Hyperaldosteronism: A condition caused by the overproduction of ALDOSTERONE. It is characterized by sodium retention and potassium excretion with resultant HYPERTENSION and HYPOKALEMIA.Aldosterone: A hormone secreted by the ADRENAL CORTEX that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium.Hypokalemia: Abnormally low potassium concentration in the blood. It may result from potassium loss by renal secretion or by the gastrointestinal route, as by vomiting or diarrhea. It may be manifested clinically by neuromuscular disorders ranging from weakness to paralysis, by electrocardiographic abnormalities (depression of the T wave and elevation of the U wave), by renal disease, and by gastrointestinal disorders. (Dorland, 27th ed)Aldosterone Synthase: A mitochondrial cytochrome P450 enzyme that catalyzes the 18-hydroxylation of steroids in the presence of molecular oxygen and NADPH-specific flavoprotein. This enzyme, encoded by CYP11B2 gene, is important in the conversion of CORTICOSTERONE to 18-hydroxycorticosterone and the subsequent conversion to ALDOSTERONE.Spironolactone: A potassium sparing diuretic that acts by antagonism of aldosterone in the distal renal tubules. It is used mainly in the treatment of refractory edema in patients with congestive heart failure, nephrotic syndrome, or hepatic cirrhosis. Its effects on the endocrine system are utilized in the treatments of hirsutism and acne but they can lead to adverse effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p827)Adrenal Gland Neoplasms: Tumors or cancer of the ADRENAL GLANDS.Adrenocortical Adenoma: A benign neoplasm of the ADRENAL CORTEX. It is characterized by a well-defined nodular lesion, usually less than 2.5 cm. Most adrenocortical adenomas are nonfunctional. The functional ones are yellow and contain LIPIDS. Depending on the cell type or cortical zone involved, they may produce ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and/or ANDROSTENEDIONE.Steroid 11-beta-Hydroxylase: A mitochondrial cytochrome P450 enzyme that catalyzes the 11-beta-hydroxylation of steroids in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP11B1 gene, is important in the synthesis of CORTICOSTERONE and HYDROCORTISONE. Defects in CYP11B1 cause congenital adrenal hyperplasia (ADRENAL HYPERPLASIA, CONGENITAL).Adrenalectomy: Excision of one or both adrenal glands. (From Dorland, 28th ed)Mineralocorticoid Receptor Antagonists: Drugs that bind to and block the activation of MINERALOCORTICOID RECEPTORS by MINERALOCORTICOIDS such as ALDOSTERONE.Gitelman Syndrome: An inherited renal disorder characterized by defective NaCl reabsorption in the convoluted DISTAL KIDNEY TUBULE leading to HYPOKALEMIA. In contrast with BARTTER SYNDROME, Gitelman syndrome includes hypomagnesemia and normocalcemic hypocalciuria, and is caused by mutations in the thiazide-sensitive SODIUM-POTASSIUM-CHLORIDE SYMPORTERS.Adrenal Glands: A pair of glands located at the cranial pole of each of the two KIDNEYS. Each adrenal gland is composed of two distinct endocrine tissues with separate embryonic origins, the ADRENAL CORTEX producing STEROIDS and the ADRENAL MEDULLA producing NEUROTRANSMITTERS.Renin: A highly specific (Leu-Leu) endopeptidase that generates ANGIOTENSIN I from its precursor ANGIOTENSINOGEN, leading to a cascade of reactions which elevate BLOOD PRESSURE and increase sodium retention by the kidney in the RENIN-ANGIOTENSIN SYSTEM. The enzyme was formerly listed as EC 3.4.99.19.Adrenal Cortex Neoplasms: Tumors or cancers of the ADRENAL CORTEX.Polydipsia: Excessive thirst manifested by excessive fluid intake. It is characteristic of many diseases such as DIABETES MELLITUS; DIABETES INSIPIDUS; and NEPHROGENIC DIABETES INSIPIDUS. The condition may be psychogenic in origin.18-Hydroxycorticosterone: 11 beta,18,21-Trihydroxypregn-4-ene-3,20-dione.Canrenone: A synthetic pregnadiene compound with anti-aldosterone activity.Adenoma: A benign epithelial tumor with a glandular organization.Hypertension: Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.Mineralocorticoids: A group of CORTICOSTEROIDS primarily associated with water and electrolyte balance. This is accomplished through the effect on ION TRANSPORT in renal tubules, resulting in retention of sodium and loss of potassium. Mineralocorticoid secretion is itself regulated by PLASMA VOLUME, serum potassium, and ANGIOTENSIN II.18-Hydroxydesoxycorticosterone: An analog of desoxycorticosterone which is substituted by a hydroxyl group at the C-18 position.Adrenocortical Hyperfunction: Excess production of ADRENAL CORTEX HORMONES such as ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and/or ANDROSTENEDIONE. Hyperadrenal syndromes include CUSHING SYNDROME; HYPERALDOSTERONISM; and VIRILISM.Adrenal Hyperplasia, Congenital: A group of inherited disorders of the ADRENAL GLANDS, caused by enzyme defects in the synthesis of cortisol (HYDROCORTISONE) and/or ALDOSTERONE leading to accumulation of precursors for ANDROGENS. Depending on the hormone imbalance, congenital adrenal hyperplasia can be classified as salt-wasting, hypertensive, virilizing, or feminizing. Defects in STEROID 21-HYDROXYLASE; STEROID 11-BETA-HYDROXYLASE; STEROID 17-ALPHA-HYDROXYLASE; 3-beta-hydroxysteroid dehydrogenase (3-HYDROXYSTEROID DEHYDROGENASES); TESTOSTERONE 5-ALPHA-REDUCTASE; or steroidogenic acute regulatory protein; among others, underlie these disorders.Adrenal Gland Diseases: Pathological processes of the ADRENAL GLANDS.G Protein-Coupled Inwardly-Rectifying Potassium Channels: A family of inwardly-rectifying potassium channels that are activated by PERTUSSIS TOXIN sensitive G-PROTEIN-COUPLED RECEPTORS. GIRK potassium channels are primarily activated by the complex of GTP-BINDING PROTEIN BETA SUBUNITS and GTP-BINDING PROTEIN GAMMA SUBUNITS.Adrenocorticotropic Hormone: An anterior pituitary hormone that stimulates the ADRENAL CORTEX and its production of CORTICOSTEROIDS. ACTH is a 39-amino acid polypeptide of which the N-terminal 24-amino acid segment is identical in all species and contains the adrenocorticotrophic activity. Upon further tissue-specific processing, ACTH can yield ALPHA-MSH and corticotrophin-like intermediate lobe peptide (CLIP).Myelolipoma: A rare benign tumor of the adrenal gland, several centimeters in diameter, composed in varying proportions of adipose tissue, lymphocytes, and primitive myeloid cells, probably a developmental abnormality. (Dorland, 27th ed)Potassium: An element in the alkali group of metals with an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the WATER-ELECTROLYTE BALANCE.Hyperplasia: An increase in the number of cells in a tissue or organ without tumor formation. It differs from HYPERTROPHY, which is an increase in bulk without an increase in the number of cells.Hydrocortisone: The main glucocorticoid secreted by the ADRENAL CORTEX. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.Receptors, Mineralocorticoid: Cytoplasmic proteins that specifically bind MINERALOCORTICOIDS and mediate their cellular effects. The receptor with its bound ligand acts in the nucleus to induce transcription of specific segments of DNA.Sodium: A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.Veins: The vessels carrying blood away from the capillary beds.Diuretics: Agents that promote the excretion of urine through their effects on kidney function.Antihypertensive Agents: Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS.Dexamethasone: An anti-inflammatory 9-fluoro-glucocorticoid.Tomography, X-Ray Computed: Tomography using x-ray transmission and a computer algorithm to reconstruct the image.Glucocorticoids: A group of CORTICOSTEROIDS that affect carbohydrate metabolism (GLUCONEOGENESIS, liver glycogen deposition, elevation of BLOOD SUGAR), inhibit ADRENOCORTICOTROPIC HORMONE secretion, and possess pronounced anti-inflammatory activity. They also play a role in fat and protein metabolism, maintenance of arterial blood pressure, alteration of the connective tissue response to injury, reduction in the number of circulating lymphocytes, and functioning of the central nervous system.

