Articles de revues : « Hypothalamic-pituitary-adrenal axis »

1

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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Kirnap, Mehmet, Hulusi Atmaca, Fatih Tanriverdi, Osman Ozsoy, Kursad Unluhizarci, and Fahrettin Kelestimur. "Hypothalamic-pituitary-adrenal axis in patients with ankylosing spondylitis." HORMONES 7, no. 3 (July 15, 2008): 255–58. http://dx.doi.org/10.14310/horm.2002.1206.

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Chez, Ronald A. "Fetal hypothalamic-pituitary-adrenal axis." American Journal of Obstetrics and Gynecology 183, no. 5 (November 2000): 1310. http://dx.doi.org/10.1067/mob.2000.107737.

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Gordon, D., C. G. Semple, G. H. Beastall, and J. A. Thomson. "A study of hypothalamic-pituitary-adrenal suppression following curative surgery for Cushing's syndrome due to adrenal adenoma." Acta Endocrinologica 114, no. 2 (February 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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Musselman, Dominique L., and Charles B. Nemeroff. "Depression and Endocrine Disorders: Focus on the Thyroid and Adrenal System." British Journal of Psychiatry 168, S30 (June 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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ARATÓ, MIHÁLY, CSABA M. BANKI, CHARLES B. NEMEROFF, and GARTH BISSETTE. "Hypothalamic-Pituitary-Adrenal Axis and Suicide." Annals of the New York Academy of Sciences 487, no. 1 Psychobiology (December 1986): 263–70. http://dx.doi.org/10.1111/j.1749-6632.1986.tb27905.x.

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BATEMAN, ANDREW, AVA SINGH, THOMAS KRAL, and SAMUEL SOLOMON. "The Immune-Hypothalamic-Pituitary-Adrenal Axis*." Endocrine Reviews 10, no. 1 (February 1989): 92–112. http://dx.doi.org/10.1210/edrv-10-1-92.

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Altamura, A. Carlo. "Hypothalamic-pituitary-adrenal axis in schizophrenia." Biological Psychiatry 40, no. 6 (September 1996): 560–61. http://dx.doi.org/10.1016/0006-3223(96)85271-1.

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Lilly, Michael P. "The Hypothalamic-Pituitary-Adrenal—Immune Axis." Archives of Surgery 127, no. 12 (December 1, 1992): 1463. http://dx.doi.org/10.1001/archsurg.1992.01420120097017.

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Watson, Paddy Burges. "The hypothalamic/pituitary/adrenal axis revisited." Stress Medicine 5, no. 3 (July 1989): 141–43. http://dx.doi.org/10.1002/smi.2460050303.

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Keller‐Wood, Maureen. "Hypothalamic‐Pituitary‐Adrenal Axis—Feedback Control." Comprehensive Physiology 5, no. 3 (July 2015): 1161–82. https://doi.org/10.1002/j.2040-4603.2015.tb00644.x.

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ABSTRACTThe hypothalamo‐pituitary‐adrenal axis (HPA) is responsible for stimulation of adrenal corticosteroids in response to stress. Negative feedback control by corticosteroids limits pituitary secretion of corticotropin, ACTH, and hypothalamic secretion of corticotropin‐releasing hormone, CRH, and vasopressin, AVP, resulting in regulation of both basal and stress‐induced ACTH secretion. The negative feedback effect of corticosteroids occurs by action of corticosteroids at mineralocorticoid receptors (MR) and/or glucocorticoid receptors (GRs) located in multiple sites in the brain and in the pituitary. The mechanisms of negative feedback vary according to the receptor type and location within the brain‐hypothalmo‐pituitary axis. A very rapid nongenomic action has been demonstrated for GR action on CRH neurons in the hypothalamus, and somewhat slower nongenomic effects are observed in the pituitary or other brain sites mediated by GR and/or MR. Corticosteroids also have genomic actions, including repression of the pro‐opiomelanocortin (POMC) gene in the pituitary and CRH and AVP genes in the hypothalamus. The rapid effect inhibits stimulated secretion, but requires a rapidly rising corticosteroid concentration. The more delayed inhibitory effect on stimulated secretion is dependent on the intensity of the stimulus and the magnitude of the corticosteroid feedback signal, but also the neuroanatomical pathways responsible for activating the HPA. The pathways for activation of some stressors may partially bypass hypothalamic feedback sites at the CRH neuron, whereas others may not involve forebrain sites; therefore, some physiological stressors may override or bypass negative feedback, and other psychological stressors may facilitate responses to subsequent stress. © 2015 American Physiological Society. Compr Physiol 5:1161‐1182, 2015.

