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Journal articles on the topic 'Mineralocorticoid deficiency'

Author: Grafiati

Published: 7 June 2025

Last updated: 2 August 2025

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1

Tolstoy, N. S., M. T. Aized, M. P. McMonagle, et al. "Mineralocorticoid Deficiency in Hemorrhagic Shock." Journal of Surgical Research 172, no. 2 (2012): 346. http://dx.doi.org/10.1016/j.jss.2011.11.808.

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2

Tolstoy, Nikolai S., Majid Aized, Morgan P. McMonagle, et al. "Mineralocorticoid deficiency in hemorrhagic shock." Journal of Surgical Research 180, no. 2 (2013): 232–37. http://dx.doi.org/10.1016/j.jss.2012.05.018.

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3

Guy, R. J., Y. Turberg, R. N. Davidson, G. Finnerty, G. A. MacGregor, and P. H. Wise. "Mineralocorticoid deficiency in HIV infection." BMJ 298, no. 6672 (1989): 496–97. http://dx.doi.org/10.1136/bmj.298.6672.496.

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4

Murphy, C. E., R. G. Ratnavel, and A. C. Davidson. "Mineralocorticoid deficiency in HIV infection." BMJ 298, no. 6681 (1989): 1181. http://dx.doi.org/10.1136/bmj.298.6681.1181-b.

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5

Alimetova, Z. R., та T. A. Bekmansurova. "Congenital dysfunction of the adrenal cortex on the background of 11β-hydroxylase deficiency". Endocrine Surgery 17, № 3 (2023): 30–33. http://dx.doi.org/10.14341/serg12834.

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Congenital adrenal dysfunction (CHD) is a variant of hereditary fermentopathies that lead to a violation of the synthesis of cortisol in the adrenal cortex. Late diagnosis of this pathology significantly impairs the quality of life of patients, and in some cases can lead to fatal consequences. The most common form of CHD, occurring in more than 90% of cases, is due to a deficiency of 21-hydroxylase, which is responsible for the synthesis of deoxycorticosterone and 11-deoxycortisol. The prevalence of this form is 1:10,000 to 1:20,000 newborns in the world, in Russia — 1:9500. In second place is

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6

Kalinchenko, N. Yu, N. A. Zubkova, and A. N. Tyulpakov. "Molecular genetic verification of isolated mineralocorticoid deficiency due to aldosterone synthase deficiency." Problems of Endocrinology 55, no. 1 (2009): 28–30. http://dx.doi.org/10.14341/probl200955128-30.

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Isolated mineralocorticoid deficiency is a rare hereditary autosomal recessive disorder that is characterized by salt wasting and that has the severest manifestations in infants. This paper is the first in the Russian literature to describe cases of isolated aldosterone deficiency. In both cases, the patients were monitored and treated for misdiagnosed congenital adrenal hyperplasia; however, the permanently low level of 17-hydroxyprogesterone could put in doubt the diagnosis and suspect isolated mineralocorticoid deficiency, by keeping in mind a history of salt wasting. By using the presented

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7

Glass, I. A., A. M. Wallace, and T. J. Beattie. "Aldosterone Deficiency in Infancy." Scottish Medical Journal 33, no. 3 (1988): 275–76. http://dx.doi.org/10.1177/003693308803300311.

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Two infants with a chronic salt wasting state secondary to a rare defect in mineralocorticoid synthesis are described. Management difficulties are illustrated highlighting the need for early definitive diagnosis based on measurement and correct interpretation of plasma renin, plasma aldosterone and urinary steroid metabolite concentrations.

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Padidela, Raja, and Peter C. Hindmarsh. "Mineralocorticoid Deficiency and Treatment in Congenital Adrenal Hyperplasia." International Journal of Pediatric Endocrinology 2010 (2010): 1–4. http://dx.doi.org/10.1155/2010/656925.

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Padidela, Raja, and PeterC Hindmarsh. "Mineralocorticoid Deficiency and Treatment in Congenital Adrenal Hyperplasia." International Journal of Pediatric Endocrinology 2010, no. 1 (2010): 656925. http://dx.doi.org/10.1186/1687-9856-2010-656925.

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10

Saffari, Fatemeh, and Banafsheh Arad. "Treatment of Hypertension in a Child with 11beta-Hydroxylase Deficiency: A case report." Journal of Pediatrics Review 10, no. 1 (2022): 8. http://dx.doi.org/10.32598/jpr.10.1.993.1.

