DOCSLIB.ORG

Hyperaldosteronism: Recent Concepts, Diagnosis, and Management

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Hyperaldosteronism: Recent Concepts, Diagnosis, and Management Postgrad Med J 2001;77:639–644 639 Hyperaldosteronism: recent concepts, diagnosis, Postgrad Med J: first published as 10.1136/pmj.77.912.639 on 1 October 2001. Downloaded from and management R Foo, K M O’Shaughnessy, M J Brown As a cause for hypertension, aldosterone excess modulate sgk gene transcription and further- is now thought to be more prevalent than previ- more, a simple hormone response element has ously quoted in textbooks. Classical features of been found in the rat sgk gene 5'-flanking hypokalaemia and metabolic alkalosis can be region.2 Sgk mRNA is rapidly stimulated by absent even in the presence of marked hyper- mineralocorticoids but receptor ligand activa- tension. This implies the need for a high index of tion results in both an early phase increase in suspicion and possibly argues the case for ENaC activity and a late phase upregulation of routine screening, especially in patients with ENaC number. Apart from action on ENaC in “diYcult to treat” hypertension. Given multisys- apical cells, aldosterone appears to also increase tem target organ damage and increased cardio- activity of the Na+/K+-ATPase pump in the vascular risk associated with chronic uncon- basolateral membrane of distal tubular cells.3 trolled hypertension, a readily treatable cause Furthermore, rapid 2–10 min eVects of aldoster- such as hyperaldosteronism is an important one have been described that are not inhibited diagnosis to make. In addition, hyperaldos- by mineralocorticoid receptor antagonist, teronism related hypertension is now known to spironolactone.4 Unknown mechanisms mediat- cover other recently identified monogenic disor- ing aldosterone receptor binding, including the ders such as glucocorticoid remediable aldos- possibility of unknown membrane receptors not teronism. These rarer monogenic hypertensive involving protein synthesis, thus remain to be disorders provide clues to cracking the mystery defined. Nevertheless aldosterone is responsible behind polygenic “essential” hypertension. physiologically for electrolyte balance in the kid- Apart from patients with hyperaldosteronism, a ney, salivary glands, sweat glands, and gastro- subset of the well recognised “low renin intestinal tract and in the kidney it has the hypertension” patient group also appears to important function of mediating sodium reten- produce a dramatic and remarkable response tion and increasing potassium excretion. when treated with spironolactone. We suggest In the renin-angiotensin-aldosterone axis, that spironolactone sensitive hypertension may decreased renal perfusion pressure stimulates represent a wider spectrum of disorders where the â-adrenoreceptor dependent release of renin blood pressure is readily controlled by the addi- that is synthesised by juxtaglomerular cells. In tion of aldosterone receptor antagonist. extracellular volume overexpansion, “excessive stretch” signals in the juxtaglomerular cells Aldosterone physiology Glucocorticoids and mineralocorticoids are syn- result in decreased renin secretion. The sub- http://pmj.bmj.com/ thesised from cholesterol mainly in the adrenal strate for renin is angiotensinogen, which is a cortex. The two forms of cytochrome P-450 glycoprotein of variable structure and molecular enzymes, CYP11B1 (aldosynthase) and weight synthesised in the liver. Ten N-terminal CYP11B2 (11â-hydroxylase), that catalyse the amino acid residues of angiotensinogen contain final step of these synthetic pathways are the amino acid sequence of angiotensin I and encoded by two closely related genes on angiotensin converting enzyme is responsible for chromosome 8. CYP11B1 synthesises corticos- the removal of two amino acids from angiotensin on October 3, 2021 by guest. Protected copyright. terone from deoxycorticosterone in the zona I to produce the key aldosterone stimulating fasiculata reticularis and is mainly regulated by factor, angiotensin II. Angiotensin II is itself a adrenocorticotrophic hormone (ACTH). potent vasoconstrictor. CYP11B2 catalyses the synthesis of aldosterone from deoxycorticosterone in the zona glomeru- Clinical features and making the diagnosis losa and its activity is principally regulated by Conn’s original description was that of a patient angiotensin II and potassium; and it is weakly with hypertension, hypokalaemia, and neuro- regulated by sodium and ACTH. As mito- muscular symptoms associated with an chondrial