*  Spiractin Incorrect Dose Administered Side Effects
Female, 54 years of age, was diagnosed with primary hyperaldosteronism, hypertension and took Spiractin 25 Mg; Daily; Oral, ... A 54-year-old female patient (weight:NA) experienced the following symptoms/conditions: primary hyperaldosteronism. The patient ...
  http://patientsville.com/spiractin/incorrect-dose-administered.htm
*  Left Ventricular Hypertrophy Precedes Other Target-Organ Damage in Primary Aldosteronism | Hypertension
hyperaldosteronism. *hypertension, essential. *hypertrophy, left ventricular. *hemodynamics. The mineralocorticoid hormone ...
  http://hyper.ahajournals.org/content/29/3/723
*  Secondary Hypertension Guide: Causes, Symptoms and Treatment Options
Hyperaldosteronism often causes weakness related to low blood potassium levels.. Diagnosis. You doctor will ask you if you have ... Hyperaldosteronism (also called Conn's syndrome). Both adrenal glands can overproduce the salt-retaining hormone aldosterone or ... For hyperaldosteronism, a blood test for potassium and aldosterone levels are measured. ...
  https://www.drugs.com/health-guide/secondary-hypertension.html
*  Most recent papers with the keyword Aldosterone producing adenoma | Read by QxMD
PA is mainly caused by unilateral hyperaldosteronism due to an aldosterone-producing adenoma, unilateral hyperplasia with or ... RECENT FINDINGS: Different inherited genetic abnormalities distinguish specific forms of familial hyperaldosteronism... ... a condition featuring hyperaldosteronism, and in APA-adjacent tissue. The effect of C21, an AT2R agonist, on CYP11B1 (cortisol ... and 4 forms of familial hyperaldosteronism (FH-I to FH-IV) have been identified... ...
  https://www.readbyqxmd.com/keyword/37039
*  2017/18 ICD-10-CM Codes E26*: Hyperaldosteronism
E26 Hyperaldosteronism* E26.0 Primary hyperaldosteronism* E26.01 Conn's syndrome. * E26.02 Glucocorticoid-remediable ... Hyperaldosteronism E26- >. Clinical Information *A condition caused by the overproduction of aldosterone. It is characterized ...
  http://www.icd10data.com/ICD10CM/Codes/E00-E89/E20-E35/E26-
*  Hyperaldosteronism: Background, Pathophysiology, Etiology
encoded search term (Hyperaldosteronism) and Hyperaldosteronism What to Read Next on Medscape. Related Conditions and Diseases ... Secondary hyperaldosteronism. Secondary hyperaldosteronism is a collective term for a diverse group of disorders characterized ... Hyperaldosteronism. Updated: Apr 20, 2017 * Author: George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London); Chief Editor: Robert ... Causes of secondary hyperaldosteronism include the following:. * Edema disorders (eg, cardiac failure and nephrotic syndrome ...
  https://emedicine.medscape.com/article/920713-overview
*  Hyperaldosteronism - primary and secondary | University of Maryland Medical Center
Hyperaldosteronism - primary and secondary. Toggle: English / Spanish Definition. Hyperaldosteronism is a disorder in which the ... Primary hyperaldosteronism caused by an adrenal gland tumor is usually treated with surgery. It can sometimes be treated with ... Primary hyperaldosteronism is due to a problem of the adrenal glands themselves, which causes them to release too much ... Primary hyperaldosteronism can cause very high blood pressure, which can damage many organs, including the eyes, kidneys, heart ...
  https://www.umm.edu/Health/Medical/Ency/Articles/Hyperaldosteronism-primary-and-secondary
*  Impaired Endothelium-Dependent Flow-Mediated Vasodilation in Hypertensive Subjects With Hyperaldosteronism | Circulation
Hyperaldosteronism was diagnosed on the basis of a renin activity ,1.0 ng · mL−1 · h−1, urinary aldosterone ,12 μg/24 h, and ... Biochemical hyperaldosteronism was determined if the PRA was suppressed (,1.0 ng · mL−1 · h−1) and the 24-hour urinary ... Hyperaldosteronism among black and white subjects with resistant hypertension. Hypertension. 2002; 40: 892-896. ... Impaired Endothelium-Dependent Flow-Mediated Vasodilation in Hypertensive Subjects With Hyperaldosteronism. Mari K. Nishizaka, ...