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Introduction: Deficiency of 11-hydroxylase is clinically presented by external genitalia virilization in girls and precocious puberty in boys. Low renin hypertension occurs in both sexes. Early diagnosis and treatment of hypertension can prevent complications. Case presentation: We described a 4.5 years old girl of 46.XX, who presented with ambiguous genitalia at birth and hypertension later in follow-up. The patient had received the appropriate dosage of hydrocortisone and the level of 17-hydroxy progesterone was within the acceptable range but the hypokalemia persisted. Both hypertension and

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11

Bobillier-Chaumont, Sylvie, Laurence Nicod, Lysiane Richert, and Alain Berthelot. "Antioxidant status in the liver of hypertensive and metallothionein-deficient mice." Canadian Journal of Physiology and Pharmacology 81, no. 10 (2003): 929–36. http://dx.doi.org/10.1139/y03-089.

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Because oxidative stress is involved in arterial hypertension, impairment of hepatic antioxidant defences could develop in the course of this disease. Metallothionein (MT), an antioxidant protein, is present in high rates in the liver. The aim of this study was to investigate the effect of a mineralocorticoid-salt treatment on blood pressure, hepatic antioxidant enzyme activities, and cardiac MT levels in transgenic MT null mice compared with control mice to further clarify the role of MT during the experimental development of arterial hypertension. Control and transgenic MT / mice were subm

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Palermo, Mario, Marcus Quinkler, and Paul M. Stewart. "Apparent mineralocorticoid excess syndrome: an overview." Arquivos Brasileiros de Endocrinologia & Metabologia 48, no. 5 (2004): 687–96. http://dx.doi.org/10.1590/s0004-27302004000500015.

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Apparent mineralocorticoid excess (AME) syndrome results from defective 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2). This enzyme is co-expressed with the mineralocorticoid receptor (MR) in the kidney and converts cortisol (F) to its inactive metabolite cortisone (E). Its deficiency allows the unmetabolized cortisol to bind to the MR inducing sodium retention, hypokalemia, suppression of PRA and hypertension. Mutations in the gene encoding 11beta-HSD2 account for the inherited form, but a similar clinical picture to AME occurs following the ingestion of bioflavonoids, licorice and

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13

Pokharel, Sunil, A. Shrestha, D. Maksey, et al. "Addisonian Crisis Precipitated By Thyroxine Therapy In A Patient With Type 2 Autoimmune Polyglandular Syndrome." Journal of Chitwan Medical College 3, no. 4 (2014): 54–56. http://dx.doi.org/10.3126/jcmc.v3i4.9557.

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Primary hypoadrenalism(Addison’s disease) refers to glucocorticoid deficiency occurring in the setting of adrenal disease(mostly due to autoimmune adrenalitis), whereas secondary hypoadrenalism arises because of deficiency of ACTH(mostly due to pituitary disease) . A major distinction between these two is that mineralocorticoid deficiency invariably accompanies primary hypoadrenalism, but this does not occur in secondary hypoadrenalism because only ACTH is deficient; the renin-angiotensin-aldosterone axis is intact and in primary hypoadrenalism skin pigmentation is always present due to inc

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14

Weinberg-Shukron, Ariella, Abdulsalam Abu-Libdeh, Fouad Zhadeh, et al. "Combined mineralocorticoid and glucocorticoid deficiency is caused by a novel founder nicotinamide nucleotide transhydrogenase mutation that alters mitochondrial morphology and increases oxidative stress." Journal of Medical Genetics 52, no. 9 (2015): 636–41. http://dx.doi.org/10.1136/jmedgenet-2015-103078.

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BackgroundFamilial glucocorticoid deficiency (FGD) reflects specific failure of adrenocortical glucocorticoid production in response to adrenocorticotropic hormone (ACTH). Most cases are caused by mutations encoding ACTH-receptor components (MC2R, MRAP) or the general steroidogenesis protein (StAR). Recently, nicotinamide nucleotide transhydrogenase (NNT) mutations were found to cause FGD through a postulated mechanism resulting from decreased detoxification of reactive oxygen species (ROS) in adrenocortical cells.Methods and resultsIn a consanguineous Palestinian family with combined mineralo

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15

Kwon, Tae-Hwan, Jakob Nielsen, Shyama Masilamani, et al. "Regulation of collecting duct AQP3 expression: response to mineralocorticoid." American Journal of Physiology-Renal Physiology 283, no. 6 (2002): F1403—F1421. http://dx.doi.org/10.1152/ajprenal.00059.2002.