enzymes, CYP11B1 and 11B2 are aldosterone-producing adrenal adenoma.5 It is Clinical Pharmacology highly sensitive to tissue oxygen concentration. now recognised that the same clinical and Unit, University of Aldosterone is the major and most potent biochemical picture can be produced by other Cambridge, Box 110, Addenbrooke’s mineralocortcoid in man. It interacts with conditions in which there is aldosterone excess Hospital, Cambridge specific intracellular receptors to form dimers without adenoma. Primary aldosteronism either CB2 2QQ, UK which in turn bind to response elements in the through adrenal adenoma or adrenal hyperplasia RFoo promoter regions of target genes to initiate hor- is characterised by low or undetectable plasma K M O’Shaughnessy mone mediated transcription. Precise aldoster- renin activity suppressed via negative feedback M J Brown one induced proteins have not been identified by autonomous aldosterone secretion. While in Correspondence to: but recent evidence suggests that a member of some instances, the plasma aldosterone level is Dr Foo the serine-threonine kinase pathway, serum glu- high as would be expected; it can also be within [email protected] cocorticoid regulated kinase (sgk) regulates the normal range. Instead the aldosterone:renin Submitted 27 February 2001 activity of the epithelial sodium channel ratio (ARR) appears to be a more reliable means Accepted 23 April 2001 (ENaC).1 Mineralocorticoids appear to directly (93% sensitivity6) of identifying patients with www.postgradmedj.com 640 Foo, O’Shaughnessy, Brown primary hyperaldosteronism and whose hyper- and aldosterone synthesis is angiotensin II Postgrad Med J: first published as 10.1136/pmj.77.912.639 on 1 October 2001. Downloaded from tension is treatable by the aldosterone receptor insensitive but ACTH sensitive. In contrast, antagonist, spironolactone. familial hyperaldosteronism II is yet another The first study using the ARR was published condition that has been described where in 1981 where out of 348 hypertensive patients patients have cortical hyperplasia,12 and in who were screened, nine were found to have many kindreds there is an associated progres- adrenal adenoma using a much higher cut oV sion to adenoma (tumour) formation where ARR of 2081 units together with subsequent aldosterone synthesis is not glucocorticoid nuclear scintigram and computed tomogram.7 remediable and remains angiotensin II sensi- In this study, only three of the nine had tive. Familial hyperaldosteronism II has re- potassium less than 3.5 mmol/l. Plasma aldos- cently been mapped to chromosome 7p22. terone levels were equally non-discriminatory. On the background of this, diVerence in All nine had suppressed plasma renin activity aldosterone levels with change of posture but so did 39% of all the other 348 patients therefore requires careful interpretation in without adenomata. If present day ARR cut oV relation to family history and adrenal imaging of 750 units were used, more patients may have results. When entire adrenal glands were been diagnosed as having primary aldos- removed in cases of a solitary benign adenoma, teronism. In the late 1990s Gordon showed that the “non-tumorous” section of zona glomeru- by screening all hypertensive patients reviewed losa often appeared histologically hyperplastic, in a tertiary centre for ARR >750 units, the consisting of multiple small cortical nodules. prevalence of primary aldosteronism was closer This may well represent a spectrum of overlap to 15% than the 1% that has previously been as seen in familial multiple neoplasia syn- quoted in textbooks.8 Percentages of prevalence dromes where both neoplasia and hyperplasia based on the finding of a raised ARR have are variously and sometimes simultaneously ranged from 2.7% to 32%.9 expressed. The genetic abnormality is unlikely In a primary care setting, a group in Dundee to be limited to cells within the adenoma. has recently shown that the prevalence of When determining the ARR, concomitant primary aldosteronism diagnosed through a antihypertensive therapy can alter renin and high ARR was 25%.10 aldosterone levels. Calcium channel antagonists In an Australian tertiary practice, Hamlet et al suppress aldosterone synthesis. Angiotensin reportedly found the recognition of hyperaldos- converting enzyme inhibitors suppress aldoster- teronism as defined by a high ARR abruptly one levels as would the newer angiotensin II increased from two to five cases per year before receptor antagonists. Thiazide diuretics lead to routine use of the ARR, to over 50 per year after increase in renin levels more marked than that of its use.11 In their screening programme, Hamlet aldosterone. All antihypertensives in these et al also found that the majority of patients classes, however, improve the discriminatory (70%) with primary aldosteronism were power of the ARR. A false negative is unlikely in normokalaemic. Patients can rarely present with view of the autonomous nature of aldosterone severe resistant hypokalaemia with symptoms of excess. However â-blockers suppress renin syn- muscle weakness and parasthesia. We have thesis and may lead to a