  http://circ.ahajournals.org/content/109/23/2857
*  Hyperaldosteronism-induced hypertension Symptoms, Diagnosis, Treatments and Causes - RightDiagnosis.com
Hyperaldosteronism-induced hypertension information including symptoms, diagnosis, misdiagnosis, treatment, causes, patient ... Contents for Hyperaldosteronism-induced hypertension: *Hyperaldosteronism-induced hypertension *What is Hyperaldosteronism- ... Hyperaldosteronism-induced hypertension: Introduction. Hyperaldosteronism-induced hypertension: Hyperaldosteronism -induced ... Prognosis for Hyperaldosteronism-induced hypertension. Prognosis for Hyperaldosteronism-induced hypertension: The prognosis ...
  http://www.rightdiagnosis.com/h/hyperaldosteronism_induced_hypertension/intro.htm
*  Hyperaldosteronism - Wikipedia
... spironolactone Secondary hyperaldosteronism (also hyperreninism, or hyperreninemic hyperaldosteronism) is due to overactivity ... Hyperaldosteronism can also be caused by plant poisoning, where the patient has been exposed to too much licorice. Licorice is ... Hyperaldosteronism, also aldosteronism, is a medical condition wherein too much aldosterone is produced by the adrenal glands, ... Primary aldosteronism (hyporeninemic hyperaldosteronism) was previously thought to be most commonly caused by an adrenal ...
  https://en.wikipedia.org/wiki/Hyperaldosteronism
*  Feline hyperaldosteronism - Wikipedia
The other type, known as idiopathic hyperaldosteronism, occurs with bilateral adrenal hyperplasia. Secondary hyperaldosteronism ... secondary hyperaldosteronism). Primary hyperaldosteronism (PHA) is a disorder of the adrenal cortex that causes increased ... Feline hyperaldosteronism is a disease in cats. The symptoms are caused by abnormally high concentrations of the hormone ... Unilateral primary hyperaldosteronism due to an adrenocortical adenoma or adrenocarcinoma can be potentially cured surgically. ...
  https://en.wikipedia.org/wiki/Feline_hyperaldosteronism
*  Familial hyperaldosteronism - Wikipedia
There are other forms of hyperaldosteronism that are not inherited. Familial hyperaldosteronism is categorized into three types ... The various types of familial hyperaldosteronism have different genetic causes. Familial hyperaldosteronism type I is caused by ... The genetic cause of familial hyperaldosteronism type II is unknown. "Familial hyperaldosteronism". Genetics home reference. ... which leads to the signs and symptoms of familial hyperaldosteronism type I. Familial hyperaldosteronism type III is caused by ...
  https://en.wikipedia.org/wiki/Familial_hyperaldosteronism
*  11 beta-hydroxylase activity in glucocorticoid suppressible hyperaldosteronism: Lessons for essential hypertension? -...
11 beta-hydroxylase activity in glucocorticoid suppressible hyperaldosteronism: Lessons for essential hypertension? ... 11 beta-hydroxylase activity in glucocorticoid suppressible hyperaldosteronism: Lessons for essential hypertension? Endocrine ...
  http://eprints.gla.ac.uk/16189/
*  Most recent papers with the keyword "Familial hyperaldosteronism" | Read by QxMD
Familial Hyperaldosteronism type 1 (FH1) or dexamethasone suppressible hyperaldosteronism, FH2, the most common form of as yet ... Familial hyperaldosteronism type III.. S Monticone, M Tetti, J Burrello, F Buffolo, R De Giovanni, F Veglio, T A Williams, P ... ARMC5 is not implicated in familial hyperaldosteronism type II (FH-II).. S M C De Sousa, M Stowasser, J Feng, A W Schreiber, P ... Familial hyperaldosteronism types I, II and III are the known genetic syndromes, in which both adrenal glands produce excessive ...
  https://www.readbyqxmd.com/keyword/80280
*  Hyperaldosteronism Habitations
For this reason, a hyperaldosteronism diagnosed in connection with essential hypertension is usually only diagnosed once an ... Neuroblastoma represents the most important hormone production in your diet can also lead to secondary hyperaldosteronism, ...