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Adrenocortical steroid hormones are importantly involved in the regulation of extracellular fluid volume. The present study was aimed at examining whether aldosterone and/or glucocorticoid regulates the abundance of aquaporin-3 (AQP3), -2, and -1 in rat kidney. In protocol 1, rats were adrenalectomized, followed by aldosterone replacement, dexamethasone replacement, or combined aldosterone and dexamethasone replacement (rats had free access to water but received a fixed amount of food). Protocol 2 was identical to protocol 1, except that all groups received fixed daily food and water intake. I

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Travers, Simon, Claire Bouvattier, Jérôme Fagart, et al. "Interaction between accumulated 21-deoxysteroids and mineralocorticoid signaling in 21-hydroxylase deficiency." American Journal of Physiology-Endocrinology and Metabolism 318, no. 2 (2020): E102—E110. http://dx.doi.org/10.1152/ajpendo.00368.2019.

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21-Hydroxylase deficiency (21OHD) is a rare genetic disorder in which salt-wasting syndrome occurs in 75% of cases, due to inability to synthesize cortisol and aldosterone. Recent mass spectrometry progress allowed identification of 21-deoxysteroids, i.e., 17-hydroxyprogesterone (17OHP), 21-deoxycortisol (21DF), and 21-deoxycorticosterone (21DB). We hypothesized that they may interfere with mineralocorticoid signaling and fludrocortisone therapy in patients with congenital adrenal hyperplasia (CAH) without effective glucocorticoid replacement and ACTH suppression. Our goal was to quantify circ

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17

Kulkarni, Abhishek J., and Poorvi Chandraprakash Agrawal. "Congenital aromatase deficiency – A virilizing masquerade!" Journal of Pediatric Endocrinology and Diabetes 2 (May 3, 2022): 31–33. http://dx.doi.org/10.25259/jped_26_2021.

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Congenital adrenal hyperplasia (CAH) is the most common cause of disorder of sex development in an XX individual. While 21-hydroxylase (CYP21A2) gene mutation is the most common subtype of CAH, aromatase deficiency due to mutations in the gene CYP19A1 is a rare subtype. We report a 46,XX infant with virilized external genitalia, no clinical signs of glucocorticoid or mineralocorticoid deficiency, normal 17-hydroxyprogesterone and adrenocorticotropic hormone, and high levels of gonadotropins and testosterone with inappropriately low estradiol and ovarian cysts. Based on this clinical and bioche

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18

Coeli, Fernanda Borchers, Lúcio Fábio Caldas Ferraz, Sofia H. V. de Lemos-Marini, Sumara Zuanazi Pinto Rigatto, Vera Maria Santoro Belangero, and Maricilda Palandi de-Mello. "Apparent mineralocorticoid excess syndrome in a Brazilian boy caused by the homozygous missense mutation p.R186C in the HSD11B2 gene." Arquivos Brasileiros de Endocrinologia & Metabologia 52, no. 8 (2008): 1277–81. http://dx.doi.org/10.1590/s0004-27302008000800012.

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The apparent mineralocorticoid excess syndrome (AME) is a rare autosomal recessive disorder due to the deficiency of 11β-hydroxysteroid dehydrogenase type 2 enzyme (11beta-HSD2). The 11beta-HSD2 enzyme, encoded by HSD11B2 gene, metabolizes active cortisol in cortisone. Mutations on HSD11B2 gene affect the enzyme activity by leading to an excess of cortisol, which causes its inappropriate access to mineralocorticoid receptor. Therefore, cortisol will bind mineralocorticoid receptor. The human HSD11B2 gene maps to chromosome 16q22 and consists of five exons encoding a protein of 405 amino acids.

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19

Chang, Julia J., Alejandro Villar-Prados, David A. Stevens, Xiao-Yan Wang, and Julie Chen. "Concurrent Pseudohyperaldosteronism and Primary Glucocorticoid Deficiency From Posaconazole." Journal of the Endocrine Society 5, Supplement_1 (2021): A124—A125. http://dx.doi.org/10.1210/jendso/bvab048.250.

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Abstract Background: Posaconazole can cause pseudohyperaldosteronism via inhibition of 11-beta hydroxylase and 11-beta-hydroxysteroid dehydrogenase type 2 (1). The accumulation of 11-deoxycorticosterone and increased cortisol-to-cortisone ratio in the kidney causes apparent mineralocorticoid excess. The effect of posaconazole on the glucocorticoid axis is less established. Clinical Case: A 56-year-old Hispanic man with a history of chronic septic arthritis of the left ankle from Coccidioides presented with 3 months of malaise, nausea, weight loss of 30 pounds, and recurrent hypokalemia. He was

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20

Doucet, A., C. Barlet-Bas, S. Siaume-Perez, C. Khadouri, and S. Marsy. "Gluco- and mineralocorticoids control adenylate cyclase in specific nephron segments." American Journal of Physiology-Renal Physiology 258, no. 4 (1990): F812—F820. http://dx.doi.org/10.1152/ajprenal.1990.258.4.f812.

