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Adrenal insufficiency
Published in Nadia Barghouthi, Jessica Perini, Endocrine Diseases in Pregnancy and the Postpartum Period, 2021
Despite the significant rise in cortisol levels, pregnant women do not demonstrate the stigmata classically associated with Cushing’s syndrome, such as ecchymoses, proximal muscle weakness, and dorsocervical adiposity.Prior theories have suggested that the anti-glucocorticoid effects of elevated progesterone levels during pregnancy lead to relatively inert cortisol actions.11,12Similarly, the physiologic cortisol elevation does not affect the developing fetus.11-β-hydroxysteroid dehydrogenase 2 (11β-HSD2) catalyzes the conversion of most of maternal cortisol to inert cortisone, thereby decreasing excess fetal glucocorticoid exposure, which could lead to intrauterine growth restriction and preeclampsia.13
Ethnomedicinal and Pharmacological Importance of Glycyrrhiza glabra L
Published in Mahendra Rai, Shandesh Bhattarai, Chistiane M. Feitosa, Wild Plants, 2020
Ashish K. Bhattarai, Sanjaya M. Dixit
High intake of licorice can cause hyper mineralocorticoidism with sodium retention and potassium loss, oedema, increased blood pressure, and depression of the renin-angiotensin-aldosterone system. As a result, the number of related clinical symptoms are reported. There is increased cortisol level in the kidneys and other mineralocorticoid selective tissues because of the inhibition of enzymes involved in the metabolism of corticosteroids. Glycyrrhetic acid inhibits the enzyme 11β-hydroxysteroid dehydrogenase involved in the metabolism of corticosteroids which is produced after glycyrrhizic acid is hydrolyzed in the intestine. This cortisol results in hyper mineralocorticoid effect. The compensatory physiological mechanisms following hyper mineralocorticoids, which is depression of the renin-angiotensin system, can last several months. The inhibitory effect on 11β-hydroxysteroid dehydrogenase is reversible. So after the withdrawal of consumption of licorice, there is physiological reversal of hyper mineralocorticoids, but it takes several months (Størmer et al. 1993).
Overview of Perinatal Maternal Stress
Published in Rosa Maria Quatraro, Pietro Grussu, Handbook of Perinatal Clinical Psychology, 2020
Dawn Kingston, Muhammad Kashif Mughal
Third, 11β-HSD2 is the gene responsible for cortisol regulation in the placenta. It codes for production of the enzyme, 11-β-hydroxysteroid dehydrogenase, which metabolizes active cortisol into inactive cortisone. Methylation of this gene has been associated with sub-optimal neurobehavioral outcomes and increased cortisol in infants (Cao-Lei et al., 2017). Another study showed that infants of women who were psychologically distressed during pregnancy had greater 11β-HSD2 methylation than infants of mothers who were not distressed, and this was associated with infant hypotonia (Conradt et al., 2013).
Neuroprotective effects of food restriction in a rat model of traumatic brain injury – the role of glucocorticoid signaling
Published in Nutritional Neuroscience, 2022
Milka Perović, Milena Jović, Smilja Todorović, Aleksandra Mladenović Đorđević, Desanka Milanović, Selma Kanazir, Nataša Lončarević-Vasiljković
Since 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) is the major regulator of the tissue-specific effects of circulating glucocorticoid excess, we next analyzed the protein level of this enzyme in the ipsilateral brain tissue (Figure 5). Two-way ANOVA with FR and time as factors revealed a significant effect of FR (F(1,40) = 15.243, p < 0.05), time (F(4,40) = 13.140, p < 0.05) and FR × time (F(4,40) = 9.544, p < 0.05) on 11β-HSD1 levels. They were significantly increased in AL group on the 2nd, 7th, 14th and 28th dpi (24%, 43%, 39%, and 37% respectively) compared to AL control (*p < 0.05). Oppositely, in the FR group, levels of 11β-HSD1 were significantly decreased on the 14th and 28th dpi (36% and 51%, respectively) compared to FR control (#p < 0.05). Post hoc analysis showed a significant decrease of 11β-HSD1 on the 2nd, 7th, 14th and 28th dpi in FR rats (28, 54, 75 and 88%, respectively) vs. AL rats at matching time points ($p < 0.05). However, WB analysis did not reveal any significant differences in 11β-HSD1 between AL and FR physiological controls.
Hydrocortisone granules in capsules for opening (Alkindi) as replacement therapy in pediatric patients with adrenal insufficiency
Published in Expert Opinion on Orphan Drugs, 2021
Helen Coope, Lotta Parviainen, Mike Withe, John Porter, Richard J Ross
Hydrocortisone has been used in humans for more than 60 years and is identical to the innate hormone cortisol. Like other steroids, cortisol binds to an intracellular receptor which, after migrating to the nucleus of the cell, upregulates or downregulates gene expression. Hydrocortisone also acts through non-genomic mechanisms [42]. Hydrocortisone is rapidly and virtually completely absorbed from the fasted alimentary system (bioavailability is ~100%) with Tmax reached about 60 minutes [43]. Cortisol is highly protein bound mostly by cortisol binding globulin, with a smaller amount of albumin binding. This leads to non-linear pharmacokinetics as higher doses of hydrocortisone are more rapidly cleared due to saturation of the protein binding [43,44]. Metabolism of cortisol is by renal 11β-Hydroxysteroid dehydrogenase type 2 (11β-HSD2) to inactive cortisone whilst hepatic and adipose 11β-HSD1 converts cortisone to cortisol. Cortisol, cortisone and downstream metabolites allo-tetrahydrocortisol, tetrahydrocortisol and tetrahydrocortisone, are all renally excreted [45].
Use of medications during pregnancy and breastfeeding for Crohn’s disease and ulcerative colitis
Published in Expert Opinion on Drug Safety, 2021
Robyn Laube, Sudarshan Paramsothy, Rupert W Leong
Corticosteroids can traverse the placenta where they undergo rapid metabolism via the 11-β-hydroxysteroid dehydrogenase type 2 enzyme into less active metabolites, therefore reducing fetal exposure. Shorter-acting formulations, such as prednisolone and methylprednisolone, are more rapidly and extensively metabolized than longer-acting formulations such as dexamethasone, 98% of which traverses the placenta intact to attain higher fetal levels [49]. Levels of endogenous glucocorticoids are markedly lower in the fetal circulation compared to the maternal circulation, therefore rendering the fetus more susceptible to iatrogenic corticosteroids [50]. Multiple studies have identified an increased risk of maternal and fetal complications with corticosteroid use during pregnancy. These include gestational diabetes (GDM), preterm birth, LBW and neonatal adrenal suppression [51–53]. However, given that these medications are generally reserved for patients with active disease, it is difficult to distinguish whether observed adverse effects arise secondary to active IBD or corticosteroid exposure.