Jill K.H. Laurin , Oyebimbola A. Oyewunmi , Emily M. Garland , Alfredo Gamboa , Victor C. Nwazue , Sachin Y. Paranjape , Bonnie K. Black , Luis E. Okamoto , Cyndya A. Shibao , Italo Biaggioni , David Robertson , André Diedrich , William D. Dupont , Robert S. Sheldon , Satish R. Raj
{"title":"体位性直立性心动过速综合征患者的肾上腺对促肾上腺皮质激素的反应是完整的。","authors":"Jill K.H. Laurin , Oyebimbola A. Oyewunmi , Emily M. Garland , Alfredo Gamboa , Victor C. Nwazue , Sachin Y. Paranjape , Bonnie K. Black , Luis E. Okamoto , Cyndya A. Shibao , Italo Biaggioni , David Robertson , André Diedrich , William D. Dupont , Robert S. Sheldon , Satish R. Raj","doi":"10.1016/j.autneu.2023.103105","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><p><span>Many patients with postural orthostatic tachycardia syndrome<span><span> (POTS) are hypovolemic with plasma volume deficits of 10–30 %. Some also have low levels of aldosterone and diminished aldosterone-renin ratios despite elevations in </span>angiotensin II, pointing to potential </span></span>adrenal dysfunction<span><span><span>. To assess adrenal gland responsiveness in POTS, we measured circulating levels of aldosterone and </span>cortisol following </span>adrenocorticotropin hormone (ACTH) stimulation.</span></p></div><div><h3>Methods</h3><p>While on a low Na<sup>+</sup> diet (∼10 mEq/day), 8 female patients with POTS and 5 female healthy controls (HC) received a low dose (1 μg) ACTH bolus following a baseline blood sample. After 60 min, a high dose (249 μg) infusion of ACTH was administered to ensure maximal adrenal response. Venous aldosterone and cortisol levels were sampled every 30 min for 2 h.</p></div><div><h3>Results</h3><p>Aldosterone increased in both groups in response to ACTH but was not different between POTS vs. HC at 60 min (53.5 ng/dL [37.8–61.8 ng/dL] vs. 46.1 ng/dL [36.7–84.9 ng/dL]; <em>P</em> = 1.000) or maximally (56.4 ng/dL [49.2–67.1 ng/dL] vs. 49.5 ng/dL [39.1–82.8 ng/dL]; <em>P</em><span> = 0.524). Cortisol increased in both groups in response to ACTH but was not different in patients with POTS vs. HC at 60 min (39.9 μg/dL [36.1–47.7 μg/dL] vs. 39.3 μg/dL [35.4–46.6 μg/dL]; </span><em>P</em> = 0.724) or maximally (39.9 μg/dL [33.9–45.4 μg/dL] vs. 42.0 μg/dL [37.6–49.7 μg/dL]; <em>P</em> = 0.354).</p></div><div><h3>Conclusions</h3><p><span>ACTH appropriately increased the aldosterone and cortisol levels in patients with POTS. These findings suggest that the response of the adrenal cortex to </span>hormonal stimulation is intact in patients with POTS.</p></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":null,"pages":null},"PeriodicalIF":3.2000,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Adrenal gland response to adrenocorticotropic hormone is intact in patients with postural orthostatic tachycardia syndrome\",\"authors\":\"Jill K.H. Laurin , Oyebimbola A. Oyewunmi , Emily M. Garland , Alfredo Gamboa , Victor C. Nwazue , Sachin Y. Paranjape , Bonnie K. Black , Luis E. Okamoto , Cyndya A. Shibao , Italo Biaggioni , David Robertson , André Diedrich , William D. Dupont , Robert S. Sheldon , Satish R. Raj\",\"doi\":\"10.1016/j.autneu.2023.103105\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><p><span>Many patients with postural orthostatic tachycardia syndrome<span><span> (POTS) are hypovolemic with plasma volume deficits of 10–30 %. Some also have low levels of aldosterone and diminished aldosterone-renin ratios despite elevations in </span>angiotensin II, pointing to potential </span></span>adrenal dysfunction<span><span><span>. To assess adrenal gland responsiveness in POTS, we measured circulating levels of aldosterone and </span>cortisol following </span>adrenocorticotropin hormone (ACTH) stimulation.</span></p></div><div><h3>Methods</h3><p>While on a low Na<sup>+</sup> diet (∼10 mEq/day), 8 female patients with POTS and 5 female healthy controls (HC) received a low dose (1 μg) ACTH bolus following a baseline blood sample. After 60 min, a high dose (249 μg) infusion of ACTH was administered to ensure maximal adrenal response. Venous aldosterone and cortisol levels were sampled every 30 min for 2 h.