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[一例特发性醛固酮增多症发病后5年血浆醛固酮浓度正常:一项12年随访研究]

[A case of idiopathic hyperaldosteronism with normal plasma aldosterone concentrations for 5 years after onset: a 12-year follow-up study].

作者信息

Nemoto T, Niimura S, Hayashi A, Gomibuchi T, Sanada H, Watanabe Y, Shigetomi S, Fukuchi S

机构信息

Third Department of Internal Medicine, Fukushima Medical College, Japan.

出版信息

Nihon Naibunpi Gakkai Zasshi. 1994 May 20;70(4):439-46. doi: 10.1507/endocrine1927.70.4_439.

DOI:10.1507/endocrine1927.70.4_439
PMID:7958093
Abstract

We report a 54-year old man diagnosed as idiopathic hyperaldosteronism (IHA) at least 12 years after the onset. At the age of 42, he showed hypertension (162/100mmHg), hypokalemia, metabolic alkalosis, low plasma renin activity (PRA) and normal plasma aldosterone concentration (PAC) in a supine posture. Both PRA and PAC were elevated after a 2-hour ambulation following furosemide (60mg) injection. Since the accumulation of radioactivity following 131I-aldosterol injection with combined administration of dexamethasone was equally detected in both adrenal areas, he was diagnosed as low-renin essential hypertension (LREH). Blood pressure (BP) decreased to the normal range after treatment with nifedipine (40mg/day). At the age of 47, however, BP was hypertensive (164/106mmHg) serum potassium (K) level was normal. Although PAC was normal in a supine posture, it increased after a 2-hour ambulation following furosemide (60mg) injection. PRA after the stimulation was still suppressed despite the increase in PAC. At the age of 54, BP was 172/94mmHg. Serum K level was 3.4mEq/L. PRA was suppressed below 0.1 ng/ml/hr, while PAC was above the normal range (170pg/ml) in a supine posture. Serum cortisol and urinary excretion of 17-OHCS and 17-KS were within normal limits. PRA was still suppressed below 0.1 ng/ml/hr after a 2-hour ambulation following furosemide (60mg) injection, but PAC was markedly increased (330pg/ml). There was a diurnal rhythm of aldosterone, which was parallel to that of ACTH.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

我们报告一名54岁男性,在发病至少12年后被诊断为特发性醛固酮增多症(IHA)。42岁时,他表现为高血压(162/100mmHg)、低钾血症、代谢性碱中毒、血浆肾素活性(PRA)降低以及仰卧位时血浆醛固酮浓度(PAC)正常。注射速尿(60mg)后步行2小时,PRA和PAC均升高。由于注射131I - 醛固酮并联合使用地塞米松后,双侧肾上腺区域放射性均有同等程度的积聚,他被诊断为低肾素性原发性高血压(LREH)。服用硝苯地平(40mg/天)治疗后血压降至正常范围。然而,47岁时血压又升高(164/106mmHg),血清钾(K)水平正常。尽管仰卧位时PAC正常,但注射速尿(60mg)后步行2小时,PAC升高。尽管PAC升高,但刺激后的PRA仍受抑制。54岁时,血压为172/94mmHg。血清钾水平为3.4mEq/L。仰卧位时PRA抑制至低于0.1 ng/ml/hr,而PAC高于正常范围(170pg/ml)。血清皮质醇以及17 - OHCS和17 - KS的尿排泄量均在正常范围内。注射速尿(60mg)后步行2小时,PRA仍抑制至低于0.1 ng/ml/hr,但PAC显著升高(330pg/ml)。醛固酮存在昼夜节律,与促肾上腺皮质激素(ACTH)的昼夜节律平行。(摘要截选至250字)

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