Load more

Recommended publications
  • Familial Hyperaldosteronism
    Familial hyperaldosteronism Description Familial hyperaldosteronism is a group of inherited conditions in which the adrenal glands, which are small glands located on top of each kidney, produce too much of the hormone aldosterone. Aldosterone helps control the amount of salt retained by the kidneys. Excess aldosterone causes the kidneys to retain more salt than normal, which in turn increases the body's fluid levels and blood pressure. People with familial hyperaldosteronism may develop severe high blood pressure (hypertension), often early in life. Without treatment, hypertension increases the risk of strokes, heart attacks, and kidney failure. Familial hyperaldosteronism is categorized into three types, distinguished by their clinical features and genetic causes. In familial hyperaldosteronism type I, hypertension generally appears in childhood to early adulthood and can range from mild to severe. This type can be treated with steroid medications called glucocorticoids, so it is also known as glucocorticoid-remediable aldosteronism (GRA). In familial hyperaldosteronism type II, hypertension usually appears in early to middle adulthood and does not improve with glucocorticoid treatment. In most individuals with familial hyperaldosteronism type III, the adrenal glands are enlarged up to six times their normal size. These affected individuals have severe hypertension that starts in childhood. The hypertension is difficult to treat and often results in damage to organs such as the heart and kidneys. Rarely, individuals with type III have milder symptoms with treatable hypertension and no adrenal gland enlargement. There are other forms of hyperaldosteronism that are not familial. These conditions are caused by various problems in the adrenal glands or kidneys. In some cases, a cause for the increase in aldosterone levels cannot be found.
    [Show full text]
  • Hyperaldosteronism: How Current Concepts Are Transforming the Diagnostic and Therapeutic Paradigm
    Kidney360 Publish Ahead of Print, published on July 23, 2020 as doi:10.34067/KID.0000922020 Hyperaldosteronism: How Current Concepts Are Transforming the Diagnostic and Therapeutic Paradigm Michael R Lattanzio(1), Matthew R Weir(2) (1) Division of Nephrology, Department of Medicine, The Chester County Hospital/University of Pennsylvania Health System (2) Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD Correspondence: Matthew R Weir University of Maryland Medical Center Division of Nephrology 22 S. Greene St. Room N3W143 Baltimore, Maryland 21201 [email protected] 1 Copyright 2020 by American Society of Nephrology. Abbreviations PA=Primary Hyperaldosteronism CVD=Cardiovascular Disease PAPY=Primary Aldosteronism Prevalence in Hypertension APA=Aldosterone-Producing Adenoma BAH=Bilateral Adrenal Hyperplasia ARR=Aldosterone Renin Ratio AF=Atrial Fibrillation OSA=Obstructive Sleep Apnea OR=Odds Ratio AHI=Apnea Hypopnea Index ABP=Ambulatory Blood Pressure AVS=Adrenal Vein Sampling CT=Computerized Tomography MRI=Magnetic Resonance Imaging SIT=Sodium Infusion Test FST=Fludrocortisone Suppression Test CCT=Captopril Challenge Test PAC=Plasma Aldosterone Concentration PRA=Plasma Renin Activity MRA=Mineralocorticoid Receptor Antagonist MR=Mineralocorticoid Receptor 2 Abstract Nearly seven decades have elapsed since the clinical and biochemical features of Primary Hyperaldosteronism (PA) were described by Conn. PA is now widely recognized as the most common form of secondary hypertension. PA has a strong correlation with cardiovascular disease and failure to recognize and/or properly diagnose this condition has profound health consequences. With proper identification and management, PA has the potential to be surgically cured in a proportion of affected individuals. The diagnostic pursuit for PA is not a simplistic endeavor, particularly since an enhanced understanding of the disease process is continually redefining the diagnostic and treatment algorithm.
