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Thematische Bibliographien / Hypothalamic-pituitary-adrenal axis / Zeitschriftenartikel

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Zeitschriftenartikel zum Thema „Hypothalamic-pituitary-adrenal axis“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 23. Februar 2023

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1

Kirnap, Mehmet, Hulusi Atmaca, Fatih Tanriverdi, Osman Ozsoy, Kursad Unluhizarci und Fahrettin Kelestimur. „Hypothalamic-pituitary-adrenal axis in patients with ankylosing spondylitis“. HORMONES 7, Nr. 3 (15.07.2008): 255–58. http://dx.doi.org/10.14310/horm.2002.1206.

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2

Honour, J. W. „Hypothalamic-pituitary-adrenal axis“. Respiratory Medicine 88 (August 1994): 9–15. http://dx.doi.org/10.1016/s0954-6111(05)80035-6.

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3

Chez, Ronald A. „Fetal hypothalamic-pituitary-adrenal axis“. American Journal of Obstetrics and Gynecology 183, Nr. 5 (November 2000): 1310. http://dx.doi.org/10.1067/mob.2000.107737.

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4

Gordon, D., C. G. Semple, G. H. Beastall und J. A. Thomson. „A study of hypothalamic-pituitary-adrenal suppression following curative surgery for Cushing's syndrome due to adrenal adenoma“. Acta Endocrinologica 114, Nr. 2 (Februar 1987): 166–70. http://dx.doi.org/10.1530/acta.0.1140166.

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Abstract. The hypothalamic-pituitary-adrenal axis was investigated in all six patients requiring glucocorticoid replacement 2.5–11 years after unilateral adrenalectomy for adrenal adenomas causing Cushing's syndrome. The hypothalamic-pituitary-adrenal axis was assessed by insulin induced hypoglycaemia and CRF testing in each patient. Two patients showed normal cortisol and ACTH responses to hypoglycaemia. Two patients showed subnormal cortisol responses to hypoglycaemia in the presence of high or normal basal ACTH concentrations. ACTH concentrations increased with both hypoglycaemia and CRF. Two patients showed subnormal cortisol responses to hypoglycaemia and CRF. One of these patients showed an ACTH rise following hypoglycaemia but not CRF. Defects at either hypothalamic-pituitary or adrenal levels were demonstrated and recovery of the axis appears to commence at the hypothalamic-pituitary level.

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5

Zapanti, Evangelia, Konstantinos Terzidis und George Chrousos. „Dysfunction of the Hypothalamic-Pituitary-Adrenal axis in HIV infection and disease“. HORMONES 7, Nr. 3 (15.07.2008): 205–16. http://dx.doi.org/10.14310/horm.2002.1200.

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6

ARATÓ, MIHÁLY, CSABA M. BANKI, CHARLES B. NEMEROFF und GARTH BISSETTE. „Hypothalamic-Pituitary-Adrenal Axis and Suicide“. Annals of the New York Academy of Sciences 487, Nr. 1 Psychobiology (Dezember 1986): 263–70. http://dx.doi.org/10.1111/j.1749-6632.1986.tb27905.x.

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7

BATEMAN, ANDREW, AVA SINGH, THOMAS KRAL und SAMUEL SOLOMON. „The Immune-Hypothalamic-Pituitary-Adrenal Axis*“. Endocrine Reviews 10, Nr. 1 (Februar 1989): 92–112. http://dx.doi.org/10.1210/edrv-10-1-92.

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8

Altamura, A. Carlo. „Hypothalamic-pituitary-adrenal axis in schizophrenia“. Biological Psychiatry 40, Nr. 6 (September 1996): 560–61. http://dx.doi.org/10.1016/0006-3223(96)85271-1.

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9

Lilly, Michael P. „The Hypothalamic-Pituitary-Adrenal—Immune Axis“. Archives of Surgery 127, Nr. 12 (01.12.1992): 1463. http://dx.doi.org/10.1001/archsurg.1992.01420120097017.

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10

Watson, Paddy Burges. „The hypothalamic/pituitary/adrenal axis revisited“. Stress Medicine 5, Nr. 3 (Juli 1989): 141–43. http://dx.doi.org/10.1002/smi.2460050303.

