Relevant bibliographies by topics / Mineralocorticoid deficiency

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Mineralocorticoid deficiency'

Author: Grafiati
Published: 7 June 2025
Last updated: 16 July 2025

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Journal articles on the topic "Mineralocorticoid deficiency"

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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Mineralocorticoid deficiency"

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Travers, Simon. "Stéroïdomique corticosurrénalienne par LC-MS/MS : applications en endocrinologie pédiatrique Multiplexed Steroid Profiling of Gluco- and Mineralocorticoids Pathways Using a Liquid Chromatography Tandem Mass Spectrometry Method Urinary Steroidomic Profiles by LC-MS/MS to Monitor Classic 21-Hydroxylase Deficiency Interaction between Accumulated 21-Deoxysteroids and Mineralocorticoid Signaling in 21-Hydroxylase Deficiency Comparative Profiling of Adrenal Steroids in Maternal and Umbilical Cord Blood Alterations of Adrenal Steroidomic Profiles in Preterm Infants at Birth." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL019.

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La corticostéroïdogénèse correspond à la synthèse de l’aldostérone, hormone régulant l’homéostasie hydrosodée, et du cortisol hormone du stress, impliquée, dans de nombreux processus physiologiques. Son exploration exhaustive nécessite un dosage précis des précurseurs de synthèse, dont certains, en pathologie, peuvent être déficitaires ou au contraire s’accumuler entrainant des conséquences cliniques graves. Grâce à la chromatographie liquide à la spectrométrie de masse en tandem (LC-MS/MS), nous avons développé deux méthodes permettant de cartographier les stéroïdomes plasmatique et urinaire
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Gardy-Godillot, Michèle. "Mise en evidence d'episodes secretoires du cortisol et de l'aldosterone au cours du nycthemere en relation avec les repas et certains acides amines de la ration." Clermont-Ferrand 2, 1988. http://www.theses.fr/1988CLF21112.

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Book chapters on the topic "Mineralocorticoid deficiency"

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Litchfield, W. Reid, and Robert G. Dluhy. "Mineralocorticoid Deficiency Syndromes." In Hormone Replacement Therapy. Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-700-0_14.

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Dluhy, Robert G. "Mineralocorticoid Deficiency Syndromes." In Endocrine Replacement Therapy in Clinical Practice. Humana Press, 2003. https://doi.org/10.1007/978-1-59259-375-0_17.

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Stewart, Paul M., and Marcus O. Quinkler. "Mineralocorticoid Deficiency." In Endocrinology: Adult and Pediatric. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-323-18907-1.00109-8.

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Stewart, Paul M., and Marcus Quinkler. "Mineralocorticoid Deficiency." In Endocrinology. Elsevier, 2010. http://dx.doi.org/10.1016/b978-1-4160-5583-9.00108-8.

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"Mineralocorticoid deficiency." In Oxford Handbook of Endocrinology and Diabetes, edited by Helen Turner and John Wass. Oxford University Press, 2009. http://dx.doi.org/10.1093/med/9780198567394.003.0047.

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Connell, John M. C., and E. Marie Freel. "Primary aldosteronism and other steroid-related causes of endocrine hypertension." In Oxford Textbook of Endocrinology and Diabetes. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.0570.

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Mineralocorticoid hypertension is characterized by increased distal renal tubular sodium reabsorption, raised body sodium content, plasma volume expansion, markedly reduced body potassium content, with a metabolic alkalosis and suppression of renin production by the juxtaglomerular cells of the kidney (and correspondingly low levels of angiotensin II). Primary aldosteronism is the most common cause of mineralocorticoid hypertension (1); less frequent causes include the rare inborn errors of adrenal steroid synthesis (11β‎-hydroxylase and 17α‎-hydroxylase deficiency), alterations in corticosteroid metabolism (syndrome of apparent mineralocorticoid excess), and constitutive activation of the epithelial sodium channel (Liddle’s syndrome).
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Krone, Nils. "Congenital adrenal hyperplasia." In Oxford Textbook of Endocrinology and Diabetes. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.0616.

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Congenital adrenal hyperplasia (CAH) represents a group of autosomal recessive disorders of steroidogenesis caused by defects in steroidogenic enzymes involved in glucocorticoid synthesis or in enzymes providing cofactors to steroidogenic enzymes (1, 2). Congenital lipoid adrenal hyperplasia (CLAH) caused by steroidogenic acute regulatory protein (StAR) deficiency is distinct in origin and presentation from the conventional variants of CAH, with the unique feature of lipid accumulation subsequently leading to destruction of adrenal function. This chapter will also mention aldosterone synthase deficiency, which is the only defect in adrenal steroidogenesis causing deficient mineralocorticoid biosynthesis without affecting glucocorticoid biosynthesis. The disorder cannot strictly be considered a CAH variant as it does not result in increased ACTH drive and thus not in adrenal hyperplasia. Novel forms of CAH have emerged during recent years. These include P450 oxidoreductase deficiency (ORD), P450 side-chain cleavage (CYP11A1) deficiency, the nonclassic form of CLAH (StAR deficiency), and apparent cortisone reductase deficiency. All forms of congenital adrenal hyperplasia resemble a disease continuum spanning from mild nonclassic presentations to classic onset with severe signs and symptoms.
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Hughes, Claire, Louise Metherell, and Adrian J. L. Clark. "Familial glucocorticoid deficiency." In Oxford Textbook of Endocrinology and Diabetes. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.0611.