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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, no. 6 (October 13, 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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Paul, Bidisha, Zachary R. Sterner, Daniel R. Buchholz, Yun-Bo Shi, and Laurent M. Sachs. "Thyroid and Corticosteroid Signaling in Amphibian Metamorphosis." Cells 11, no. 10 (May 10, 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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Zapanti, Evangelia, Konstantinos Terzidis, and George Chrousos. "Dysfunction of the Hypothalamic-Pituitary-Adrenal axis in HIV infection and disease." HORMONES 7, no. 3 (July 15, 2008): 205–16. http://dx.doi.org/10.14310/horm.2002.1200.

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Miller, Walter L. "The Hypothalamic-Pituitary-Adrenal Axis: A Brief History." Hormone Research in Paediatrics 89, no. 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, and 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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Wand, Gary S. "Alcohol and the Hypothalamic-Pituitary–Adrenal Axis." Endocrinologist 9, no. 5 (September 1999): 333–41. http://dx.doi.org/10.1097/00019616-199909000-00003.

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Stokes, Peter E., and Carolyn R. Sikes. "Hypothalamic-Pituitary-Adrenal Axis in Psychiatric Disorders." Annual Review of Medicine 42, no. 1 (February 1991): 519–31. http://dx.doi.org/10.1146/annurev.me.42.020191.002511.

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&NA;. "Dexamethasone suppresses the hypothalamic-pituitary-adrenal axis." Inpharma Weekly &NA;, no. 753 (September 1990): 16–17. http://dx.doi.org/10.2165/00128413-199007530-00052.

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KARIMA A. ABDEL KHALAK, M.D.*;, HANAN A. E. ABDELNABY, M. Sc *. and. "Hypothalamic Pituitary Adrenal Axis in Asthmatic Children." Medical Journal of Cairo University 92, no. 09 (September 1, 2024): 705–8. http://dx.doi.org/10.21608/mjcu.2024.389770.

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Besnier, Emmanuel, Thomas Clavier, and Vincent Compere. "The Hypothalamic–Pituitary–Adrenal Axis and Anesthetics." Anesthesia & Analgesia 124, no. 4 (April 2017): 1181–89. http://dx.doi.org/10.1213/ane.0000000000001580.

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Imrich, Richard, and Jozef Rovenský. "Hypothalamic-Pituitary-Adrenal Axis in Rheumatoid Arthritis." Rheumatic Disease Clinics of North America 36, no. 4 (November 2010): 721–27. http://dx.doi.org/10.1016/j.rdc.2010.09.003.

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HARBUZ, M. S., G. L. CONDE, O. MARTI, S. L. LIGHTMAN, and D. S. JESSOP. "The Hypothalamic-Pituitary-Adrenal Axis in Autoimmunity." Annals of the New York Academy of Sciences 823, no. 1 Neuropsychiat (August 1997): 214–24. http://dx.doi.org/10.1111/j.1749-6632.1997.tb48393.x.

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Young, Elizabeth A., and William Coryell. "Suicide and the hypothalamic-pituitary-adrenal axis." Lancet 366, no. 9490 (September 2005): 959–61. http://dx.doi.org/10.1016/s0140-6736(05)67348-5.

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Thorén, Marja, Carina Stenfors, Bo Apéria, and Aleksander A. Mathé. "Hypothalamic-pituitary-adrenal axis interaction with prostaglandins." Progress in Neuro-Psychopharmacology and Biological Psychiatry 14, no. 3 (January 1990): 319–26. http://dx.doi.org/10.1016/0278-5846(90)90020-h.