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11

Musselman, Dominique L., und Charles B. Nemeroff. „Depression and Endocrine Disorders: Focus on the Thyroid and Adrenal System“. British Journal of Psychiatry 168, S30 (Juni 1996): 123–28. http://dx.doi.org/10.1192/s0007125000298504.

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Of the various hypothalamic–pituitary–end organ axes, the thyroid and adrenal systems have been implicated most often in affective disorders. Patients with primary thyroid disease have high rates of depression, and patients with Addison's disease or Cushing's syndrome have relatively high rates of affective and anxiety symptoms. However, the major support for these endocrine axes in the pathophysiology of mood disorders comes from studies in which alterations in components of the hypothalamic–pituitary–thyroid (HPT) and the hypothalamic–pituitary–adrenal (HPA) axes have been documented in patients with primary depression. Concerning the HPT axis, depressed patients have been reported to have: (a) alterations in thyroid-stimulating hormone response to thyrotropin-releasing hormone (TRH); (b) an abnormally high rate of antithyroid antibodies; and (c) elevated cerebrospinal fluid (CSF) TRH concentrations. Moreover, tri-iodothyronine has been shown conclusively to augment the efficacy of various antidepressants. Concerning the HPA axis, depressed patients have been reported to exhibit: (a) adrenocorticoid hypersecretion; (b) enlarged pituitary and adrenal gland size; and (c) elevated CSF corticotropin-releasing factor concentrations. All of the HPA axis alterations in depression studied thus far are state-dependent, whereas the HPT axis alterations may be partially trait and partially state markers.

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12

Kalaria, Tejas, Mayuri Agarwal, Sukhbir Kaur, Lauren Hughes, Hayley Sharrod-Cole, Rahul Chaudhari, Carolina Gherman-Ciolac et al. „Hypothalamic–pituitary–adrenal axis suppression – The value of salivary cortisol and cortisone in assessing hypothalamic–pituitary–adrenal recovery“. Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 57, Nr. 6 (13.10.2020): 456–60. http://dx.doi.org/10.1177/0004563220961745.

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Background The 0.25 mg short synacthen test is used to assess recovery from hypothalamic–pituitary–adrenal suppression due to chronic glucocorticoid administration. We assessed the potential role of salivary cortisol and cortisone in predicting hypothalamic–pituitary–adrenal function using the short synacthen test as the gold standard test. Method Between 09:00 and 10:30, salivary and blood samples were collected just prior to a short synacthen test to assess hypothalamic–pituitary–adrenal axis recovery in patients previously treated with oral glucocorticoids. The cut-off for a normal short synacthen test was a 30-min cortisol ≥450 nmol/L. Results Fifty-six short synacthen tests were performed on 47 patients. Of these, 15 were normal. The area under receiver operating characteristic curves for serum cortisol, salivary cortisone and salivary cortisol were 0.772, 0.785 and 0.770, respectively. From the receiver operating characteristic analysis, the cut-offs for baseline serum cortisol (≥365 nmol/L) and salivary cortisone (≥37.2 nmol) predicted hypothalamic–pituitary–adrenal axis recovery with 100% specificity in 26.7% of pass short synacthen tests, whereas salivary cortisol predicted none. Baseline serum cortisol (≤170 nmol/L), salivary cortisone (≤9.42 nmol/L) and salivary cortisol (≤1.92 nmol/L) predicted hypothalamic–pituitary–adrenal suppression with 100% sensitivity in 58.5%, 53.7% and 51.2% of failed short synacthen tests, respectively. Using these cut-offs, baseline serum cortisol, salivary cortisone and salivary cortisol could reduce the need for short synacthen tests by 50%, 46% and 37%, respectively. Conclusion Although marginally inferior to early morning serum cortisol, early morning salivary cortisone may be used as a first-line test for assessing hypothalamic–pituitary–adrenal function. We plan to incorporate salivary cortisone into a home-based patient pathway to identify patients with hypothalamic–pituitary–adrenal recovery, continuing hypothalamic–pituitary–adrenal suppression and those who require a short synacthen test.

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13

Wand, Gary S. „Alcohol and the Hypothalamic-Pituitary–Adrenal Axis“. Endocrinologist 9, Nr. 5 (September 1999): 333–41. http://dx.doi.org/10.1097/00019616-199909000-00003.