    [Show full text]
  • High and Non-Suppressible Plasma Renin Activity in a Patient with Aldosterone Producing Adenoma: Pathophysiologic and Diagnostic Implications
    Journal of Human Hypertension (1999) 13, 75–78 1999 Stockton Press. All rights reserved 0950-9240/99 $12.00 http://www.stockton-press.co.uk/jhh CASE REPORT High and non-suppressible plasma renin activity in a patient with aldosterone producing adenoma: pathophysiologic and diagnostic implications E Shyong Tai and PHK Eng Department of Endocrinology, Singapore General Hospital, Singapore We describe a case of primary aldosteronism due to an possible pathophysiological causes of a rise in PRA in aldosterone producing adenoma with high and non-sup- this clinical setting and suggest that underlying arteri- pressible plasma renin activity (PRA). She had sup- olar disease due to prolonged hypertension may be the pressed PRA at initial diagnosis. This rose above the cause of increased and non-suppressible PRA in pri- reference range for normal individuals over a period of mary aldosteronism. 7 years with untreated hypertension. We discuss the Keywords: primary aldosteronism; plasma renin activity; diagnosis Introduction Case report Primary aldosteronism is classically associated with Our patient was a 34-year-old woman who was hypertension, hypokalaemia and suppressed plasma found to have hypertension during the fifteenth renin activity (PRA). Most cases are due to an aldo- week of pregnancy. Plasma aldosterone was sterone producing adenoma (APA). We present a 2039 pmol/l, PRA Ͻ0.15 ␮g/l/h and a diagnosis of case of prolonged, untreated, primary aldosteronism primary aldosteronism was made. Following the due to an APA. She had suppressed PRA at the time delivery of her child, she defaulted follow-up and of diagnosis, which became elevated and non-sup- was not treated with any antihypertensives nor pot- pressible by intravenous salt loading.
    [Show full text]
  • A Case of Gitelman's Syndrome with Decreased Angiotensin II–Forming Activity
    545 Hypertens Res Vol.29 (2006) No.7 p.545-549 Case Report A Case of Gitelman’s Syndrome with Decreased Angiotensin II–Forming Activity Kimika ETO1), Uran ONAKA1), Takuya TSUCHIHASHI1), Takashi HIRANO2), Masaru NAKAYAMA2), Kosuke MASUTANI3), Hideki HIRAKATA3), Hidenori URATA4), and Minoru YASUJIMA5) Gitelman’s syndrome (GS) is a variant of Bartter’s syndrome (BS) characterized by hypokalemic alkalosis, hypomagnesemia, hypocalciuria and secondary aldosteronism without hypertension. A 31-year old Japa- nese man who had suffered from mild hypokalemia for 10 years was admitted to our hospital. He had met- abolic alkalosis, hypokalemia and hypocalciuria. Since he had two missense mutations (R261C and L623P) in the thiazide-sensitive Na-Cl cotransporter (TSC) gene (SLC12A3), he was diagnosed as having GS. He showed hyperreninism and a high angiotensin I (Ang I) level, whereas his angiotensin II (Ang II) and aldo- sterone levels were not elevated. His angiotensin converting enzyme (ACE) activities were normal, and administration of captopril inhibited the production of Ang II and aldosterone. We evaluated the Ang II–form- ing activity (AIIFA) of other enzymes in his lymphocytes. Interestingly, chymase-dependent AIIFA was not detected in the lymphocytes. Together, these results suggest that the lack of chymase activity resulted in the manifestation of GS without hyperaldosteronism. (Hypertens Res 2006; 29: 545–549) Key Words: Gitelman’s syndrome, angiotensin II, aldosterone, chymase several TSC gene mutations have been reported (5–10). Introduction Moreover, GS is characterized by sodium wasting, low blood pressure, and secondary hyperaldosteronism. Here, we report In 1966, Gitelman et al. reported three adult patients with a case of GS with hyperreninism and high angiotensin I (Ang intermittent episodes of muscle weakness and tetany, I) but without elevated angiotensin II (Ang II) or hyperaldos- hypokalemia, and hypomagnesemia, but no history of poly- teronism.