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Daban, C., E. Vieta, P. Mackin, and A. H. Young. "Hypothalamic-pituitary-adrenal Axis and Bipolar Disorder." Psychiatric Clinics of North America 28, no. 2 (June 2005): 469–80. http://dx.doi.org/10.1016/j.psc.2005.01.005.

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MEROLA, B., S. LONGOBARDI, A. COLAO, C. DI SOMMA, D. FERONE, E. ROSSI, V. COVELLI, and G. LOMBARDI. "Hypothalamic-Pituitary-Adrenal Axis in Neuropsychiatric Disorders." Annals of the New York Academy of Sciences 741, no. 1 Neuroimmunomo (November 1994): 263–70. http://dx.doi.org/10.1111/j.1749-6632.1994.tb23109.x.

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Papadimitriou, Anastasios, and Kostas N. Priftis. "Regulation of the Hypothalamic-Pituitary-Adrenal Axis." Neuroimmunomodulation 16, no. 5 (2009): 265–71. http://dx.doi.org/10.1159/000216184.

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Blackburn, Susan. "The Hypothalamic-Pituitary-Adrenal Axis During Pregnancy." Journal of Perinatal & Neonatal Nursing 24, no. 1 (January 2010): 10–11. http://dx.doi.org/10.1097/jpn.0b013e3181cf5bec.

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Hermus, A. R. M. M., and C. G. J. Sweep. "Cytokines and the hypothalamic-pituitary-adrenal axis." Journal of Steroid Biochemistry and Molecular Biology 37, no. 6 (December 1990): 867–71. http://dx.doi.org/10.1016/0960-0760(90)90434-m.

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Chalew, Stuart, Heinz Nagel, and Shirah Shore. "The Hypothalamic-Pituitary-Adrenal Axis in Obesity." Obesity Research 3, no. 4 (July 1995): 371–82. http://dx.doi.org/10.1002/j.1550-8528.1995.tb00163.x.

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Gupta, Deepashree, and John E. Morley. "Hypothalamic‐Pituitary‐Adrenal (HPA) Axis and Aging." Comprehensive Physiology 4, no. 4 (October 2014): 1495–510. https://doi.org/10.1002/j.2040-4603.2014.tb00585.x.

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AbstractHuman aging is associated with increasing frailty and morbidity which can result in significant disability. Dysfunction of the hypothalamic‐pituitary‐adrenal (HPA) axis may contribute to aging‐related diseases like depression, cognitive deficits, and Alzheimer's disease in some older individuals. In addition to neuro‐cognitive dysfunction, it has also been associated with declining physical performance possibly due to sarcopenia. This article reviews the pathophysiology of HPA dysfunction with respect to increased basal adrenocorticotropic hormone (ACTH) and cortisol secretion, decreased glucocorticoid (GC) negative feedback at the level of the paraventricular nucleus (PVN) of the hypothalamus, hippocampus (HC), and prefrontal cortex (PFC), and flattening of diurnal pattern of cortisol release. It is possible that the increased cortisol secretion is secondary to peripheral conversion from cortisone. There is a decline in pregnolone secretion and C‐19 steroids (DHEA) with aging. There is a small decrease in aldosterone with aging, but a subset of the older population have a genetic predisposition to develop hyperaldosteronism due to the increased ACTH stimulation. The understanding of the HPA axis and aging remains a complex area with conflicting studies leading to controversial interpretations. © 2014 American Physiological Society. Compr Physiol 4:1495‐1510, 2014.

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Igaz, Péter, Károly >Rácz, Miklós Tóth, Edit Gláz, and Zsolt Tulassay. "Treatment of iatrogenic Cushing’s syndrome: questions of glucocorticoid withdrawal." Orvosi Hetilap 148, no. 5 (February 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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Kobzina-Didukh, D. S. "The influence of scorpion venom on the hypothalamo-pituitary-adrenal axis (review)." Reports of Vinnytsia National Medical University 28, no. 3 (September 25, 2024): 524–29. http://dx.doi.org/10.31393/reports-vnmedical-2024-28(3)-24.