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Adrenal insufficiency is associated with an impairment of kidney diluting and concentrating ability, defects that may result from alterations of vasopressin-induced adenosine 3',5'-cyclic monophosphate (cAMP) production. The purpose of this study were 1) to localize the sites of decreased vasopressin-stimulated adenylate cyclase (AC) activity along the nephron of adrenalectomized rats; 2) to determine whether the response of AC to other hormones is altered by adrenalectomy; 3) to evaluate whether changes in AC are due to the deficiency in mineralocorticoids and/or glucocorticoids; and 4) to ch

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21

de Lange, W. E., та H. Doorenbos. "Incomplete virilization and subclinical mineralocorticoid excess in a boy with partial 17,20-desmolase/17 α-hydroxylase deficiency". Acta Endocrinologica 122, № 2 (1990): 263–66. http://dx.doi.org/10.1530/acta.0.1220263.

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Abstract A 17-year-old boy is described with impaired virilization and subclinical mineralocorticoid excess owing to combined 17,20-desmolase/17 α-hydroxylase deficiency. His basal plasma progesterone was 20.9 nmol/l (reference value 0.50-1.88), 17-hydroxyprogesterone 21.3 nmol/l (reference value 3.05-4.84), testosterone 6.85 nmol/l (reference value 14.1-22.0), and his excretion of tetrahydro-11-deoxycorticosterone 11.8 μmol/24 h (reference value 1.0-1.5). The differential effects of this combined enzyme deficiency on adrenal and testicular function were studied by ACTH stimulation, dexamethas

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22

Yao, Bing, Raymond C. Harris та Ming-Zhi Zhang. "Interactions between 11β-hydroxysteroid dehydrogenase and COX-2 in kidney". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, № 6 (2005): R1767—R1773. http://dx.doi.org/10.1152/ajpregu.00786.2004.

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The syndrome of apparent mineralocorticoid excess (SAME) is an autosomal recessive form of salt-sensitive hypertension caused by deficiency of the kidney type 2 11β-hydroxysteroid dehydrogenase (11βHSD2). In this disorder, cortisol is not inactivated by 11βHSD2, occupies mineralocorticoid receptors (MRs), and causes excessive sodium retention and hypertension. In renal medulla, prostaglandins derived from cyclooxygenase-2 (COX-2) stimulate sodium and water excretion, and renal medullary COX-2 expression increases after mineralocorticoid administration. We investigated whether medullary COX-2 a

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23

Potier, Louis, Ludovic Waeckel, Christine Richer, Ronan Roussel, Nadine Bouby, and Francois Alhenc-Gelas. "Tissue kallikrein, blood pressure regulation, and hypertension: insight from genetic kallikrein deficiency." Biological Chemistry 394, no. 3 (2013): 329–33. http://dx.doi.org/10.1515/hsz-2012-0332.

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Abstract Tissue kallikrein has been suggested to be involved in blood pressure regulation and in protection against hypertension. However, this hypothesis remains debated. Recently, murine genetic models of kallikrein deficiency have been engineered and partial genetic deficiency in kallikrein activity has been characterized in humans. Studies in kallikrein-deficient mice indicate that kallikrein indeed influences blood pressure in the setting of mineralocorticoid excess and salt retention but not in normotensive animals and in high renin hypertension. These observations suggest that kallikrei

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RONGEN-WESTERLAKEN, C., S. L. S. DROP, and J. N. VAN DEN ANKER. "Primary adrenocortical insufficiency in childhood." Acta Endocrinologica 113, no. 4_Suppl (1986): S279—S283. http://dx.doi.org/10.1530/acta.0.112s279.

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SUMMARY Seven patients with primary glucocorticoid or glucocorticoid and mineralocorticoid deficiency are described with emphasis on the clinical presentation and laboratory investigations. Two patients presented with irreversible shock and at autopsy adrenal tissue was recognized only microscopically. In 3 patients adrenal antibodies were present. One girl had the polyglandular autoimmune disorder type I and one boy had glucocorticoid deficiency only. The histories of the patients illustrate that the presenting symptoms of primary adrenocortical insufficiency are very insiduous and that it ma

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Stewart, PM. "Tissue-specific Cushing's syndrome, 11beta-hydroxysteroid dehydrogenases and the redefinition of corticosteroid hormone action." European Journal of Endocrinology 149, no. 3 (2003): 163–68. http://dx.doi.org/10.1530/eje.0.1490163.