    [Show full text]
  • Primary Hyperaldosteronism: a Case of Unilateral Adrenal Hyperplasia with Contralateral Incidentaloma Sujit Vakkalanka,1 Andrew Zhao,1 Mohammed Samannodi2
    Unexpected outcome (positive or negative) including adverse drug reactions CASE REPORT Primary hyperaldosteronism: a case of unilateral adrenal hyperplasia with contralateral incidentaloma Sujit Vakkalanka,1 Andrew Zhao,1 Mohammed Samannodi2 1University at Buffalo, Buffalo, SUMMARY palpitations or any difficulty breathing in the past. New York, USA Primary hyperaldosteronism is one of the most common She was being managed in an outpatient setting for 2Department of Medicine, Buffalo, New York, USA causes of secondary hypertension but clear hypokalaemia and hypertension since 2009. She differentiation between its various subtypes can be a has been taking three antihypertensives (amlodi- Correspondence to clinical challenge. We report the case of a 37-year-old pine, benazepril and labetalol) and supplemental Dr Mohammed Samannodi, African-American woman with refractory hypertension potassium (2 tablets of 10 mEq three times a day) [email protected] who was admitted to our hospital for palpitations, but was very recently switched to hydralazine, ver- Accepted 28 June 2016 shortness of breath and headache. Her laboratory results apamil and doxazosin mesylate, and two potassium showed hypokalaemia and an elevated aldosterone/renin tablets of 20 mEq three times a day. ratio. An abdominal CT scan showed a nodule in the left On physical examination, her heart rate was adrenal gland but adrenal venous sampling showed 110 bpm while the blood pressure was 170/ elevated aldosterone/renin ratio from the right adrenal 110 mm Hg. Cardiac, abdominal, neurological and vein. The patient began a new medical regimen but musculoskeletal examinations were unimpressive declined any surgical options. We recommend with no signs of clubbing or oedema.
    [Show full text]
  • Monogenic Forms of Mineralocorticoid Hypertension: Insights Into the Pathogenesis of ‘Essential’ Hypertension?
    Journal of Human Hypertension (1998) 12, 7–12 1998 Stockton Press. All rights reserved 0950-9240/98 $12.00 REVIEW ARTICLE Monogenic forms of mineralocorticoid hypertension: insights into the pathogenesis of ‘essential’ hypertension? M Petrelli and PM Stewart Department of Medicine, University of Birmingham, Queen Elizabeth Hospital, Edgbaston, Birmingham B15 2TH, UK Keywords: hyperaldosteronism; mineralocorticoid; Liddle’s syndrome; inheritance; cortisol; 11␤-hydroxysteroid dehydrogen- ase Hypertension is a common condition, which, mary aldosteronism due to an adrenocortical tumour depending on its definition, affects 10–25% of the (Conn’s Syndrome).1 Both subjects had a mineral- population. Because it is an established risk factor ocorticoid excess syndrome, characterised by pot- for coronary and cerebrovascular disease, hyperten- assium deficiency, suppressed plasma renin activity sion has, quite rightly, been targeted as an important (PRA) and increased aldosterone secretion rate, factor in determining the health of the nation. which, in contrast to tumorous aldosteronism, Despite this we can explain the underlying cause of responded to treatment with the synthetic glucocort- a patient’s hypertension in Ͻ5% of cases; the icoid, dexamethasone. Shortly afterwards, an remainder are labelled ‘essential’ hypertension, an additional, well-documented case was described, elegant way of stating that the aetiology is unknown. confirming the existence of this new ‘glucocorticoid As a result, in the vast majority of cases treatment remediable’ aldosteronism syndrome.2 Sub- is given on an empirical basis. sequently it was shown to be inherited in an autoso- In the last 5 years, significant advances have been mal dominant fashion and approximately 100 cases made in our understanding of the pathogenesis of were reported in the world literature up to the early hypertension with the characterisation of three 1990’s.3–9 forms of inherited hypertension.