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Familial glucocorticoid deficiency (FGD), also known as isolated glucocorticoid deficiency or hereditary unresponsiveness to ACTH, is a rare, genetically heterogeneous autosomal recessive disorder. It is characterized by resistance of the adrenal cortex to ACTH, resulting in adrenal failure with isolated glucocorticoid deficiency. Mineralocorticoid production by the adrenal gland remains near normal. Patients with FGD usually present in early childhood with symptoms relating to cortisol deficiency, including hypoglycaemia, jaundice, recurrent infection, and failure to thrive. Patients are hyperpigmented due to grossly elevated ACTH levels. FGD was first described in 1959 by Shepard et al. who reported two sisters as having Addison’s disease without hypoaldosteronism (1). Subsequently, a number of patients were reported with an inherited form of adrenal insufficiency also without hypoaldosteronism (2–5). In contrast to Addison’s disease (see Chapter 5.9), FGD is a genetic disorder resulting from mutations in genes encoding essential proteins involved in the early response to ACTH.
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Auchus, Richard J. "Modern Management of Congenital Adrenal Hyperplasia and Prospects for the Future." In Oxford Textbook of Endocrinology and Diabetes 3e, edited by John A. H. Wass, Wiebke Arlt, and Robert K. Semple. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198870197.003.0105.

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Congenital adrenal hyperplasia (CAH) refers to a group of genetic cortisol biosynthesis defects, with 21-hydroxylase deficiency (21OHD) being the most common form. The treatment of CAH first involves replacing the deficient hormones of adrenal and sometimes also gonadal origin. In addition, the accumulation of cortisol precursors typically leads to excess androgen and/or mineralocorticoid production. Thus, the second goal is to attenuate the production of unwanted adrenal steroids or to block their action in target tissues. Historically, the two goals were primarily accomplished with glucocorticoid therapy, both to replace the cortisol deficiency and to lower adrenocorticotropin secretion and the production of unwanted steroids. This chapter will review the principles and practical approaches to therapy for patients with CAH, focusing on the adult with 21OHD and their transition from paediatric care. The later sections will review differences in treatment strategies for other forms of CAH and potential novel therapies for the future.
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Samani, Nilesh J., and Maciej Tomaszewski. "Mendelian disorders causing hypertension." In Oxford Textbook of Medicine, edited by Jeremy Dwight. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0380.

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Several rare mendelian disorders where hypertension is the predominant manifestation have been characterized at the molecular level. These include glucocorticoid-remediable aldosteronism, the syndrome of apparent mineralocorticoid excess, Liddle’s syndrome, and Gordon’s syndrome. Hypertension and hypokalaemia are features of 11β‎-hydroxylase and 17β‎-hydroxylase deficiency—two rare recessive gene disorders of adrenal steroid-synthesizing enzymes that, among others, cause congenital adrenal hyperplasia. 11β‎-Hydroxylase deficiency usually presents in infancy or early childhood with virilization of both sexes, while presentation of 17β‎-hydroxylase deficiency may be delayed until adolescence or adulthood. Hypertension due to a phaeochromocytoma may be a feature of multiple endocrine neoplasia type 2 (MEN2, Sipple’s syndrome), which when familial is inherited in an autosomal dominant pattern, or rarely to be a feature of neurofibromatosis (von Recklinghausen’s disease).
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Conference papers on the topic "Mineralocorticoid deficiency"

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CAMARGO, DANIELA DA SILVA, and MIRIAN SILIANE BATISTA DE SOUZA. "HIPOADRENOCORTICISMO CANINO: RELATO DE CASO." In I Congresso Nacional de Especialidades Veterinárias On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/convesp/6457.

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INTRODUÇÃO: O hipoadrenocorticismo canino também chamada de doença de Addison é uma endrocrinopatia considerada rara em cães, resultado da produção deficiente de mineralocorticóide e/ou glicocorticoide e assim consequentemente reduzindo o teor de cortisol basal. Ocorre com maior predisposição em cães adultos jovens com idade média de 4 a 5 anos, sendo mais frequente em fêmeas e nas raças Cão-d’água português, Great Dane, Rottweiler, Wheaten Terrier, West Highland White Terrier e Poodle padrão, tendo neste a herdabilidade sendo influenciada por um único locus gênico recessivo. OBJETIVO: O prese
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