</p></div><div><h3>Results</h3><p>Aldosterone increased in both groups in response to ACTH but was not different between POTS vs. HC at 60 min (53.5 ng/dL [37.8–61.8 ng/dL] vs. 46.1 ng/dL [36.7–84.9 ng/dL]; <em>P</em> = 1.000) or maximally (56.4 ng/dL [49.2–67.1 ng/dL] vs. 49.5 ng/dL [39.1–82.8 ng/dL]; <em>P</em><span> = 0.524). Cortisol increased in both groups in response to ACTH but was not different in patients with POTS vs. HC at 60 min (39.9 μg/dL [36.1–47.7 μg/dL] vs. 39.3 μg/dL [35.4–46.6 μg/dL]; </span><em>P</em> = 0.724) or maximally (39.9 μg/dL [33.9–45.4 μg/dL] vs. 42.0 μg/dL [37.6–49.7 μg/dL]; <em>P</em> = 0.354).</p></div><div><h3>Conclusions</h3><p><span>ACTH appropriately increased the aldosterone and cortisol levels in patients with POTS. These findings suggest that the response of the adrenal cortex to </span>hormonal stimulation is intact in patients with POTS.</p></div>\",\"PeriodicalId\":55410,\"journal\":{\"name\":\"Autonomic Neuroscience-Basic & Clinical\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":3.2000,\"publicationDate\":\"2023-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Autonomic Neuroscience-Basic & Clinical\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1566070223000346\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Autonomic Neuroscience-Basic & Clinical","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1566070223000346","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
Adrenal gland response to adrenocorticotropic hormone is intact in patients with postural orthostatic tachycardia syndrome
Background
Many patients with postural orthostatic tachycardia syndrome (POTS) are hypovolemic with plasma volume deficits of 10–30 %. Some also have low levels of aldosterone and diminished aldosterone-renin ratios despite elevations in angiotensin II, pointing to potential adrenal dysfunction. To assess adrenal gland responsiveness in POTS, we measured circulating levels of aldosterone and cortisol following adrenocorticotropin hormone (ACTH) stimulation.
Methods
While on a low Na+ diet (∼10 mEq/day), 8 female patients with POTS and 5 female healthy controls (HC) received a low dose (1 μg) ACTH bolus following a baseline blood sample. After 60 min, a high dose (249 μg) infusion of ACTH was administered to ensure maximal adrenal response. Venous aldosterone and cortisol levels were sampled every 30 min for 2 h.
Results
Aldosterone increased in both groups in response to ACTH but was not different between POTS vs. HC at 60 min (53.5 ng/dL [37.8–61.8 ng/dL] vs. 46.1 ng/dL [36.7–84.9 ng/dL]; P = 1.000) or maximally (56.4 ng/dL [49.2–67.1 ng/dL] vs. 49.5 ng/dL [39.1–82.8 ng/dL]; P = 0.524). Cortisol increased in both groups in response to ACTH but was not different in patients with POTS vs. HC at 60 min (39.9 μg/dL [36.1–47.7 μg/dL] vs. 39.3 μg/dL [35.4–46.6 μg/dL]; P = 0.724) or maximally (39.9 μg/dL [33.9–45.4 μg/dL] vs. 42.0 μg/dL [37.6–49.7 μg/dL]; P = 0.354).
Conclusions
ACTH appropriately increased the aldosterone and cortisol levels in patients with POTS. These findings suggest that the response of the adrenal cortex to hormonal stimulation is intact in patients with POTS.
期刊介绍:
This is an international journal with broad coverage of all aspects of the autonomic nervous system in man and animals. The main areas of interest include the innervation of blood vessels and viscera, autonomic ganglia, efferent and afferent autonomic pathways, and autonomic nuclei and pathways in the central nervous system.
The Editors will consider papers that deal with any aspect of the autonomic nervous system, including structure, physiology, pharmacology, biochemistry, development, evolution, ageing, behavioural aspects, integrative role and influence on emotional and physical states of the body. Interdisciplinary studies will be encouraged. Studies dealing with human pathology will be also welcome.