    [Show full text]
  • Prevalence of Primary Hyperaldosteronism Assessed by Aldosterone/Renin Ratio and Spironolactone Testing
    I ORIGINAL PAPERS Prevalence of primary hyperaldosteronism assessed by aldosterone/renin ratio and spironolactone testing Sue Hood, John Cannon, Roger Foo and Morris Brown ABSTRACT – Recent studies have suggested that Aldosterone-secreting adenomas were long consid- Sue Hood RGN primary hyperaldosteronism may be present in ered a rare cause of hypertension, with bilateral Research Sister more than 10% of patients with hypertension. We micronodular hyperplasia accounting for a similarly *John Cannon MB aimed to estimate the prevalence in unselected small proportion – less than 2% – of all hyperten- FRCGP General patients in primary care, and investigate the sion.1 But recent studies have suggested that primary Practitioner influence of current drug treatment upon the hyperaldosteronism (PHA) may be present in at least Roger Foo MD aldosterone/renin ratio (ARR) and its prediction 10% of patients.2–5 These studies have used biochem- MRCP Specialist of blood pressure response to spironolactone. We ical measures of autonomous aldosterone secretion, Registrar measured blood pressure, plasma electrolytes, usually the ratio of plasma aldosterone to renin and Morris Brown MSc renin activity and aldosterone in 846 patients the failure of aldosterone to suppress during treat- MD FRCP FMedSci, Professor of with hypertension. Spironolactone 50 mg was ment with salt supplementation. However, as often Clinical prescribed for one month to patients with blood occurs when the arbiter for diagnosis changes – here, Pharmacology pressure ≥130/85 mmHg and ARR ≥400. The from anatomical to biochemical – the question arises primary outcome measure was to discover the whether the definition of the condition has also Clinical Pharmacology Unit, proportion of patients with plasma aldosterone changed.
    [Show full text]
  • Pseudo Bartter Syndrome from Surreptitious Purging Behaviour In
    al Dis ion ord rit e t rs u N & f T o h Gentile, J Nutr Disorders Ther 2012, 2:1 l e a r n a r DOI: 10.4172/2161-0509.1000107 p u y o Journal of Nutritional Disorders & Therapy J ISSN: 2161-0509 Case Report Open Access Pseudo Bartter Syndrome from Surreptitious Purging Behaviour in Anorexia Nervosa Maria Gabriella Gentile* Eating Disorder Unit, Niguarda Hospital, Piazza Ospedale Maggiore 3, 20126 Milan, Italy Abstract Pseudo Bartter syndrome is a rare disorder characterized by metabolic alkalosis, hypokalaemia, hyperaldosteronism, hyperreninism, normal blood pressure and hyperplasia of the juxtaglomerular apparatus. The most dangerous complication of Pseudo Bartter syndrome is hypokalemia. Hypokalemia caused by vomiting, diarrhea, prolonged fasting, abuse of potassium-depleting drugs, may be present in patients with binge /purging form of anorexia or bulimia nervosa. We report a case of a 19-year-old girl with anorexia nervosa (BMI 16.15 kg/m2) and severe prolonged hypokalemia (1.9 mEq/l), metabolic alkalosis and severe protracted secondary hyperaldosteronism (i.e. Pseudo Bartter’s syndrome) from surreptitious purging behaviour (vomit and laxative abuse). An intensive multidisciplinary day-hospital treatment including long-term potassium supplementation, a potassium- sparing diuretic was necessary to resolve the case and to allow the young girl to admit her previous purging behaviour and after three months to get at a normal kalemia without any potassium supplementation and BMI at a normal value (20 kg/m2). Given the dangers to the heart electrical and mechanical functions set by severe potassium deficiency, it is mandatory to find out the true cause so that a proper treatment can be started.