  http://hyperaldosteronismhabitations.blogspot.com
*  wwecatch • View topic - Immunosuppressive hyperaldosteronism, type-specific young, b
Immunosuppressive hyperaldosteronism, type-specific young, b. wwecatch Faq-Have any questions?The answers are here. Post a ... Immunosuppressive hyperaldosteronism, type-specific young, b. by paweiresuci on Fri Apr 21, 2017 10:23 am ...
  http://wwecatch.phpbb.net/viewtopic.php?f=7&t=9071&hilit=&sid=8f11bafaa2d2534e200b542619f92e29&p=9139
*  CLCN2 mutation analysis - Molecular diagnostic of familial hyperaldosteronism type II
Hyperaldosteronism is supposed to be the most common reason for secondary hypertension accounting for 5 to 12 percent of ... Keywords: Molekulare Diagnostik, Bluthochdruck, Hyperaldosteronismus, Molecular diagnostic, hypertension, hyperaldosteronism. ... In addition, this technology may give rise to novel therapy options for hyperaldosteronism targeting the mutated chloride ... 2018) CLCN2 chloride channel mutations in familial hyperaldo-steronism type II. Nature Genetics doi: 10.1038/s41588-018-0048-5. ...
  https://provendis.info/technologien/alle/technologie/clcn2-mutation-analysis-molecular-diagnostic-of-familial-hyperaldosteronism-type-ii/
*  Chapter 13. Hyperaldosteronism | McGraw-Hill Manual: Endocrine Surgery | AccessSurgery | McGraw-Hill Medical
In 1% of cases, familial hyperaldosteronism type I (FH1), also known as glucocorticoid-remediable hyperaldosteronism (GRA) and ... Hyperaldosteronism." McGraw-Hill Manual: Endocrine Surgery Morita SY, Dackiw AB, Zeiger MA. Morita S.Y., Dackiw A.B., Zeiger M. ... Hyperaldosteronism. In: Morita SY, Dackiw AB, Zeiger MA. Morita S.Y., Dackiw A.B., Zeiger M.A. Eds. Shane Y. Morita, et al.eds. ... Most cases of hyperaldosteronism affect younger adults between the ages of 30 and 50 years, with a female preponderance three ...
  http://accesssurgery.mhmedical.com/content.aspx?bookid=440§ionid=40161247
*  Causes of Low Potassium & Low Calcium | LIVESTRONG.COM
Primary hyperaldosteronism is caused by problems with your adrenal glands, whereas secondary hyperaldosteronism is caused by ... Hyperaldosteronism. Hyperaldosteronism can cause decreased potassium and calcium levels. The National Adrenal Diseases ... Common signs and symptoms associated with hyperaldosteronism include low potassium and calcium levels, fatigue, headache, ... There are two principal types of hyperaldosteronism: primary and secondary. ...
  https://www.livestrong.com/article/285434-causes-of-low-potassium-low-calcium/
*  Evaluation and Management of the Patient with Difficult-to-Control or Resistant Hypertension - American Family Physician
... or hyperaldosteronism, all of which can lead to fluid retention. Higher doses of diuretics (or a change to a loop diuretic) are ... PRIMARY HYPERALDOSTERONISM. Primary hyperaldosteronism may be one of the most common contributors to resistant hypertension. ... Management of hyperaldosteronism and hypercortisolismIzzo JL Jr, Sica DA, Black HR. Hypertension Primer: The Essentials of High ... Approximately 20 percent of patients referred to hypertension subspecialty clinics have hyperaldosteronism.37-39 Many of these ...
  https://www.aafp.org/afp/2009/0515/p863.html
*  Table of Contents - September 01, 2016, 68 (3) | Hypertension
Primary Hyperaldosteronism. *. You have accessRestricted access. Small-Conductance Ca2+-Activated Potassium Channels Negatively ...
  http://hyper.ahajournals.org/content/68/3
*  Aldosterone - Wikipedia
HyperaldosteronismEdit. Primary aldosteronism, also known as primary hyperaldosteronism, is characterized by the overproduction ... Secondary hyperaldosteronism, on the other hand, is due to overactivity of the renin-angiotensin system. ... Hyperaldosteronism is abnormally increased levels of aldosterone, while hypoaldosteronism is abnormally decreased levels of ... Depending on cause and other factors, hyperaldosteronism can be treated by surgery and/or medically, such as by aldosterone ...
  https://en.m.wikipedia.org/wiki/Aldosterone