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14

Stokes, Peter E., und Carolyn R. Sikes. „Hypothalamic-Pituitary-Adrenal Axis in Psychiatric Disorders“. Annual Review of Medicine 42, Nr. 1 (Februar 1991): 519–31. http://dx.doi.org/10.1146/annurev.me.42.020191.002511.

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15

&NA;. „Dexamethasone suppresses the hypothalamic-pituitary-adrenal axis“. Inpharma Weekly &NA;, Nr. 753 (September 1990): 16–17. http://dx.doi.org/10.2165/00128413-199007530-00052.

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16

Besnier, Emmanuel, Thomas Clavier und Vincent Compere. „The Hypothalamic–Pituitary–Adrenal Axis and Anesthetics“. Anesthesia & Analgesia 124, Nr. 4 (April 2017): 1181–89. http://dx.doi.org/10.1213/ane.0000000000001580.

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17

Imrich, Richard, und Jozef Rovenský. „Hypothalamic-Pituitary-Adrenal Axis in Rheumatoid Arthritis“. Rheumatic Disease Clinics of North America 36, Nr. 4 (November 2010): 721–27. http://dx.doi.org/10.1016/j.rdc.2010.09.003.

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18

HARBUZ, M. S., G. L. CONDE, O. MARTI, S. L. LIGHTMAN und D. S. JESSOP. „The Hypothalamic-Pituitary-Adrenal Axis in Autoimmunity“. Annals of the New York Academy of Sciences 823, Nr. 1 Neuropsychiat (August 1997): 214–24. http://dx.doi.org/10.1111/j.1749-6632.1997.tb48393.x.

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19

Young, Elizabeth A., und William Coryell. „Suicide and the hypothalamic-pituitary-adrenal axis“. Lancet 366, Nr. 9490 (September 2005): 959–61. http://dx.doi.org/10.1016/s0140-6736(05)67348-5.

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20

Thorén, Marja, Carina Stenfors, Bo Apéria und Aleksander A. Mathé. „Hypothalamic-pituitary-adrenal axis interaction with prostaglandins“. Progress in Neuro-Psychopharmacology and Biological Psychiatry 14, Nr. 3 (Januar 1990): 319–26. http://dx.doi.org/10.1016/0278-5846(90)90020-h.

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21

Daban, C., E. Vieta, P. Mackin und A. H. Young. „Hypothalamic-pituitary-adrenal Axis and Bipolar Disorder“. Psychiatric Clinics of North America 28, Nr. 2 (Juni 2005): 469–80. http://dx.doi.org/10.1016/j.psc.2005.01.005.

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22

MEROLA, B., S. LONGOBARDI, A. COLAO, C. DI SOMMA, D. FERONE, E. ROSSI, V. COVELLI und G. LOMBARDI. „Hypothalamic-Pituitary-Adrenal Axis in Neuropsychiatric Disorders“. Annals of the New York Academy of Sciences 741, Nr. 1 Neuroimmunomo (November 1994): 263–70. http://dx.doi.org/10.1111/j.1749-6632.1994.tb23109.x.

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23

Papadimitriou, Anastasios, und Kostas N. Priftis. „Regulation of the Hypothalamic-Pituitary-Adrenal Axis“. Neuroimmunomodulation 16, Nr. 5 (2009): 265–71. http://dx.doi.org/10.1159/000216184.

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24

Blackburn, Susan. „The Hypothalamic-Pituitary-Adrenal Axis During Pregnancy“. Journal of Perinatal & Neonatal Nursing 24, Nr. 1 (Januar 2010): 10–11. http://dx.doi.org/10.1097/jpn.0b013e3181cf5bec.

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25

Chalew, Stuart, Heinz Nagel und Shirah Shore. „The Hypothalamic-Pituitary-Adrenal Axis in Obesity“. Obesity Research 3, Nr. 4 (Juli 1995): 371–82. http://dx.doi.org/10.1002/j.1550-8528.1995.tb00163.x.

