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  1. Article ; Online: Emerging treatment for congenital adrenal hyperplasia.

    White, Perrin C

    Current opinion in endocrinology, diabetes, and obesity

    2022  Volume 29, Issue 3, Page(s) 271–276

    Abstract: Purpose of review: Although the basic treatment of congenital adrenal hyperplasia (CAH) is well established, there are active clinical research projects to more closely mimic the normal diurnal rhythm of cortisol secretion and to reduce total ... ...

    Abstract Purpose of review: Although the basic treatment of congenital adrenal hyperplasia (CAH) is well established, there are active clinical research projects to more closely mimic the normal diurnal rhythm of cortisol secretion and to reduce total glucocorticoid doses to minimize adverse metabolic effects.
    Recent findings: We review clinical studies on CAH treatment published in the last 18 months or currently underway according to ClinicalTrials.gov listings. These can be grouped into several broad themes: alternative dosing forms of hydrocortisone with altered pharmacokinetics or easier dose titration; corticotropin-releasing hormone receptor antagonists that reduce corticotropin (ACTH) secretion and thereby reduce adrenal androgen secretion; androgen biosynthesis inhibitors; a first clinical trial of a gene therapy vector.
    Summary: Alternative dosing forms of hydrocortisone are, or will shortly be, marketed, but cost may be a barrier to utilization, at least in the US market. Trials of corticotropin releasing hormone receptor antagonists and androgen biosynthesis inhibitors are currently underway. The author believes that trials of gene therapy for CAH are premature.
    MeSH term(s) Adrenal Hyperplasia, Congenital/drug therapy ; Adrenocorticotropic Hormone ; Androgens/therapeutic use ; Glucocorticoids/therapeutic use ; Humans ; Hydrocortisone/therapeutic use
    Chemical Substances Androgens ; Glucocorticoids ; Adrenocorticotropic Hormone (9002-60-2) ; Hydrocortisone (WI4X0X7BPJ)
    Language English
    Publishing date 2022-03-13
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 2272017-0
    ISSN 1752-2978 ; 1752-296X
    ISSN (online) 1752-2978
    ISSN 1752-296X
    DOI 10.1097/MED.0000000000000723
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Letter to the Editor: "Genetic Link Between Gender Dysphoria and Sex Hormone Signaling".

    White, Perrin C

    The Journal of clinical endocrinology and metabolism

    2019  Volume 104, Issue 10, Page(s) 4418–4419

    MeSH term(s) Gender Dysphoria ; Gonadal Steroid Hormones ; Humans ; Signal Transduction ; Transsexualism
    Chemical Substances Gonadal Steroid Hormones
    Language English
    Publishing date 2019-04-15
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 3029-6
    ISSN 1945-7197 ; 0021-972X
    ISSN (online) 1945-7197
    ISSN 0021-972X
    DOI 10.1210/jc.2019-00487
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  3. Article ; Online: History of Adrenal Research: From Ancient Anatomy to Contemporary Molecular Biology.

    Miller, Walter L / White, Perrin C

    Endocrine reviews

    2022  Volume 44, Issue 1, Page(s) 70–116

    Abstract: The adrenal is a small, anatomically unimposing structure that escaped scientific notice until 1564 and whose existence was doubted by many until the 18th century. Adrenal functions were inferred from the adrenal insufficiency syndrome described by ... ...

    Abstract The adrenal is a small, anatomically unimposing structure that escaped scientific notice until 1564 and whose existence was doubted by many until the 18th century. Adrenal functions were inferred from the adrenal insufficiency syndrome described by Addison and from the obesity and virilization that accompanied many adrenal malignancies, but early physiologists sometimes confused the roles of the cortex and medulla. Medullary epinephrine was the first hormone to be isolated (in 1901), and numerous cortical steroids were isolated between 1930 and 1949. The treatment of arthritis, Addison's disease, and congenital adrenal hyperplasia (CAH) with cortisone in the 1950s revolutionized clinical endocrinology and steroid research. Cases of CAH had been reported in the 19th century, but a defect in 21-hydroxylation in CAH was not identified until 1957. Other forms of CAH, including deficiencies of 3β-hydroxysteroid dehydrogenase, 11β-hydroxylase, and 17α-hydroxylase were defined hormonally in the 1960s. Cytochrome P450 enzymes were described in 1962-1964, and steroid 21-hydroxylation was the first biosynthetic activity associated with a P450. Understanding of the genetic and biochemical bases of these disorders advanced rapidly from 1984 to 2004. The cloning of genes for steroidogenic enzymes and related factors revealed many mutations causing known diseases and facilitated the discovery of new disorders. Genetics and cell biology have replaced steroid chemistry as the key disciplines for understanding and teaching steroidogenesis and its disorders.
    MeSH term(s) Humans ; Adrenal Hyperplasia, Congenital/genetics ; Hormones ; Mixed Function Oxygenases ; Molecular Biology ; Steroids ; Adrenal Gland Diseases/genetics ; Adrenal Gland Diseases/history ; Adrenal Gland Diseases/pathology ; Adrenal Gland Diseases/therapy ; Adrenal Glands/anatomy & histology ; Biomedical Research/history
    Chemical Substances Hormones ; Mixed Function Oxygenases (EC 1.-) ; Steroids
    Language English
    Publishing date 2022-08-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 603096-8
    ISSN 1945-7189 ; 0163-769X
    ISSN (online) 1945-7189
    ISSN 0163-769X
    DOI 10.1210/endrev/bnac019
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  4. Article ; Online: A Brief History of Congenital Adrenal Hyperplasia.