Aldosterone-to-renin ratio: Aldosterone-to-renin ratio (ARR) is the mass concentration of aldosterone divided by the plasma renin activity in blood plasma. The aldosterone/renin ratio is recommended as screening tool for primary hyperaldosteronism.Aldosterone escape: In physiology, aldosterone escape is a term that has been used to refer to two distinct phenomena involving aldosterone that are exactly opposite each other:HypokalemiaSpironolactoneAdrenal tumorAdrenocortical adenoma: A adrenocortical adenoma (or adrenal cortical adenoma) is a benign tumor of the adrenal cortex.Gitelman syndromeAbsent adrenal glandRenin: Renin, Iran}}Polydipsia in birds: Polydipsia is an excessively large water intake. Its occurrence in captive birds has been recorded, although it is a relatively rare abnormal behaviour.Thyroid adenomaHypertensionInborn errors of steroid metabolism: An inborn error of steroid metabolism is an inborn error of metabolism due to defects in steroid metabolism.Adrenocortical hyperfunctionCongenital adrenal hyperplasia due to 21-hydroxylase deficiencyG protein-gated ion channelMyelolipomaTrans-tubular potassium gradient: The trans-tubular potassium gradient (TTKG) is an index reflecting the conservation of potassium in the cortical collecting ducts (CCD) of the kidneys. It is useful in diagnosing the causes of hyperkalemia or hypokalemia.Hyperplasia: Hyperplasia (from ancient Greek ὑπέρ huper, "over" + πλάσις plasis, "formation"), or hypergenesis, is an increase in the amount of organic tissue that results from cell proliferation. It may lead to the gross enlargement of an organ and the term is sometimes confused with benign neoplasia or benign tumor.Alcohol and cortisol: Recent research has looked into the effects of alcohol on the amount of cortisol that is produced in the human body. Continuous consumption of alcohol over an extended period of time has been shown to raise cortisol levels in the body.Aortic pressure: Central aortic blood pressure (CAP or CASP) is the blood pressure at the root of aorta. Studies have shown the importance of central aortic pressure and its implications in assessing the efficacy of antihypertensive treatment with respect to cardiovascular risk factors.RU28362Fractional sodium excretion: The fractional excretion of sodium (FENa) is the percentage of the sodium filtered by the kidney which is excreted in the urine. It is measured in terms of plasma and urine sodium, rather than by the interpretation of urinary sodium concentration alone, as urinary sodium concentrations can vary with water reabsorption.Superficial vein: Superficial vein is a vein that is close to the surface of the body. This differs from deep veins that are far from the surface.Loop diureticLidanserin: Lidanserin (INN; ZK-33,839) is a drug which acts as a combined 5-HT2A and α1-adrenergic receptor antagonist. It was developed as an antihypertensive agent but was never marketed.Dense artery sign: In medicine, the dense artery sign or hyperdense artery sign is a radiologic sign seen on computer tomography (CT) scans suggestive of early ischemic stroke. In earlier studies of medical imaging in patients with strokes, it was the earliest sign of ischemic stroke in a significant minority of cases.