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Two isoforms of 11beta-hydroxysteroid dehydrogenase (11beta-HSD) interconvert the active glucocorticoid, cortisol, and inactive cortisone. 11beta-HSD1 acts predominantly as an oxo-reductase in vivo using NADP(H) as a cofactor to generate cortisol. In contrast, 11beta-HSD2 is a NAD-dependent dehydrogenase inactivating cortisol to cortisone, thereby protecting the mineralocorticoid receptor from occupation by cortisol. In peripheral tIssues, both enzymes serve to control the availability of cortisol to bind to corticosteroid receptors. 11beta-HSD2 protects the mineralocorticoid receptor from cor

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Biglieri, E. G., and C. E. Kater. "Steroid characteristics of mineralocorticoid adrenocortical hypertension." Clinical Chemistry 37, no. 10 (1991): 1843–48. http://dx.doi.org/10.1093/clinchem/37.10.1843.

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Abstract Adrenocortical causes of hypertension are established by examining the mineralocorticoid hormones produced in the zona glomerulosa and zona fasciculata. In the zona glomerulosa, aldosterone excess leads to hypertension, hypokalemia, and suppressed plasma renin activity, with increased concentrations of urinary aldosterone (either as the 18-glucuronide or free aldosterone) as an index of its production. Identifying a tumor by computed tomography scan verifies the diagnosis of a correctable lesion. If no tumor is found, several maneuvers are used to identify primary adrenal hyperplasia,

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27

McGonigle, Kathryn M., John F. Randolph, Sharon A. Center, and Richard E. Goldstein. "Mineralocorticoid Before Glucocorticoid Deficiency in a Dog with Primary Hypoadrenocorticism and Hypothyroidism." Journal of the American Animal Hospital Association 49, no. 1 (2013): 54–57. http://dx.doi.org/10.5326/jaaha-ms-5820.

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A dog with an unexpected presentation of primary hypoadrenocorticism was evaluated for clinical signs and electrolyte abnormalities characteristic of Addison’s disease. Although the initial adrenocorticotropic hormone (ACTH) stimulation test documented serum cortisol concentrations within the reference range, subsequent assessments confirmed hypoaldosteronism. Mineralocorticoid replacement promptly normalized electrolytes and transiently improved clinical illness. Six weeks after initial ACTH stimulation testing, the dog became glucocorticoid deficient. Concurrent primary hypothyroidism was al

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28

HOCHBER, ZEEV, AVRAHAM BENDERLY, LUNA KAHANA та ZVI ZADIK. "Requirement of Mineralocorticoid in Congenital Adrenal Hyperplasia due to 11β-Hydroxylase Deficiency". Journal of Clinical Endocrinology & Metabolism 63, № 1 (1986): 36–40. http://dx.doi.org/10.1210/jcem-63-1-36.

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Li, Chao, Yu Yao Zhang, Ryan A. Frieler, et al. "Myeloid Mineralocorticoid Receptor Deficiency Inhibits Aortic Constriction-Induced Cardiac Hypertrophy in Mice." PLoS ONE 9, no. 10 (2014): e110950. http://dx.doi.org/10.1371/journal.pone.0110950.

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30

Valentino, R., M. Wallace, M. Wallace, D. Burt, and C. R. W. Edwards. "17 Liquorice Induced Mineralocorticoid Excess: 11 ??- Hydroxysteroid Dehydrogenase Deficiency Comes of Age." Journal of Hypertension 5, no. 6 (1987): 768–69. http://dx.doi.org/10.1097/00004872-198712000-00038.

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31

Verrijn Stuart, A. A., G. Ozisik, M. A. de Vroede, et al. "An Amino-Terminal DAX1 (NROB1) Missense Mutation Associated with Isolated Mineralocorticoid Deficiency." Journal of Clinical Endocrinology & Metabolism 92, no. 3 (2007): 755–61. http://dx.doi.org/10.1210/jc.2005-2429.

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32

Treesaranuwattana, Thitinan, Kelly Yin Han Wong, Danielle L. Brooks, et al. "Lysine-Specific Demethylase-1 Deficiency Increases Agonist Signaling Via the Mineralocorticoid Receptor." Hypertension 75, no. 4 (2020): 1045–53. http://dx.doi.org/10.1161/hypertensionaha.119.13821.