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Annotation. Scorpion venom is an important subject of research because of its potential impact on the hypothalamic-pituitary-adrenal axis, which plays a key role in regulating the body's stress response. Studying this effect may contribute to the development of new therapeutic approaches for the treatment of stress and endocrine disorders. The purpose of this study is to review modern scientific sources devoted to the study of scorpion venom on the organs of the hypothalamic-pituitary-adrenal axis. For this, a search for literary sources related to the research topic in the period 2014-2024 was performed on the basis of Google Scholar, Scopus using keywords and inclusion/exclusion criteria, in particular, the presence of previous review of articles, the representativeness of the sample, and the presence of statistical analysis of the obtained data. An analysis of the literature on the effects of scorpion venom on the hypothalamic-pituitary-adrenal axis revealed several key aspects. First, the presence of specific biological mechanisms through which venom components affect the activity of this axis, including the secretion of corticosteroids, adrenocorticotropic hormone, or other stress hormones, has been confirmed. Secondly, the results of the analysis indicated the possible therapeutic prospects of using individual components of the venom to regulate the work of this system, which may be important in the treatment of various endocrine and stress disorders. Finally, the analysis helped identify gaps in existing research and outline directions for further experiments, which will contribute to a deeper understanding of the effects of scorpion venom on the hypothalamic-pituitary-adrenal axis.

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Gifford, Robert M., Thomas J. O’Leary, Sophie L. Wardle, Rebecca L. Double, Natalie Z. M. Homer, A. Forbes Howie, Julie P. Greeves, Richard A. Anderson, David R. Woods, and Rebecca M. Reynolds. "Reproductive and metabolic adaptation to multistressor training in women." American Journal of Physiology-Endocrinology and Metabolism 321, no. 2 (August 1, 2021): E281—E291. http://dx.doi.org/10.1152/ajpendo.00019.2021.

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We characterized reproductive endocrine adaptation to prolonged arduous multistressor training in women. We identified marked suppression of hypothalamic-pituitary-gonadal (HPG) axis function during training but found no evidence of low energy availability despite high energy requirements. Our findings suggest a complex interplay of psychological and environmental stressors with suppression of the HPG axis via activation of the hypothalamic-pituitary adrenal (HPA) axis. The neuroendocrine impact of nonexercise stressors on the HPG axis during arduous training should be considered.

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Ozcan, Lale. "A new player in hunger games." Science Translational Medicine 11, no. 499 (July 3, 2019): eaay3569. http://dx.doi.org/10.1126/scitranslmed.aay3569.

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Zhang, Dongyun, and Anthony P. Heaney. "Nuclear Receptors as Regulators of Pituitary Corticotroph Pro-Opiomelanocortin Transcription." Cells 9, no. 4 (April 7, 2020): 900. http://dx.doi.org/10.3390/cells9040900.

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The hypothalamic–pituitary–adrenal (HPA) axis plays a critical role in adaptive stress responses and maintaining organism homeostasis. The pituitary corticotroph is the central player in the HPA axis and is regulated by a plethora of hormonal and stress related factors that synergistically interact to activate and temper pro-opiomelanocortin (POMC) transcription, to either increase or decrease adrenocorticotropic hormone (ACTH) production and secretion as needed. Nuclear receptors are a family of highly conserved transcription factors that can also be induced by various physiologic signals, and they mediate their responses via multiple targets to regulate metabolism and homeostasis. In this review, we summarize the modulatory roles of nuclear receptors on pituitary corticotroph cell POMC transcription, describe the unique and complex role these factors play in hypothalamic–pituitary–adrenal axis (HPA) regulation and discuss potential therapeutic targets in disease states.

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Alkalay, Arie L., Jeffrey J. Pomerance, Asha R. Puri, Berwyn J. C. Lin, Arnold L. Vinstein, Naomi D. Neufeld, and Alan H. Klein. "Hypothalamic-Pituitary-Adrenal Axis Function in Very Low Birth Weight Infants Treated With Dexamethasone." Pediatrics 86, no. 2 (August 1, 1990): 204–10. http://dx.doi.org/10.1542/peds.86.2.204.