(1/516) Primary aldosteronism with aldosterone-producing adrenal adenoma in a pregnant woman.

A 30-year-old pregnant woman complained of muscle weakness at 29 weeks' gestation. She was hypertensive with severe hypokalemia. Lower plasma renin activity and higher aldosterone level than the normal values in pregnancy suggested primary aldosteronism. A cesarean delivery was performed at 31 weeks' gestation because of pulmonary congestion. The neonatal course was uncomplicated. The laparoscopic adrenalectomy for a 2.0-cm right adrenal adenoma resulted in normalizing of her blood pressure and serum potassium level. Although primary aldosteronism is rare, especially during pregnancy, it should be always considered as one of etiologies of hypertension in pregnancy.  (+info)

(2/516) A case of aldosterone-producing adenoma with severe postoperative hyperkalemia.

It is known that some patients with primary aldosteronism show postoperative hyperkalemia, which is due to inability of the adrenal gland to secrete sufficient amounts of aldosterone. However, hyperkalemia is generally neither severe nor prolonged, in which replacement therapy with mineralocorticoid is seldom necessary. We report a case of a 46-year-old woman with an aldosterone-producing adenoma associated with severe postoperative hyperkalemia. After unilateral adrenalectomy, the patient showed episodes of severe hyperkalemia for four months, which required not only cation-exchange resin, but also mineralocorticoid replacement. Plasma aldosterone concentration (PAC) was low, although PAC was increased after rapid ACTH test. Histological examination indicated the presence of adrenocortical tumor and paradoxical hyperplasia of zona glomerulosa in the adjacent adrenal. Immunohistochemistry demonstrated that the enzymes involved in aldosterone synthesis, such as cholesterol side chain cleavage (P-450scc), 3beta-hydroxysteroid dehydrogenase (3beta-HSD), and 21-hydroxylase (P-450c21), or the enzyme involved in glucocorticoid synthesis, 11beta-hydroxylase (P-450c11beta), were expressed in the tumor, but they were completely absent in zona glomerulosa of the adjacent adrenal. These findings were consistent with the patterns of primary aldosteronism. Serum potassium level was gradually decreased with concomitant increase in PAC. These results suggest that severe postoperative hyperkalemia of the present case was attributable to severe suppression of aldosterone synthesis in the adjacent and contralateral adrenal, which resulted in slow recovery of aldosterone secretion. It is plausible that aldosterone synthesis of adjacent and contralateral adrenal glands is severely impaired in some cases with primary aldosteronism, as glucocorticoid synthesis in Cushing syndrome.  (+info)

(3/516) Gene targeting approaches to analyzing hypertension.