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Stewart, PaulM, Rossella Valentino, A. Michael Wallace, Daniel Burt, CedricH L. Shackleton, and ChristopherR W. Edwards. "MINERALOCORTICOID ACTIVITY OF LIQUORICE: 11-BETA-HYDROXYSTEROID DEHYDROGENASE DEFICIENCY COMES OF AGE." Lancet 330, no. 8563 (1987): 821–24. http://dx.doi.org/10.1016/s0140-6736(87)91014-2.

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Alves da Silva, Isabelle, Juliana de P. Nhanharelli, and Vanessa U. da Fonseca. "Deoxycorticosterone pivalate in the control of canine hypoadrenocorticism – case reports." Clínica Veterinária XXVIII, no. 163 (2023): 36–45. http://dx.doi.org/10.46958/rcv.2023.xxviii.n.163.p.36-45.

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Primary hypoadrenocorticism or Addison’s disease is an endocrinopathy involving glucocorticoid deficiency, commonly associated with mineralocorticoid deficiency. The most commonly used treatment for hormone replacement involves the combination of fludrocortisone and prednisone. Deoxycorticosterone pivalate (DOCP) has been shown in the literature to be superior in electrolyte control in patients with hypoadrenocorticism, and should always be associated with prednisone/prednisolona. In this study, we report the benefit of DOCP and the two-stage dose adjustment protocol for this drug in 2 differe

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Orlova, E. M., M. A. Kareva, M. A. Melikian, A. N. Tiul'pakov, and V. A. Peterkova. "Familial isolated glucocorticoid deficiency: three clinical cases and a brief overview of the current literature." Problems of Endocrinology 59, no. 3 (2013): 30–35. http://dx.doi.org/10.14341/probl201359330-35.

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Familial isolated glucocorticoid deficiency (FIGD) is a rare form of primary adrenal insufficiency associated with the resistance of the adrenal cortex to the action of ACTH. This pathology manifests itself in the form of cortisol deficiency despite the normal mineralocorticoid function. Approximately 50% of all FIGD cases are attributable to mutations in two genes (melanocortin 2 receptor gene, MC2R, and melanocortin 2 receptor accessory protein gene, MRAP). In addition, the relationship between FIGD and mutations in nicotinamide nucleotide transhydrogenase gene, NNT, minichromosome maintenan

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Perelló, Marina Hernández, and Carolina Albuquerque. "Primary hypoaldosteronism in a dog with concurrent suspected chronic hepatitis." Companion Animal 29, no. 2 (2024): 1–7. http://dx.doi.org/10.12968/coan.2023.0043.

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A 3-year-old female spayed English Cocker Spaniel presented with a 2-month history of lethargy. The owner reported a single tonic-clonic seizure 7 months before presentation and intermittent mild gastrointestinal signs for the past 18 months. Initial investigations revealed hyponatraemia, hyperkalaemia and increased levels of liver enzymes. An adrenocorticotropic hormone stimulation test excluded hypocortisolism. The gastrointestinal signs resolved following a dietary change, suggesting that chronic enteropathy and most primary and secondary causes of hepatic disease were excluded, leaving idi

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Walker, Brian R., Alan A. Connacher, David J. Webb, and Christopher R. W. Edwards. "Glucocorticoids and blood pressure: a role for the cortisol/cortisone shuttle in the control of vascular tone in man." Clinical Science 83, no. 2 (1992): 171–78. http://dx.doi.org/10.1042/cs0830171.

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1. 11β-Hydroxysteroid dehydrogenase converts cortisol to inactive cortisone in man. In distal renal tubules, this inactivation protects mineralocorticoid receptors from cortisol. Congenital 11β-hydroxysteroid dehydrogenase deficiency and inhibition of 11β-hydroxysteroid dehydrogenase by liquorice or carbenoxolone result in cortisol-dependent hypokalaemia and hypertension. 2. 11β-Hydroxysteroid dehydrogenase is expressed in vascular smooth muscle. Both glucocorticoids and mineralocorticoids potentiate vascular responses to noradrenaline. 11β-Hydroxysteroid dehydrogenase activity may therefore i

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Breder, Ikaro Soares Santos, Heraldo Mendes Garmes, Tais Nitsch Mazzola, Andrea Trevas Maciel-Guerra, Maricilda Palandi de Mello та Gil Guerra-Júnior. "Three new Brazilian cases of 17α-hydroxylase deficiency: clinical, molecular, hormonal, and treatment features". Journal of Pediatric Endocrinology and Metabolism 31, № 8 (2018): 937–42. http://dx.doi.org/10.1515/jpem-2017-0521.