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26

Hermus, A. R. M. M., und C. G. J. Sweep. „Cytokines and the hypothalamic-pituitary-adrenal axis“. Journal of Steroid Biochemistry and Molecular Biology 37, Nr. 6 (Dezember 1990): 867–71. http://dx.doi.org/10.1016/0960-0760(90)90434-m.

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27

Paul, Bidisha, Zachary R. Sterner, Daniel R. Buchholz, Yun-Bo Shi und Laurent M. Sachs. „Thyroid and Corticosteroid Signaling in Amphibian Metamorphosis“. Cells 11, Nr. 10 (10.05.2022): 1595. http://dx.doi.org/10.3390/cells11101595.

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In multicellular organisms, development is based in part on the integration of communication systems. Two neuroendocrine axes, the hypothalamic–pituitary–thyroid and the hypothalamic–pituitary–adrenal/interrenal axes, are central players in orchestrating body morphogenesis. In all vertebrates, the hypothalamic–pituitary–thyroid axis controls thyroid hormone production and release, whereas the hypothalamic–pituitary–adrenal/interrenal axis regulates the production and release of corticosteroids. One of the most salient effects of thyroid hormones and corticosteroids in post-embryonic developmental processes is their critical role in metamorphosis in anuran amphibians. Metamorphosis involves modifications to the morphological and biochemical characteristics of all larval tissues to enable the transition from one life stage to the next life stage that coincides with an ecological niche switch. This transition in amphibians is an example of a widespread phenomenon among vertebrates, where thyroid hormones and corticosteroids coordinate a post-embryonic developmental transition. The review addresses the functions and interactions of thyroid hormone and corticosteroid signaling in amphibian development (metamorphosis) as well as the developmental roles of these two pathways in vertebrate evolution.

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28

Miller, Walter L. „The Hypothalamic-Pituitary-Adrenal Axis: A Brief History“. Hormone Research in Paediatrics 89, Nr. 4 (2018): 212–23. http://dx.doi.org/10.1159/000487755.

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The hypothalamic-pituitary-adrenal (HPA) axis is central to homeostasis, stress responses, energy metabolism, and neuropsychiatric function. The history of this complex system involves discovery of the relevant glands (adrenal, pituitary, hypothalamus), hormones (cortisol, corticotropin, corticotropin-releasing hormone), and the receptors for these hormones. The adrenal and pituitary were identified by classical anatomists, but most of this history has taken place rather recently, and has involved complex chemistry, biochemistry, genetics, and clinical investigation. The integration of the HPA axis with modern neurology and psychiatry has cemented the role of endocrinology in contemporary studies of behavior.

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Tian, Yu-Feng, Cheng-Hsien Lin, Shu-Fen Hsu und Mao-Tsun Lin. „Melatonin Improves Outcomes of Heatstroke in Mice by Reducing Brain Inflammation and Oxidative Damage and Multiple Organ Dysfunction“. Mediators of Inflammation 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/349280.

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We report here that when untreated mice underwent heat stress, they displayed thermoregulatory deficit (e.g., animals display hypothermia during room temperature exposure), brain (or hypothalamic) inflammation, ischemia, oxidative damage, hypothalamic-pituitary-adrenal axis impairment (e.g., decreased plasma levels of both adrenocorticotrophic hormone and corticosterone during heat stress), multiple organ dysfunction or failure, and lethality. Melatonin therapy significantly reduced the thermoregulatory deficit, brain inflammation, ischemia, oxidative damage, hypothalamic-pituitary-adrenal axis impairment, multiple organ dysfunction, and lethality caused by heat stroke. Our data indicate that melatonin may improve outcomes of heat stroke by reducing brain inflammation, oxidative damage, and multiple organ dysfunction.

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Igaz, Péter, Károly >Rácz, Miklós Tóth, Edit Gláz und Zsolt Tulassay. „Treatment of iatrogenic Cushing’s syndrome: questions of glucocorticoid withdrawal“. Orvosi Hetilap 148, Nr. 5 (Februar 2007): 195–202. http://dx.doi.org/10.1556/oh.2007.27964.