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The effect of dexamethasone therapy on hypothalamic-pituitary-adrenal axis function was prospectively investigated in very low birth weight infants with bronchopulmonary dysplasia. Ten infants (mean ± SD birth weight 825 ± 265 g, gestation 25.8 ± 1.9 weeks, postnatal age 33.1 ± 17.7 days) initially received intravenous dexamethasone, 0.5 mg/kg per day for 3 days, and then were weaned over a period of 45 ± 19.0 days to a replacement dose, followed by a metyrapone test. Morning plasma cortisol and 11-deoxycortisol levels were measured before and after an oral metyrapone dose given at midnight. Five infants (group A: birth weight 876 ± 313 g, gestation 26.2 ± 1.3 weeks, age of entry 31.8 ± 22.8 days) had normal metyrapone test results, and five infants (group B: 778 ± 234 g, 25.4 ± 2.5 weeks, 34.4 ± 13.4 days) had suppressed test results. Group A infants, in comparison with group B infants, had higher basal cortisol plasma levels (14.52 ± 12.53 and 3.00 ± 1.38 µg/dL, P = .047), higher postmetyrapone 11-deoxycortisol plasma levels (3.11 ± 3.93 and 0.55 ± 0.51 µg/dL, P = .028), larger differences between basal and postmetyrapone cortisol levels (7.10 ± 4.67 and 2.12 ± 1.31 µg/dL, P = .047), and larger differences between basal and postmetyrapone 11-deoxycortisol levels (2.99 ± 3.93 and 0.29 ± 0.25 µg/dL, P = .009). The hypothalamic-pituitary-adrenal axis function in group B infants eventually returned to normal when they continued to receive low-dose dexamethasone therapy after a period of 36.8 ± 16.6 days. The results suggest that dexamethasone therapy given for several weeks or more may be associated with prolonged suppression of hypothalamic-pituitary-adrenal axis function in a substantial number of very low birth weight infants with bronchopulmonary dysplasia. Evaluation of hypothalamic-pituitary-adrenal axis function before discontinuation of dexamethasone therapy is necessary to ensure proper adrenal secretory response.

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Brooks, A. N., and J. R. G. Challis. "Regulation of the hypothalamic–pituitary–adrenal axis in birth." Canadian Journal of Physiology and Pharmacology 66, no. 8 (August 1, 1988): 1106–12. http://dx.doi.org/10.1139/y88-182.

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In sheep an increase in fetal pituitary–adrenal function, reflected in rising concentrations of plasma ACTH and cortisol, is important in relation to fetal organ maturation and the onset of parturition. This review presents evidence that implicates the hypothalamic–pituitary–adrenal axis in the control of parturition and describes recent experiments that explore in detail the maturation of the fetal hypothalamus and pituitary in relation to fetal adrenal function. Recent improvements for the measurement of ACTH in unextracted plasma and the ability to maintain vascular catheters in chronically catheterized fetal sheep have enabled subtle changes in fetal ACTH concentrations to be detected. As a result of these advances it has now been established that the terminal rise in cortisol, which is responsible for the onset of parturition in sheep, is preceded by an increase in fetal plasma ACTH concentrations. This has led to the hypothesis that birth results from the sequential development of the fetal hypothalamic–pituitary–adrenal axis with the signal originating from the fetal brain. This increase in trophic drive to the fetal adrenal may result from changes in the responsiveness of the fetal pituitary gland to factors that stimulate the release of ACTH. Corticotropin releasing factor (CRF) and arginine vasopressin are two such factors that stimulate the secretion of ACTH and cortisol secretion in the chronically catheterized fetal sheep. The response to these factors increases with gestational age and is sensitive to glucocorticoid feedback. Furthermore, repeated administration of CRF to immature fetal sheep results in pituitary and adrenal activation and in some cases may lead to premature parturition. Until recently, little was known of the controls of CRF secretion from the fetal hypothalamus. However, CRF has now been detected in the fetal sheep hypothalamus by radioimmunoassay and with immunohistochemistry, during the last third of pregnancy. The CRF material detected by radioimmunoassay co-elutes with synthetic ovine CRF on Sephadex G75 chromatography and also stimulates the release of ACTH from adult sheep pituitary cells maintained in culture. Furthermore at d100 of pregnancy (term of 145 days), CRF is released from fetal sheep hypothalami perifused in vitro both under basal conditions and in response to potassium-induced nerve terminal depolarization. Dexamethasone does not affect the release of CRF under these conditions. At d140, the hypothalamus contains similar quantities of immunoreactive and bioactive CRF which are released at a higher rate during in vitro perifusion. Potassium causes a similar release of CRF compared with d100 and again is unaffected by the presence of dexamethasone. However, at d140, dexamethasone does reduce basal CRF release. These results provide evidence for maturation of glucocorticoid feedback mechanisms at the level of the fetal hypothalamus and, together with the additional data presented in this review, illustrate the complexity of neuroendocrine control of the hypothalamic–pituitary–adrenal axis in birth.

