Effects of pre-operative Trilostane treatment on pituitary-adrenal function in primary hyperaldosteronism (Conn's syndrome)

The primary hyperaldosteronism also known as Conns syndrome, is a rarely diagnosed disease that commonly runs under a mask of ischemic heart disease and the primary arteria hypertension (AH). Nevertheless, the incidence of the given pathology among all patients with AH makes almost 17%. On the other hand, the absence of specific clinical manifestations of the disease makes its timely and correct diagnosis difficult which is fraught with serious complications. In the article a clinical case of Conns syndrome and peculiarities of its diagnosis are described.

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Conn’s syndrome (primary hyperaldosteronism) simulating polymyositis

Rheumatology International ◽

10.1007/s00296-004-0462-0 ◽

2004 ◽

Vol 25 (2) ◽

pp. 133-134 ◽

Cited By ~ 4

Author(s):

Timuçin Kaşifoğlu ◽

Cengiz Korkmaz ◽

Özgül Paşaoğlu

Keyword(s):

Primary Hyperaldosteronism ◽

Conn’S Syndrome

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Hypertension and Recurrent Hypokalaemia in Young Woman - A Case Report of Primary Hyperaldosteronism (Conn’s Syndrome)

University Heart Journal ◽

10.3329/uhj.v12i2.36393 ◽

2018 ◽

Vol 12 (2) ◽

pp. 102-104

Author(s):

Md Nazmul Hasan ◽

Md Abdur Rahim ◽

Quazi Mamtaz Uddin Ahmed ◽

Md Syedul Islam ◽

Md Rasul Amin ◽

...

Keyword(s):

Case Report ◽

Young Woman ◽

Clinical Features ◽

Resistant Hypertension ◽

Plasma Aldosterone ◽

Primary Hyperaldosteronism ◽

Adrenal Hyperplasia ◽

Conn’S Syndrome ◽

Bilateral Adrenal Hyperplasia ◽

Aldosterone Producing Adenoma

Primary hyperaldosteronism is caused by most commonly due to aldosterone producing adenoma(conn’s syndrome) or bilateral adrenal hyperplasia. Clinical features may be of different type which includes hypertension in young age or resistant hypertension, recurrent hypokalaemia and characterized by increased ratio of plasma aldosterone (ng/dl) to rennin (ng/ml per hour) activity. We report a case of young woman presented with hypertension and recurrent hypokalaemia.University Heart Journal Vol. 12, No. 2, July 2016; 102-104

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Symptomatic arterial hypertension associated with primary hyperaldosteronism

Arterial’naya Gipertenziya (Arterial Hypertension) ◽

10.18705/1607-419x-2017-23-3-224-230 ◽

2017 ◽

Vol 23 (3) ◽

pp. 224-230 ◽

Cited By ~ 2

Author(s):

A. N. Kalyagin ◽

V. A. Beloborodov ◽

T. M. Maksikova

Keyword(s):

Surgical Treatment ◽

Lactate Dehydrogenase ◽

Arterial Hypertension ◽

Resistant Hypertension ◽

Creatine Phosphokinase ◽

Primary Hyperaldosteronism ◽

Adrenal Tumors ◽

Therapeutic Practice ◽

Conn’S Syndrome ◽

Rare Phenomenon

Objective.Primary hyperaldosteronism (PGA) (Conn’s syndrome) is a relatively rare phenomenon in therapeutic practice, occurring in 4,7–9%. In resistant hypertension (HTN) the rate of PGA achieves 10–20%. Often it results from the aldosterone-producing adrenal tumors and manifests by symptomatic HTN, neuromuscular, and renal symptoms. We present the cases of successful verification and surgical treatment of PGA. HTN patients and patients with rhabdomyolysis symptoms (increased creatine phosphokinase or lactate dehydrogenase) require further examination to exclude PGA.

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Atrial Fibrillation Associated with Hypokalemia Due to Primary Hyperaldosteronism (Conn's Syndrome)

Pacing and Clinical Electrophysiology ◽

10.1111/j.1540-8159.2006.00536.x ◽

2006 ◽

Vol 29 (11) ◽

pp. 1303-1305 ◽

Cited By ~ 8

Author(s):

BASEL AL. ALOUL ◽

JIAN-MING LI ◽

DAVID BENDITT ◽

VENKATAKRISHNA THOLAKANAHALLI

Keyword(s):

Atrial Fibrillation ◽

Primary Hyperaldosteronism ◽

Conn’S Syndrome

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Polymorphic differences from normal in the aldosterone synthase gene (CYP11B2) in patients with primary hyperaldosteronism and adrenal tumour (Conn's syndrome)

Clinical Endocrinology ◽

10.1046/j.1365-2265.2001.01287.x ◽

2001 ◽

Vol 54 (6) ◽

pp. 725-730 ◽

Cited By ~ 14

Author(s):

Gordon C. Inglis ◽

Pierre F. Plouin ◽

Elaine C. Friel ◽

Eleanor Davies ◽

Robert Fraser ◽

...

Keyword(s):

Primary Hyperaldosteronism ◽

Adrenal Tumour ◽

Aldosterone Synthase ◽

Conn’S Syndrome

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KCNJ5 mutations in the National Institutes of Health cohort of patients with primary hyperaldosteronism: an infrequent genetic cause of Conn's syndrome

Endocrine Related Cancer ◽

10.1530/erc-12-0022 ◽

2012 ◽

Vol 19 (3) ◽

pp. 255-260 ◽

Cited By ~ 27

Author(s):

Paraskevi Xekouki ◽

Michael M Hatch ◽

Lin Lin ◽

De Alexandre Rodrigo ◽

Monalisa Azevedo ◽

...

Keyword(s):

Amino Acid ◽

Amino Acid Substitution ◽

Reversal Potential ◽

Zona Glomerulosa ◽

National Institutes Of Health ◽

Primary Hyperaldosteronism ◽

Conn’S Syndrome ◽

Variable Expression ◽

Functional Studies ◽

Channel Selectivity

KCNJ5 mutations were recently described in primary hyperaldosteronism (PH or Conn's syndrome). The frequency of these mutations in PH and the way KCNJ5 defects cause disease remain unknown. A total of 53 patients with PH have been seen at the National Institutes of Health over the last 12 years. Their peripheral and tumor DNAs (the latter from 16 that were operated) were screened for KCNJ5 mutations; functional studies on the identified defects were performed after transient transfection. Only two mutations were identified, and both in the tumor DNA only. There were no germline sequencing defects in any of the patients except for known synonymous variants of the KCNJ5 gene. One mutation was the previously described c.G451C alteration; the other was a novel one in the same codon: c.G451A; both lead to the same amino acid substitution (G151R) in the KCNJ5 protein. Functional studies confirmed previous findings that both mutations caused loss of channel selectivity and a positive shift in the reversal potential. In conclusion, the KCNJ5 protein was strongly expressed in the zona glomerulosa of normal adrenal glands but showed variable expression in the aldosterone-producing adenomas with and without mutation. The rate of KCNJ5 mutations among patients with PH and/or their tumors is substantially lower than what was previously reported. The G151R amino acid substitution appears to be the most frequent one so far detected in PH, despite additional nucleotide changes. The mutation causes loss of this potassium channel's selectivity and may assist in the design of new therapies for PH.

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