    Miller, Walter L / White, Perrin C

    Hormone research in paediatrics

    2022  Volume 95, Issue 6, Page(s) 529–545

    Abstract: The adrenal has played a major role in the history of pediatric endocrinology. Cases of congenital adrenal hyperplasia (CAH) were reported in the 19th century, leading to the understanding that the adrenal influenced sexual phenotypes as well as being ... ...

    Abstract The adrenal has played a major role in the history of pediatric endocrinology. Cases of congenital adrenal hyperplasia (CAH) were reported in the 19th century, leading to the understanding that the adrenal influenced sexual phenotypes as well as being mysteriously required for survival. Numerous adrenal steroids were isolated in the early 20th century, and bioassays eventually distinguished glucocorticoids, mineralocorticoids, and androgens. Treatment of CAH with cortisone in 1950 by Wilkins and by Bartter and Albright revolutionized clinical endocrinology and launched a productive era of pediatric adrenal research. Through careful clinical studies, Wilkins established the contemporary approach to treating CAH. Alfred Bongiovanni identified defective 21-hydroxylation in CAH in 1957, followed by deficiencies of 3β-hydroxysteroid dehydrogenase and 11β-hydroxylase. P450 enzymes were described in 1962-1964, and 21-hydroxylation was the first activity ascribed to a P450. Accurate assays for 17OH-progesterone in newborns and in response to ACTH permitted the diagnosis of CAH in children and families. Application of the techniques of molecular genetics elucidated genetic and biochemical bases of these disorders from 1984 to 2004. Pediatric endocrinologists played central roles in identifying the genes responsible for both common and rare forms of congenital adrenal hyperplasia and determining their most appropriate treatments.
    MeSH term(s) Humans ; Adrenal Hyperplasia, Congenital/diagnosis ; Adrenal Hyperplasia, Congenital/genetics ; Mineralocorticoids ; Endocrinology ; Glucocorticoids/therapeutic use ; Androgens
    Chemical Substances Mineralocorticoids ; Glucocorticoids ; Androgens
    Language English
    Publishing date 2022-11-29
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2537278-6
    ISSN 1663-2826 ; 1663-2818
    ISSN (online) 1663-2826
    ISSN 1663-2818
    DOI 10.1159/000526468
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  5. Article ; Online: Fluid Infusion Rates for Pediatric Diabetic Ketoacidosis.

    White, Perrin C

    The New England journal of medicine

    2018  Volume 379, Issue 12, Page(s) 1182–1183

    MeSH term(s) Child ; Diabetic Ketoacidosis ; Fluid Therapy ; Humans ; Insulin
    Chemical Substances Insulin
    Language English
    Publishing date 2018-09-27
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMc1810064
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  6. Article ; Online: Alterations of Cortisol Metabolism in Human Disorders.

    White, Perrin C

    Hormone research in paediatrics

    2018  Volume 89, Issue 5, Page(s) 320–330

    Abstract: 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 ... ...