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Bailey, Michael, Harald Engler, John Hunzeker, and John F. Sheridan. "The Hypothalamic-Pituitary-Adrenal Axis and Viral Infection." Viral Immunology 16, no. 2 (June 2003): 141–57. http://dx.doi.org/10.1089/088282403322017884.

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Johnson, Karen L., and Cindy Renn RN. "The Hypothalamic-Pituitary-Adrenal Axis in Critical Illness." AACN Clinical Issues: Advanced Practice in Acute and Critical Care 17, no. 1 (January 2006): 39–49. http://dx.doi.org/10.1097/00044067-200601000-00006.

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Imrich, R. "Hypothalamic-pituitary-adrenal axis function in ankylosing spondylitis." Annals of the Rheumatic Diseases 63, no. 6 (March 17, 2004): 671–74. http://dx.doi.org/10.1136/ard.2003.006940.

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Pyter, Leah M., Jaimie D. Adelson, and Randy J. Nelson. "Short Days Increase Hypothalamic-Pituitary-Adrenal Axis Responsiveness." Endocrinology 148, no. 7 (July 1, 2007): 3402–9. http://dx.doi.org/10.1210/en.2006-1432.

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Bussone, Gennaro, Massimo Leone, Boris M. Zappacosta, Giorgia Patruno, Sergio Valentini, Fabio Frediani, and Eugenio A. Parati. "Hypothalamic-Pituitary-Adrenal Axis Evaluation in Cluster Headache." Cephalalgia 11, no. 11_suppl (June 1991): 244–45. http://dx.doi.org/10.1177/0333102491011s11131.

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Arnett, Melinda G., Lisa M. Muglia, Gloria Laryea, and Louis J. Muglia. "Genetic Approaches to Hypothalamic-Pituitary-Adrenal Axis Regulation." Neuropsychopharmacology 41, no. 1 (July 20, 2015): 245–60. http://dx.doi.org/10.1038/npp.2015.215.

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Morsi, Amr, Donald DeFranco, and Selma F. Witchel. "The Hypothalamic-Pituitary-Adrenal Axis and the Fetus." Hormone Research in Paediatrics 89, no. 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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Tsigos, Constantine, and George P. Chrousos. "Hypothalamic–pituitary–adrenal axis, neuroendocrine factors and stress." Journal of Psychosomatic Research 53, no. 4 (October 2002): 865–71. http://dx.doi.org/10.1016/s0022-3999(02)00429-4.

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Kjaer, A., P. J. Larsen, U. Knigge, and J. Warberg. "Histaminergic activation of the hypothalamic-pituitary-adrenal axis." Endocrinology 135, no. 3 (September 1994): 1171–77. http://dx.doi.org/10.1210/endo.135.3.8070360.

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Ng, P. C. "The fetal and neonatal hypothalamic-pituitary-adrenal axis." Archives of Disease in Childhood - Fetal and Neonatal Edition 82, no. 3 (May 1, 2000): 250F—254. http://dx.doi.org/10.1136/fn.82.3.f250.

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GROSSMAN, ASHLEY, ALFREDO COSTA, MARY FORSLING, RICHARD JACOBS, PIERLUIGI NAVARRA, and MARIA SATTA. "Immune Modulation of the Hypothalamic-Pituitary-Adrenal Axis." Annals of the New York Academy of Sciences 823, no. 1 Neuropsychiat (August 1997): 225–33. http://dx.doi.org/10.1111/j.1749-6632.1997.tb48394.x.

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