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Abstract Background: Deficiency of 17α-hydroxylase (17OHD) is a rare form of adrenal hyperplasia. Diagnosis is generally delayed, impairing appropriate treatment. Case presentation: Here, we report the clinical, molecular, hormonal, and treatment data of three unrelated 17OHD patients, aged 14–16 years with hypergonadotrophic hypogonadism; uncontrolled hypertension; primary adrenal insufficiency; and high progesterone, low to normal potassium, and low dehydroepiandrosterone, androstenedione, and testosterone levels. Liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS) at base

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White, Perrin C. "Alterations of Cortisol Metabolism in Human Disorders." Hormone Research in Paediatrics 89, no. 5 (2018): 320–30. http://dx.doi.org/10.1159/000485508.

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The interconversion of active and inactive corticosteroids – cortisol and cortisone, respectively, in humans – is modulated by isozymes of 11β-hydroxysteroid dehydrogenase (11-HSD). Studies of this process have provided crucial insights into glucocorticoid effects in a wide variety of tissues. The 11-HSD1 isozyme functions mainly as an oxoreductase (cortisone to cortisol) and is expressed at high levels in the liver and other glucocorticoid target tissues. Because it is required for full physiological effects of cortisol, it has emerged as a drug target for metabolic syndrome and type 2 diabet

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Carvajal, Cristian A., Alejandra Tapia-Castillo, Andrea Vecchiola, Rene Baudrand, and Carlos E. Fardella. "Classic and Nonclassic Apparent Mineralocorticoid Excess Syndrome." Journal of Clinical Endocrinology & Metabolism 105, no. 4 (2019): e924-e936. http://dx.doi.org/10.1210/clinem/dgz315.

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Abstract Context Arterial hypertension (AHT) is one of the most frequent pathologies in the general population. Subtypes of essential hypertension characterized by low renin levels allowed the identification of 2 different clinical entities: aldosterone-mediated mineralocorticoid receptor (MR) activation and cortisol-mediated MR activation. Evidence Acquisition This review is based upon a search of Pubmed and Google Scholar databases, up to August 2019, for all publications relating to endocrine hypertension, apparent mineralocorticoid excess (AME) and cortisol (F) to cortisone (E) metabolism.

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Inada, Mitsuo. "A 87-year-old woman with mineralocorticoid excess due to 11β-HSD2 deficiency". Nippon Ronen Igakkai Zasshi. Japanese Journal of Geriatrics 44, № 4 (2007): 513–16. http://dx.doi.org/10.3143/geriatrics.44.513.

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BOSSON, Danièle, Ursula KUHNLE, Nicole MEES, et al. "Generalized unresponsiveness to mineralocorticoid hormones: familial recessive pseudohypoaldosteronism due to aldosterone-receptor deficiency." Acta Endocrinologica 113, no. 4_Suppl (1986): S376—S380. http://dx.doi.org/10.1530/acta.0.112s376.

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ABSTRACT The present report describes two sibs - born from consanguineous parents - presenting with severe salt wasting. Generalized pseudohypoaldosteronism (PHA) was diagnosed on the basis of markedly elevated sodium concentration in urine (84 & 63 mmol/L respectively), sweat (181 & 196), saliva (- & 120) and stool (- & 189), hyponatremia (112 & 132) and hyperkalemia (10.7 & 7.3) in the presence of increased plasma aldosterone (> 8.5 & 5.4 ng/ml), plasma renin activity (40 & 18.9 ng/ml/hr) and urinary aldosterone (> 32 & 11.6 μg/day). Both parents inv

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Seckl, J. R. "The syndrome of apparent mineralocorticoid excess and deficiency of 11 β-hydroxysteroid dehydrogenase". Clinical Endocrinology 43, № 2 (1995): 247–48. http://dx.doi.org/10.1111/j.1365-2265.1995.tb01924.x.

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Khadse, Savita, Karishma Bhade, Nikhil Shah, and Radha Ghildiyal. "Follow up of a rare case of adrenal insufficiency due toNNTmutation." BMJ Case Reports 17, no. 2 (2024): e258842. http://dx.doi.org/10.1136/bcr-2023-258842.