Essential hypertension probably results from combinations of small genetic variations that are partly normal variations and may not be appreciably harmful individually. Strategies to identify genes contributing to hypertension are discussed in this review. Gene targeting approaches, especially gene titration, have been used in these studies of hypertension. Gene titration experiments vary the expression of a chosen gene product by generating animals having different numbers of copies of the gene coding for the product. Gene titration is powerful for analyzing quantitative variations seen in common polygenic disorders, such as kidney diseases, diabetes mellitus, and atherosclerosis, as well as hypertension, because it allows tests of causation by determining the effects on a phenotype by changes in expression of the altered gene and because it matches normal quantitative variations more closely than is possible with classic transgenic mice. The use of zero-copy (gene "knockout") animals generated by gene disruption for studies of qualitative gene effects is also discussed. These various gene targeting experiments help identify genes regulating BP, promote a better understanding of the pathophysiology of the condition, and help identify potential targets for therapies.  (+info)

(4/516) Maximizing efficacy of endocrine tests: importance of decision-focused testing strategies and appropriate patient preparation.

The efficacy of endocrine tests depends on the choice of tests, the preparation of the patients, the integrity of the specimens, the quality of the measurements, and the validity of the reference data. Close dialogue among the clinicians, the laboratory, and the patients is a key factor for optimal patient care. The characteristics of urine and plasma samples and the advantages and limitations of paired test measurements are presented. The importance of test sequence strategies, provocative or inhibitory procedures, and elimination of drug interferences is illustrated with four cases involving Cushing syndrome, pheochromocytoma, primary aldosteronism, and hypercalcemia. For each of these scenarios, key clinical issues are highlighted, along with discussions of the best test strategies, including which medications are likely to interfere. The importance of targeting laboratory tests to answer well-focused clinical decisions is emphasized. The roles of some time-honored provocative procedures are questioned in light of more sensitive and specific analytic methods. The importance of decision-focused analytical tolerance limits is emphasized by demonstrating the impact of analytic bias on downstream medical resource utilization. User-friendly support systems to facilitate the implementation of test strategies and postanalytic tracking of patient outcomes are presented as essential requirements for quality medical practice.  (+info)

(5/516) A probable relationship between an endogenous digitalis-like substance and concentric cardiac hypertrophy in primary aldosteronism.

A 44-year-old woman was admitted to our hospital due to severe hypertension. An electrocardiogram (ECG) and an echocardiogram showed severe left ventricular hypertrophy. Her plasma aldosterone level was elevated. Magnetic resonance imaging revealed a small mass in the right adrenal gland. Before removal of the tumor, plasma endogenous digitalis-like substance (EDLS) levels were elevated. After removal of the tumor, EDLS levels quickly returned to the normal level. A series of echocardiograms and ECGs over a 6- year period after removal of the tumor showed marked regression of cardiac hypertrophy. These findings suggest that EDLS may be closely related to the development of concentric cardiac hypertrophy in primary aldosteronism.  (+info)

(6/516) Aldosterone-producing adenoma without hypertension: a report of two cases.

Normotensive primary hyperaldosteronism is exceedingly rare. We report two new cases of this syndrome in two middle-aged women, one of Asian origin. The presenting signs were tetany in one case and an adrenal mass in the other. Neither patient had hypertension, despite repeated measurements with a manual armlet. A typical biological profile of primary hyperaldosteronism was demonstrated in both patients, including hypokalemia with inappropriate kaliuresis, elevated resting plasma aldosterone, and undetectable plasma renin activity. The circadian rhythm of blood pressure was studied by ambulatory monitoring pre- and post-operatively. It confirmed the lack of hypertension, but the circadian rhythm of blood pressure was lost before surgery in one patient. Surgical removal of the histologically typical aldosterone-producing adenomas normalized the kalemia. The main finding in these two patients was spontaneously low blood pressure in the post-operative period. This suggests that excess aldosterone induced relative hypertension in these patients whose blood pressure was spontaneously very low. Genetic screening for dexamethasone-sensitive hyperaldosteronism was negative in both patients.  (+info)

(7/516) Accuracy of CT scanning and adrenal vein sampling in the pre-operative localization of aldosterone-secreting adrenal adenomas.