    [Show full text]
  • Primary Hyperaldosteronism As One of the Most Common Forms of Secondary Arterial Hypertension- Clinical Case
    Journal of Endocrinology and Thyroid Research ISSN: 2573-2188 Case Report J Endocrinol Thyroid Res Volume 4 Issue 4 - June 2019 Copyright © All rights are reserved by O V Tsygankova DOI: 10.19080/JETR.2019.04.555645 Primary Hyperaldosteronism as one of the most common forms of Secondary Arterial Hypertension- Clinical Case O V Tsygankova1,2*, T I Batluk1, L D Latyntseva1 and E V Akhmerova3 1Research Institute of Internal and Preventive Medicine – Branch of the Institute of Cytology and Genetics, Siberian Branch of Russian Academy of Science, Russia 2Ministry of Health of Russia, Novosibirsk State Medical University, Russia 3Novosibirsk City Clinical Polyclinic N16, City Endocrinology Center, Russia Submission: June 10, 2019; Published: June 21, 2019 *Corresponding author: Oksana V Tsygankova, Department of Emergency Therapy with Endocrinology and Occupational Pathology, Institute of Internal and Preventive Medicine – Branch of the Institute of Cytology and Genetics, Siberian Branch of Russian Academy of Science, Laboratory of clinical, biochemical and hormonal studies of therapeutic diseases, Novosibirsk State Medical University, Ministry of Health of Russia, Novosibirsk, Russia Abstract Primary hyperaldosteronism is a common cause of hypertension. Its prevalence reaches 15% among the forms of arterial hypertension. Prolonged exposure to elevated aldosterone concentrations is associated with target organ damage in the heart, kidney, arterial wall, and high cardiovascular risk in patients with primary hyperaldosteronism. However, the lack of attention to this problem persists among doctors of various specialties, especially general practitioners. Timely diagnosis and treatment of these patients depends on the correct choice of screening and clarifying diagnostic methods. A long ten-year diagnostic way to identify primary hyperaldosteronism in a young person with refractory hypertension is described below.
    [Show full text]
  • Diagnosis and Management of Primary Aldosteronism
    review Diagnosis and management of primary aldosteronism Leticia A. P. Vilela1, Madson Q. Almeida1,2 ABSTRACT Primary aldosteronism (PA) is the most common form of secondary hypertension (HTN), with an 1 Unidade de Suprarrenal, estimated prevalence of 4% of hypertensive patients in primary care and around 10% of referred Endocrinologia do patients. Patients with PA have higher cardiovascular morbidity and mortality than age- and sex- Desenvolvimento, Laboratório de matched patients with essential HTN and the same degree of blood pressure elevation. PA is Hormônios e Genética Molecular – LIM42, Divisão de Endocrinologia characterized by an autonomous aldosterone production causing sodium retention, plasma renin e Metabologia, Hospital das supression, HTN, cardiovascular damage, and increased potassium excretion, leading to variable Clínicas, Faculdade de Medicina degrees of hypokalemia. Aldosterone-producing adenomas (APAs) account for around 40% and da Universidade de São Paulo idiopathic hyperaldosteronism for around 60% of PA cases. The aldosterone-to-renin ratio is the (HCFMUSP), São Paulo, SP, Brasil most sensitive screening test for PA. There are several confirmatory tests and the current literature 2 Instituto do Câncer do Estado does not identify a “gold standard” confirmatory test for PA. In our institution, we recommend de São Paulo (Icesp), FMUSP, São Paulo, SP, Brasil starting case confirmation with the furosemide test. After case confirmation, all patients with PA should undergo adrenal CT as the initial study in subtype testing to exclude adrenocortical Correspondence to: carcinoma. Bilateral adrenal vein sampling (AVS) is the gold standard method to define the PA Madson Q. Almeida Unidade de Suprarrenal, subtype, but it is not indicated in all cases.