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Iatrogenic Cushing’s syndrome is the most common form of hypercortisolism. Glucocorticoids are widely used for the treatment of various diseases, often in high doses that may lead to the development of severe hypercortisolism. Iatrogenic hypercortisolism is unique, as the application of exogenous glucocorticoids leads to the simultaneous presence of symptoms specific for hypercortisolism and the suppression of the endogenous hypothalamic-pituitary-adrenal axis. The principal question of its therapy is related to the problem of glucocorticoid withdrawal. There is considerable interindividual variability in the suppression and recovery of the hypothalamic-pituitary-adrenal axis, therefore, glucocorticoid withdrawal and substitution can only be conducted in a stepwise manner with careful clinical follow-up and regular laboratory examinations regarding endogenous hypothalamic-pituitary-adrenal axis activity. Three major complications which can be associated with glucocorticoid withdrawal are: i. reactivation of the underlying disease, ii. secondary adrenal insufficiency, iii. steroid withdrawal syndrome. Here, the authors summarize the most important aspects of this area based on their clinical experience and the available literature data.

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31

Bailey, Michael, Harald Engler, John Hunzeker und John F. Sheridan. „The Hypothalamic-Pituitary-Adrenal Axis and Viral Infection“. Viral Immunology 16, Nr. 2 (Juni 2003): 141–57. http://dx.doi.org/10.1089/088282403322017884.

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32

Johnson, Karen L., und Cindy Renn RN. „The Hypothalamic-Pituitary-Adrenal Axis in Critical Illness“. AACN Clinical Issues: Advanced Practice in Acute and Critical Care 17, Nr. 1 (Januar 2006): 39–49. http://dx.doi.org/10.1097/00044067-200601000-00006.

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33

Imrich, R. „Hypothalamic-pituitary-adrenal axis function in ankylosing spondylitis“. Annals of the Rheumatic Diseases 63, Nr. 6 (17.03.2004): 671–74. http://dx.doi.org/10.1136/ard.2003.006940.

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34

Pyter, Leah M., Jaimie D. Adelson und Randy J. Nelson. „Short Days Increase Hypothalamic-Pituitary-Adrenal Axis Responsiveness“. Endocrinology 148, Nr. 7 (01.07.2007): 3402–9. http://dx.doi.org/10.1210/en.2006-1432.

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35

Bussone, Gennaro, Massimo Leone, Boris M. Zappacosta, Giorgia Patruno, Sergio Valentini, Fabio Frediani und Eugenio A. Parati. „Hypothalamic-Pituitary-Adrenal Axis Evaluation in Cluster Headache“. Cephalalgia 11, Nr. 11_suppl (Juni 1991): 244–45. http://dx.doi.org/10.1177/0333102491011s11131.

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36

Arnett, Melinda G., Lisa M. Muglia, Gloria Laryea und Louis J. Muglia. „Genetic Approaches to Hypothalamic-Pituitary-Adrenal Axis Regulation“. Neuropsychopharmacology 41, Nr. 1 (20.07.2015): 245–60. http://dx.doi.org/10.1038/npp.2015.215.

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37

Morsi, Amr, Donald DeFranco und Selma F. Witchel. „The Hypothalamic-Pituitary-Adrenal Axis and the Fetus“. Hormone Research in Paediatrics 89, Nr. 5 (2018): 380–87. http://dx.doi.org/10.1159/000488106.

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Glucocorticoids (GCs), cortisol in humans, influence multiple essential maturational events during gestation. In the human fetus, fetal hypothalamic-pituitary-adrenal (HPA) axis function, fetal adrenal steroidogenesis, placental 11β- hydroxysteroid dehydrogenase type 2 activity, maternal cortisol concentrations, and environmental factors impact fetal cortisol exposure. The beneficial effects of synthetic glucocorticoids (sGCs), such as dexamethasone and betamethasone, on fetal lung maturation have significantly shifted the management of preterm labor and threatened preterm birth. Accumulating evidence suggests that exposure to sGCs in utero at critical developmental stages can alter the function of organ systems and that these effects may have sequelae that extend into adult life. Maternal stress and environmental influences may also impact fetal GC exposure. This article explores the vulnerability of the fetal HPA axis to endogenous GCs and exogenous sGCs.

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38

Tsigos, Constantine, und George P. Chrousos. „Hypothalamic–pituitary–adrenal axis, neuroendocrine factors and stress“. Journal of Psychosomatic Research 53, Nr. 4 (Oktober 2002): 865–71. http://dx.doi.org/10.1016/s0022-3999(02)00429-4.

