxyprogesterone involves radioiodination. A single extraction with toluene/hexane removes an average 93% of the hormone from 0.1 mL of plasma. The extract is evaporated and the hormone is estimated by a simple, precise, and accurate 125I RIA involving a specific rabbit antiserum. A suspension of dextran-coated charcoal is used to separate free and bound steroid. Inter- and intra-assay CVs were less than 15 and less than 10%, respectively, and the sensitivity was 3 pg per assay tube. The regression equation for data on 17 alpha-hydroxyprogesterone added to steroid-free plasmas was y = 0.94x + 2.2 (r = 0.99). However, the turnaround time is only one-half to one-tenth that for most 3H RIA (3 h vs 6 to 30 h). The ranges of values found for plasma from normal subjects, treated and untreated patients with congenital adrenal hyperplasia, and infants with newly detected congenital adrenal hyperplasia were, respectively, 1 to 11, 0 to 20, 30 to 620, and 270 to 4900 nmol/L.     

原发醛固酮增多症亚型实验室检验结果分析

目的分析原发醛固酮增多症不同亚型的实验室检查结果差异。方法 92例原发醛固酮增多症患者,依据术后组织病理结果分为肾上腺腺瘤组（76例）和肾上腺增生组（16例）,比较2组血钾、血钠、血醛固酮、肾素、血管紧张素Ⅱ和醛固酮肾素比值。结果增生组血钾水平（（3.78±0.38）mmol/L）高于腺瘤组（（3.34±0.66）mmol/L）（P〈0.05）,血钠、血醛固酮、肾素、血管紧张素Ⅱ及醛固酮肾素比值（（143.61±2.45）mmol/L、13.5（6.8,245.0）ng/（L·h）、（0.66±0.72）mg/L、（36.90±23.37）ng/L、170.0（7.7,9 450.0））与腺瘤组（（144.53±3.16）mmol/L、21.2（2.1,375.0）ng/（L·h）、（0.62±1.23）mg/L、（33.84±24.51）ng/L、111.0（2.1,6 820.0））比较差异无统计学意义（P〉0.05）。结论原发醛固酮增多症肾上腺腺瘤和肾上腺增生患者临床表现相似,术前检测血钾有助于亚型判定。     

Primary aldosteronism in childhood due to primary adrenal hyperplasia

We present an unusual case of primary aldosteronism in childhood. A 9-year-old boy had hypertension, hypokalemia, hyporeninemia and hyperaldosteronism. Dexamethasone administration decreased plasma aldosterone transiently but failed to correct the hyperaldosteronism, excluding dexamethasone-suppressible hyperaldosteronism. Plasma aldosterone decreased with upright posture and showed a circadian rhythm. Spironolactone treatment normalized blood pressure and serum potassium and lowered aldosterone secretion. During the studies, plasma aldosterone correlated with serum cortisol but not with plasma renin. Preoperative results indicated that this patient presented the functional features of aldosteronoma. Adrenal computed tomography, scintigraphy and left venography were not diagnostic of adrenal lesions. The left adrenal venous sampling showed hypersecretion of aldosterone from the left adrenal gland. The left adrenalectomy revealed micronodular hyperplasia but resulted in a prompt and sustained reversal of hypertension and hyperaldosteronism. These findings suggest that primary aldosteronism in this patient resulted from primary adrenal hyperplasia. Thus, adrenal hyperplasia is a heterogenous group of disorders and carefully selected studies allow prospective selection of appropriate treatment.     

(131)I-MIBG核素显像在肾上腺髓质嗜铬细胞瘤诊断中的初步应用

目的 探讨^131I-MIBG肾上腺髓质显像在嗜铬细胞瘤诊断中的应用，同时与CT、B超及尿VMA测定结果进行比较。方法 病例选择经手术，病理确诊的3例嗜铬细胞瘤患者及经临床确诊的2例高血压患者，4例肾上腺肿大患者及1例肾上腺皮质瘤患者，受检者静脉缓注^131I-MIBG111MBg，注射后24h,48h使用SPECT进行全身和局部显像。结果 3例嗜铬细胞瘤患者可见患侧有异常放射性浓聚区，心肌，肝脏不显影，其他7例非嗜铬细胞瘤患者肾上腺不显影，但有6例心肌，肝脏显影。^131I-MIBG显像阳性率为100%，CT检查阳性率为66.7%，B超检查3例患者只能定位，不能定性，VMA检测阳性率为100%，结论 ^131I-MIBG显像对嗜铬细胞瘤的诊断优于CT、B超和尿VMA测定。