    Abstract 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 diabetes. Mutations in the corresponding HSD11B1 gene, or in the H6PD gene encoding hexose-6-phosphate dehydrogenase (which supplies the NADPH required for the oxoreductase activity of 11-HSD1), cause apparent cortisone reductase deficiency, a rare syndrome of adrenocortical hyperactivity and hyperandrogenism. In contrast, the 11-HSD2 isozyme functions as a dehydrogenase (cortisol to cortisone) and is expressed mainly in mineralocorticoid target tissues, where it bars access of cortisol to the mineralocorticoid receptor. Mutations in the HSD11B2 gene encoding 11-HSD2 cause the syndrome of apparent mineralocorticoid excess, a severe form of familial hypertension. The role of this enzyme in the pathogenesis of common forms of low-renin hypertension remains uncertain.
    MeSH term(s) 11-beta-Hydroxysteroid Dehydrogenase Type 1/genetics ; 11-beta-Hydroxysteroid Dehydrogenase Type 1/metabolism ; Carbohydrate Dehydrogenases/genetics ; Carbohydrate Dehydrogenases/metabolism ; Diabetes Mellitus, Type 2/enzymology ; Diabetes Mellitus, Type 2/genetics ; Humans ; Hydrocortisone/genetics ; Hydrocortisone/metabolism ; Hyperandrogenism/epidemiology ; Hyperandrogenism/genetics ; Hypertension/enzymology ; Hypertension/genetics ; Isoenzymes ; Metabolic Syndrome/enzymology ; Metabolic Syndrome/genetics
    Chemical Substances Isoenzymes ; Carbohydrate Dehydrogenases (EC 1.1.-) ; galactose-6-phosphate dehydrogenase (EC 1.1.1.-) ; 11-beta-Hydroxysteroid Dehydrogenase Type 1 (EC 1.1.1.146) ; HSD11B1 protein, human (EC 1.1.1.146) ; Hydrocortisone (WI4X0X7BPJ)
    Language English
    Publishing date 2018-05-29
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2537278-6
    ISSN 1663-2826 ; 1663-2818
    ISSN (online) 1663-2826
    ISSN 1663-2818
    DOI 10.1159/000485508
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  7. Article ; Online: Update on diagnosis and management of congenital adrenal hyperplasia due to 21-hydroxylase deficiency.

    White, Perrin C

    Current opinion in endocrinology, diabetes, and obesity

    2018  Volume 25, Issue 3, Page(s) 178–184

    Abstract: Purpose of review: Congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency is a relatively common inherited disorder of cortisol biosynthesis that can be fatal if untreated.: Recent findings: The basic biochemistry and genetics of CAH ... ...

    Abstract Purpose of review: Congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency is a relatively common inherited disorder of cortisol biosynthesis that can be fatal if untreated.
    Recent findings: The basic biochemistry and genetics of CAH have been known for decades but continue to be refined by the discoveries of an alternative 'backdoor' metabolic pathway for adrenal androgen synthesis and the secretion of 11-hydroxy and 11-keto analogs of known androgens, by the elucidation of hundreds of new mutations, and by the application of high-throughput sequencing techniques to noninvasive prenatal diagnosis. Although hydrocortisone is a mainstay of treatment, overtreatment may have adverse effects on growth, risk of obesity, and cardiovascular disease; conversely, undertreatment may increase risk of testicular adrenal rest tumors in affected men.
    Summary: Refinements to screening techniques may improve the positive predictive value of newborn screening programs. Alternative dosing forms of hydrocortisone and additional therapeutic modalities are under study. Although surgical treatment of virilized female genitalia is widely accepted by families and patients, it is not without complications or controversy, and some families choose to defer it.
    MeSH term(s) Adrenal Glands/metabolism ; Adrenal Hyperplasia, Congenital/complications ; Adrenal Hyperplasia, Congenital/diagnosis ; Adrenal Hyperplasia, Congenital/therapy ; Androgens/biosynthesis ; Female ; Humans ; Hydrocortisone/biosynthesis ; Hydrocortisone/therapeutic use ; Infant, Newborn ; Male ; Neonatal Screening ; Pregnancy ; Prenatal Diagnosis ; Virilism/etiology ; Virilism/surgery
    Chemical Substances Androgens ; Hydrocortisone (WI4X0X7BPJ)
    Language English
    Publishing date 2018-05-01
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2272017-0
    ISSN 1752-2978 ; 1752-296X
    ISSN (online) 1752-2978
    ISSN 1752-296X
    DOI 10.1097/MED.0000000000000402
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  8. Article ; Online: Impact of the COVID-19 pandemic on management of children and adolescents with Type 1 diabetes.

    Choudhary, Abha / Adhikari, Soumya / White, Perrin C

    BMC pediatrics

    2022  Volume 22, Issue 1, Page(s) 124

    Abstract: Background: The coronavirus disease-2019 (COVID-19) pandemic had widespread impacts on the lives of parents and children. We determined how the pandemic affected Type 1 diabetes patients at a large urban pediatric teaching hospital.: Methods: We ... ...