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39

Kjaer, A., P. J. Larsen, U. Knigge und J. Warberg. „Histaminergic activation of the hypothalamic-pituitary-adrenal axis.“ Endocrinology 135, Nr. 3 (September 1994): 1171–77. http://dx.doi.org/10.1210/endo.135.3.8070360.

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40

Ng, P. C. „The fetal and neonatal hypothalamic-pituitary-adrenal axis“. Archives of Disease in Childhood - Fetal and Neonatal Edition 82, Nr. 3 (01.05.2000): 250F—254. http://dx.doi.org/10.1136/fn.82.3.f250.

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41

GROSSMAN, ASHLEY, ALFREDO COSTA, MARY FORSLING, RICHARD JACOBS, PIERLUIGI NAVARRA und MARIA SATTA. „Immune Modulation of the Hypothalamic-Pituitary-Adrenal Axis.“ Annals of the New York Academy of Sciences 823, Nr. 1 Neuropsychiat (August 1997): 225–33. http://dx.doi.org/10.1111/j.1749-6632.1997.tb48394.x.

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42

Priftis, Kostas N., Anastasios Papadimitriou, Polyxeni Nicolaidou und George P. Chrousos. „The hypothalamic–pituitary–adrenal axis in asthmatic children“. Trends in Endocrinology & Metabolism 19, Nr. 1 (Januar 2008): 32–38. http://dx.doi.org/10.1016/j.tem.2007.10.005.

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43

Wand, Gary S., und Robert L. Ney. „2 Disorders of the hypothalamic-pituitary-adrenal axis“. Clinics in Endocrinology and Metabolism 14, Nr. 1 (Februar 1985): 33–53. http://dx.doi.org/10.1016/s0300-595x(85)80064-5.

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44

Licinio, Júlio, Ma-Li Wong und Philip W. Gold. „The hypothalamic-pituitary-adrenal axis in anorexia nervosa“. Psychiatry Research 62, Nr. 1 (April 1996): 75–83. http://dx.doi.org/10.1016/0165-1781(96)02991-5.

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45

Schuetz, Philipp, und Beat Müller. „The Hypothalamic-Pituitary-Adrenal Axis in Critical Illness“. Endocrinology and Metabolism Clinics of North America 35, Nr. 4 (Dezember 2006): 823–38. http://dx.doi.org/10.1016/j.ecl.2006.09.013.

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46

Martin, Wrivu N., Craig E. Pennell, Carol A. Wang und Rebecca Reynolds. „Developmental programming and the hypothalamic–pituitary–adrenal axis“. Current Opinion in Endocrine and Metabolic Research 13 (August 2020): 13–19. http://dx.doi.org/10.1016/j.coemr.2020.07.010.

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47

Roy, Monique, Bronwyn Collier und Alec Roy. „Hypothalamic-pituitary-adrenal axis dysregulation among diabetic outpatients“. Psychiatry Research 31, Nr. 1 (Januar 1990): 31–37. http://dx.doi.org/10.1016/0165-1781(90)90106-f.

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48

Catena, M., S. Gorini Amedei, L. Faravelli, F. Rotella, A. Scarpato, A. Palla, A. Veltri et al. „Stress related disorders: Hypothalamic-pituitary-adrenal axis dysfunctions.“ European Psychiatry 22 (März 2007): S269. http://dx.doi.org/10.1016/j.eurpsy.2007.01.906.

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49

Hirai, Masaharu, Susumu Miyabo, Eiichi Ooya, Ken Miyanaga, Naoki Aoyagi, Kazuhiro Kimura, Shigeru Kishida und Tsuguhiko Nakai. „Endothelin-3 stimulates the hypothalamic-pituitary-adrenal axis“. Life Sciences 48, Nr. 24 (Januar 1991): 2359–63. http://dx.doi.org/10.1016/0024-3205(91)90273-e.

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Kent, Pam, Hymie Anisman und Zul Merali. „Central Bombesin Activates the Hypothalamic-Pituitary-Adrenal Axis“. Neuroendocrinology 73, Nr. 3 (2001): 203–14. http://dx.doi.org/10.1159/000054637.

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