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Hypoglycaemia is one of the most common causes of convulsions in neonatal period. Repeated hypoglycaemic convulsions have to be addressed with utmost urgency to prevent its morbid sequelae. Repeated ketotic hypoglycaemia in the infantile period needs detailed endocrine evaluation. Our patient is a boy in the third year of his life, had presented in infancy with hypoglycaemic convulsions and hyperpigmentation of skin and mucous membrane. Investigations revealed ketotic hypoglycaemia, hypocortisolaemia with high adrenocorticotropic hormone (ACTH) and normal aldosterone, 17-hydroxyprogesterone (1

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Nesterov, Viatcheslav, Marko Bertog, Jérémie Canonica, et al. "Critical role of the mineralocorticoid receptor in aldosterone-dependent and aldosterone-independent regulation of ENaC in the distal nephron." American Journal of Physiology-Renal Physiology 321, no. 3 (2021): F257—F268. http://dx.doi.org/10.1152/ajprenal.00139.2021.

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Using a mouse model with inducible nephron-specific mineralocorticoid receptor (MR) deficiency, we demonstrated that MR is not only critical for maintaining aldosterone-dependent ENaC activity in CNT/CCD but also for aldosterone-independent ENaC activity in DCT2/CNT. Furthermore, we demonstrated that cells of this latter nephron segment express little 11β-HSD2, which probably allows glucocorticoids to stimulate MR, resulting in aldosterone-independent ENaC activity in DCT2/CNT. This site-specific ENaC regulation has physiologically relevant implications for renal sodium and potassium homeostas

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Bienvenu, Laura A., James Morgan, Amanda J. Rickard, et al. "Macrophage Mineralocorticoid Receptor Signaling Plays a Key Role in Aldosterone-Independent Cardiac Fibrosis." Endocrinology 153, no. 7 (2012): 3416–25. http://dx.doi.org/10.1210/en.2011-2098.

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Mineralocorticoid receptor (MR) activation promotes the development of cardiac fibrosis and heart failure. Clinical evidence demonstrates that MR antagonism is protective even when plasma aldosterone levels are not increased. We hypothesize that MR activation in macrophages drives the profibrotic phenotype in the heart even when aldosterone levels are not elevated. The aim of the present study was to establish the role of macrophage MR signaling in mediating cardiac tissue remodeling caused by nitric oxide (NO) deficiency, a mineralocorticoid-independent insult. Male wild-type (MRflox/flox) an

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Martin, Regina M., Chin J. Lin, Elaine M. F. Costa, et al. "P450c17 Deficiency in Brazilian Patients: Biochemical Diagnosis through Progesterone Levels Confirmed by CYP17 Genotyping." Journal of Clinical Endocrinology & Metabolism 88, no. 12 (2003): 5739–46. http://dx.doi.org/10.1210/jc.2003-030988.

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Abstract P450c17 deficiency is an autosomal recessive disorder and a rare cause of congenital adrenal hyperplasia characterized by hypertension, hypokalemia, and impaired production of sex hormones. We performed a clinical, hormonal, and molecular study of 11 patients from 6 Brazilian families with the combined 17α-hydroxylase/17,20-lyase deficiency phenotype. All patients had elevated basal serum levels of progesterone (1.8–38 ng/ml; 0.57–12 pmol/liter) and suppressed plasma renin activity. CYP17 genotyping identified 5 missense mutations. The compound heterozygous mutation R362C/W406R was fo

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Whitehead, Malcolm. "Hormone replacement therapy with estradiol and drospirenone: An overview of the clinical data." British Menopause Society Journal 12, no. 1_suppl (2006): 4–7. http://dx.doi.org/10.1258/136218006775992185.

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A new form of continuous combined hormone replacement therapy has become available that contains estradiol and drospirenone as the progestogen component. Drospirenone is a synthetic progestogen, the only one in hormone replacement therapy in the UK that possesses clinically relevant anti-mineralocorticoid activity. The combination of estradiol and drospirenone has been shown to provide relief from estrogen-deficiency symptoms of the menopause. It also helps to prevent osteoporosis in postmenopausal women by increasing bone density. Further, it has been shown to provide protection against endom

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Tejera-Muñoz, A., R. R. Rodrigues-Diez, V. Esteban, et al. "CTGF deficiency predisposes to aneurysm generation and rupture. Mineralocorticoid antagonist as potential therapeutic treatment." Atherosclerosis 331 (August 2021): e246-e247. http://dx.doi.org/10.1016/j.atherosclerosis.2021.06.754.

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Shen, Zhu-Xia, Xiao-Qing Chen, Xue-Nan Sun, et al. "Mineralocorticoid Receptor Deficiency in Macrophages Inhibits Atherosclerosis by Affecting Foam Cell Formation and Efferocytosis." Journal of Biological Chemistry 292, no. 3 (2016): 925–35. http://dx.doi.org/10.1074/jbc.m116.739243.

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