    [Show full text]
  • Aldactone® Spironolactone Tablets, USP
    NDA 12-151/S-062 Page 2 Aldactone® spironolactone tablets, USP WARNING Aldactone has been shown to be a tumorigen in chronic toxicity studies in rats (see Precautions). Aldactone should be used only in those conditions described under Indications and Usage. Unnecessary use of this drug should be avoided. DESCRIPTION Aldactone oral tablets contain 25 mg, 50 mg, or 100 mg of the aldosterone antagonist spironolactone, 17-hydroxy-7α-mercapto-3-oxo-17α-pregn-4-ene-21-carboxylic acid γ-lactone acetate, which has the following structural formula: Spironolactone is practically insoluble in water, soluble in alcohol, and freely soluble in benzene and in chloroform. Inactive ingredients include calcium sulfate, corn starch, flavor, hypromellose, iron oxide, magnesium stearate, polyethylene glycol, povidone, and titanium dioxide. ACTIONS / CLINICAL PHARMACOLOGY Mechanism of action: Aldactone (spironolactone) is a specific pharmacologic antagonist of aldosterone, acting primarily through competitive binding of receptors at the aldosterone-dependent sodium-potassium exchange site in the distal convoluted renal tubule. Aldactone causes increased amounts of sodium and water to be excreted, while potassium is retained. Aldactone acts both as a diuretic and as an antihypertensive drug by this mechanism. It may be given alone or with other diuretic agents which act more proximally in the renal tubule. Aldosterone antagonist activity: Increased levels of the mineralocorticoid, aldosterone, are present in primary and secondary hyperaldosteronism. Edematous states in which secondary aldosteronism is usually involved include congestive heart failure, hepatic cirrhosis, and the nephrotic syndrome. By competing with aldosterone for receptor sites, Aldactone provides effective therapy for the edema and ascites in those conditions.
    [Show full text]
  • Case Report Posaconazole-Induced Hypertension Masquerading As Congenital Adrenal Hyperplasia in a Child with Cystic Fibrosis
    Hindawi Case Reports in Medicine Volume 2020, Article ID 8153012, 5 pages https://doi.org/10.1155/2020/8153012 Case Report Posaconazole-Induced Hypertension Masquerading as Congenital Adrenal Hyperplasia in a Child with Cystic Fibrosis Neha Agarwal ,1 Louise Apperley,1 Norman F. Taylor,2 David R. Taylor,2 Lea Ghataore,2 Ellen Rumsby,3 Catherine Treslove,3 Richard Holt,4 Rebecca Thursfield,5 and Senthil Senniappan 1 1Department of Paediatric Endocrinology, Alder Hey Children’s NHS Foundation Trust, Liverpool, UK 2Department of Clinical Biochemistry (Viapath), King’s College Hospital NHS Foundation Trust, London, UK 3Department of Biochemistry, Alder Hey Children’s NHS Foundation Trust, Liverpool, UK 4Department of Paediatric Nephrology, Alder Hey Children’s NHS Foundation Trust, Liverpool, UK 5Department of Paediatric Respiratory Medicine, Alder Hey Children’s NHS Foundation Trust, Liverpool, UK Correspondence should be addressed to Senthil Senniappan; [email protected] Received 25 June 2020; Accepted 17 August 2020; Published 28 August 2020 Academic Editor: Mark E. Shaffrey Copyright © 2020 Neha Agarwal et al. )is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background. Deficiency of 11β-hydroxylase is the second most common cause of congenital adrenal hyperplasia (CAH), pre- senting with hypertension, hypokalaemia, precocious puberty, and adrenal insufficiency. We report the case of a 6-year-old boy with cystic fibrosis (CF) found to have hypertension and cortisol insufficiency, which were initially suspected to be due to CAH, but were subsequently identified as being secondary to posaconazole therapy.
    [Show full text]