In primary hyperaldosteronism, it is important to distinguish between unilateral and bilateral disease, as management strategies differ. In the period 1983-95, we identified 34 patients with primary hyperaldosteronism. Following further investigations, a diagnosis of aldosterone-secreting adenoma was made in 17 patients, and surgery was performed. Computed tomography clearly localized an apparent adenoma (discrete adenoma=1 cm diameter; normal contralateral gland) in only 10 of these patients (59%); two of these 'adenomas' were subsequently shown to be hyperplastic glands without adenomas. Histological examination showed adrenal adenomas in the remaining 15 patients. An 'adenoma' also appeared to be clearly localized in 3/17 patients later classified as having bilateral adrenal hyperplasia by adrenal vein sampling. CT scanning, therefore clearly localizes adenomas in only 50% of histologically proven cases, and can also produce misleading results. Adrenal vein sampling results altered our management approach in one third of cases. On the basis of our detailed results we would recommend surgery if there is clear evidence of unilateral aldosterone secretion along with CT findings which may not be strictly localizing but are in keeping with the dominant side on adrenal vein sampling. The decision to refer for surgery in primary hyperaldosteronism can be difficult, and we would caution against too heavy a reliance on CT results when recommending adrenalectomy, and suggest that adrenal vein sampling should remain a routine part of the investigation of patients with primary hyperaldosteronism.  (+info)

(8/516) Hyperaldosteronemia in rabbits inhibits the cardiac sarcolemmal Na(+)-K(+) pump.

Aldosterone upregulates the Na(+)-K(+) pump in kidney and colon, classical target organs for the hormone. An effect on pump function in the heart is not firmly established. Because the myocardium contains mineralocorticoid receptors, we examined whether aldosterone has an effect on Na(+)-K(+) pump function in cardiac myocytes. Myocytes were isolated from rabbits given aldosterone via osmotic minipumps and from controls. Electrogenic Na(+)-K(+) pump current, arising from the 3:2 Na(+):K(+) exchange ratio, was measured in single myocytes using the whole-cell patch clamp technique. Treatment with aldosterone induced a decrease in pump current measured when myocytes were dialyzed with patch pipette solution containing Na(+) in a concentration of 10 mmol/L, whereas there was no effect measured when the solution contained 80 mmol/L Na(+). Aldosterone had no effect on myocardial Na(+)-K(+) pump concentration evaluated by vanadate-facilitated [(3)H]ouabain binding or by K(+)-dependent paranitrophenylphosphatase activity in crude homogenates. Aldosterone induced an increase in intracellular Na(+) activity. The aldosterone-induced decrease in pump current and increased intracellular Na(+) were prevented by cotreatment with the mineralocorticoid receptor antagonist spironolactone. Our results indicate that hyperaldosteronemia decreases the apparent Na(+) affinity of the Na(+)-K(+) pump, whereas it has no effect on maximal pump capacity.  (+info)



  • mineralocorticoids
  • The increased blood pressure will lead to increased glomerular filtration rate and cause a decrease in renin release from the granular cells of the juxtaglomerular apparatus in the kidney decreasing sodium reabsorption and returning sodium renal excretion to near normal levels allowing sodium to 'escape' the effect of mineralocorticoids (also known as Aldosterone escape mechanism in primary hyperaldosteronism also contributed to by increased ANP level). (wikipedia.org)
  • excretion
  • Instead, experiments isolating the perfusion pressures seen by glomerular capillaries from heightened systemic pressures due to hyperaldosteronism have shown that Na+ excretion remains minimal until the kidney is exposed to heightened perfusion pressures. (wikipedia.org)
  • When hydrostatic pressures are raised in the peritubular capillaries such as seen in hyperaldosteronism, Starling forces begin to favor "backflow" of Na+ and water from the interstitium into the tubules-thus, increasing Na+ excretion. (wikipedia.org)
  • novel
  • Breakthrough discoveries include the role of somatic variants in the KCNJ5, CACNA1D, ATP1A1, and ATP2B3 genes as causes of aldosterone-producing adenomas (APAs), and the recognition of three novel hyperaldosteronism syndromes with germline variants in the KCNJ5, CACNA1D, and CACNA1H genes. (readbyqxmd.com)
  • In addition, this technology may give rise to novel therapy options for hyperaldosteronism targeting the mutated chloride channel ClC-2. (provendis.info)