    Abstract Background: The coronavirus disease-2019 (COVID-19) pandemic had widespread impacts on the lives of parents and children. We determined how the pandemic affected Type 1 diabetes patients at a large urban pediatric teaching hospital.
    Methods: We compared patient characteristics, glycemic control, PHQ-9 depression screen, in person and virtual outpatient encounters, hospitalizations and continuous glucose monitor (CGM) utilization in approximately 1600 patients in 1 year periods preceding and following the local imposition of COVID-related restrictions on 3/15/2020 ("2019" and "2020" groups, respectively).
    Results: In a generalized linear model, increasing age, non-commercial insurance, Black and Hispanic race/ethnicity, and non-utilization of CGMs were all associated with higher hemoglobin A1c (HbA1c), but there was no difference between the 2019 and 2020 groups. The time in range in CGM users was lower with non-commercial insurance and in Black and Hispanic patients; it improved slightly from 2019 to 2020. CGM utilization by patients with non-commercial insurance (93% of such patients were in government programs, 7% uninsured or "other") increased markedly. In 2020, patients with commercial insurance (i.e., private-pay or provided by an employer) had fewer office visits, but insurance status did not influence utilization of the virtual visit platform. There was no change in hospitalization frequency from 2019 to 2020 in either commercially or non-commercially insured patients, but patients with non-commercial insurance were hospitalized at markedly higher frequencies in both years. PHQ-9 scores were unchanged.
    Conclusions: Hospitalization frequency, glycemic control and depression screening were unchanged in our large urban pediatric teaching hospital during the COVID pandemic. Increased utilization of CGM and rapid adoption of telemedicine may have ameliorated the impact of the pandemic on disease management.
    MeSH term(s) Adolescent ; COVID-19/epidemiology ; Child ; Diabetes Mellitus, Type 1/epidemiology ; Diabetes Mellitus, Type 1/therapy ; Humans ; Insurance Coverage ; Pandemics ; SARS-CoV-2
    Language English
    Publishing date 2022-03-10
    Publishing country England
    Document type Journal Article
    ZDB-ID 2041342-7
    ISSN 1471-2431 ; 1471-2431
    ISSN (online) 1471-2431
    ISSN 1471-2431
    DOI 10.1186/s12887-022-03189-2
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  9. Article ; Online: Optimizing fluid management of diabetic ketoacidosis.

    White, Perrin C

    Pediatric diabetes

    2015  Volume 16, Issue 5, Page(s) 317–319

    MeSH term(s) Brain Edema/epidemiology ; Diabetic Ketoacidosis/epidemiology ; Diabetic Ketoacidosis/therapy ; Female ; Fluid Therapy/methods ; Humans ; Male
    Language English
    Publishing date 2015-08
    Publishing country Denmark
    Document type Comment ; Editorial
    ZDB-ID 1502504-4
    ISSN 1399-5448 ; 1745-1426 ; 1399-543X
    ISSN (online) 1399-5448
    ISSN 1745-1426 ; 1399-543X
    DOI 10.1111/pedi.12274
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  10. Article: Alterations of Cortisol Metabolism in Human Disorders

    White, Perrin C.

    Hormone Research in Paediatrics

    2018  Volume 89, Issue 5, Page(s) 320–330

    Abstract: 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 ... ...

    Institution Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas, USA
    Abstract 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 diabetes. Mutations in the corresponding HSD11B1 gene, or in the H6PD gene encoding hexose-6-phosphate dehydrogenase (which supplies the NADPH required for the oxoreductase activity of 11-HSD1), cause apparent cortisone reductase deficiency, a rare syndrome of adrenocortical hyperactivity and hyperandrogenism. In contrast, the 11-HSD2 isozyme functions as a dehydrogenase (cortisol to cortisone) and is expressed mainly in mineralocorticoid target tissues, where it bars access of cortisol to the mineralocorticoid receptor. Mutations in the HSD11B2 gene encoding 11-HSD2 cause the syndrome of apparent mineralocorticoid excess, a severe form of familial hypertension. The role of this enzyme in the pathogenesis of common forms of low-renin hypertension remains uncertain.
    Keywords 11β-Hydroxysteroid dehydrogenase ; Hexose-6-phosphate dehydrogenase ; Hypertension ; Cortisol ; Cortisone ; Type 2 diabetes
    Language English
    Publishing date 2018-05-29
    Publisher S. Karger AG
    Publishing place Basel, Switzerland
    Document type Article
    Note Mini Review
    ZDB-ID 2537278-6
    ISBN 978-3-318-06359-2 ; 3-318-06359-2
    ISSN 1663-2826 ; 1663-2818
    ISSN (online) 1663-2826
    ISSN 1663-2818
    DOI 10.1159/000485508
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