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Immunomodulating Agents in Gastrointestinal Disease
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Samir A. Shah, Athos Bousvaros, A. Christopher Stevens
Corticosteroids are well absorbed from the gastrointestinal tract, primarily in the proximal jejunum; up to 30% of corticosteroid may be absorbed from retention enemas [68]. Once absorbed, 90% of cortisol is bound to albumin and corticosteroid-binding globulin. The liver metabolizes cortisol and other corticosteroids by reduction and glucuronidation. Inducers of hepatic conjugation such as phenobarbital and rifampin can increase hepatic metabolism and excretion of steroids [69]. Although the plasma half-life of corticosteroids is less than 5 hr, the biological effects last much longer [69], Suppression of the hypothalamic-pituitary-adrenal axis can occur with just 5 days of high-dose oral steroids and is inevitably seen with more than 2 weeks of treatment [68,70].
Steroids and Infection
Published in Herman Friedman, Thomas W. Klein, Andrea L. Friedman, Psychoneuroimmunology, Stress, and Infection, 2020
Yoshimasa Yamamoto, Herman Friedman
The levels of steroid in body fluids are dependent on the amount used for therapy. In general, these substances are carried in the plasma bound to corticosteroid binding globulin (CBG) and to albumin. Both CBG-bound and albumin-bound steroids are biologically inactive. Therefore, the physiological plasma cortisol levels from 8 to 220 ng/ml during the diurnal cycle in healthy subjects may provide a biologically available concentration of free cortisol of 0.8 - 28 ng/ml.23 In patients with Cushing’s syndrome, severe infections occur at cortisol levels ranging from 0.4 to 1.8 µg/ml.4 When steroid is administered in a dose of 100–500 mg, drug levels can reach 1–2 µg/ml for sustained periods.24,25
Pregnancy-Related Protein Concentrations and Hormone Levels in Trophoblastic Diseases
Published in Gábor N. Than, Hans Bohn, Dénes G. Szabó, Advances in Pregnancy-Related Protein Research, 2020
It was first demonstrated by Mercier et al.101 that there was a sex-steroid-binding activity in plasma which could not be assigned to corticosteroid binding globulin (CBG). The sex hormone binding globulin is of particular importance primarily for endocrinologists. Consequently, it has not been extensively studied with regard to pregnancy and neoplasia.
Evaluation of Adrenal Reserve in Patients with Differentiated Thyroid Cancer Receiving Thyroid Hormone Suppression Therapy- case-control Comparative Study
Published in Endocrine Research, 2023
Muhammet Cuneyt Bilginer, Abbas Ali Tam, Sevgul Faki, Nagihan Bestepe, Fatma Dilek Dellal, Didem Ozdemir, Oya Topaloglu, Reyhan Ersoy, Bekir Cakir
The main limitation of this study is its single-center design. Furthermore, we screened the control group only using basal cortisol measurements. The cortisol level of these healthy volunteers was above 10 mcg/dl and there was no clinical finding suggestive for adrenal insufficiency. Therefore, we did not measure ACTH levels and perform ACTH stimulation test in this group. In addition, it is suggested by some authors that this dose of ACTH is supraphysiological and 1 mcg ACTH should be used for the diagnosis of adrenal insufficiency.27 However we used 250 mcg ACTH stimulation test for this purpose since it is still the standard test recommended by Endocrine Society Clinical Practice Guideline.23 Another limitation of our study is not measuring the corticosteroid-binding globulin (CBG) adjusted free cortisol. Previous studies shows that although CBG-level increase after treatment of apparent thyrotoxicosis compared to pre-treatment, total cortisol level did not change at all or is only slightly affected.14,28 In our patient group, thyrotoxicosis was subclinical level, and we suggest that not measuring the CBG adjusted free cortisol level may not be a significant limitation on our study results. Performing subgroup analyses with a larger patient group and comparing different test protocols might help to clarify effect of suppression treatment on adrenal reserve in DTC patients.
A proposed role for glucocorticoids in mediating dopamine-dependent cue-reward learning
Published in Stress, 2021
Sofia A. Lopez, Shelly B. Flagel
Historically, the hypothalamic-pituitary-adrenal (HPA) axis has been viewed as the primary biological system activated by stress (e.g. Dallman & Jones, 1973). Upon perceiving a stressor (see Figure 1), neural signals are elicited throughout the brain, including the prefrontal cortex, hippocampus, amygdala and brainstem (for review see Herman & Cullinan, 1997). This information converges at the paraventricular nucleus (PVN) of the hypothalamus via direct projections or indirectly through the bed nucleus of the stria terminalis (BNST) and neighboring hypothalamic nuclei (for review see Herman et al., 2003). The HPA axis is thereby activated by secretion of corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) from the PVN. Adrenocorticotropic hormone (ACTH) is subsequently released from the pituitary, and ultimately, GCs are synthesized and released from the cortex of the adrenal glands (for review see Herman et al., 2016; Spencer & Deak, 2017). Even in the absence of stress, GCs—cortisol in humans and corticosterone in rodents—circulate both peripherally and centrally in fluctuating concentrations that follow an ultra-radian and circadian rhythm (Kalsbeek et al., 2012; Lightman & Conway-Campbell, 2010; Qian et al., 2012; Sarabdjitsingh et al., 2010; Spiga et al., 2014). Approximately 85% of circulating GCs are inactive and bound to a glycoprotein, corticosteroid-binding globulin (CBG) (for review see Moisan et al., 2014). At baseline, ∼5% of GCs are free to enter the brain, however, under circadian peak or stress levels this percentage is increased (McEwen et al., 1968; Qian et al., 2012).
Placental glucocorticoid receptor and 11β-hydroxysteroid dehydrogenase-2 recruitment indicates impact of prenatal adversity upon postnatal development in mice
Published in Stress, 2018
Moshe Gross, Hava Romi, Yelena Gilimovich, Elyashiv Drori, Albert Pinhasov
In this study, recruitment of placental GR and 11βHSD2 protein expression preceded rapid recovery from fetal growth retardation due to PRS among Dom mice. In contrast, PRS reduced GR and did not recruit 11βHSD2 among Sub placentae, which was associated with long-term growth impairment. These findings suggest that divergent transgenerational effects of PRS upon postnatal development of Dom and Sub mice may be mediated by differential changes of placental GR and 11βHSD2 levels in response to PRS. Increased placental GR may improve Dom placental function while recruiting 11βHSD2 which in turn may protect the developing fetuses from the effects of prenatal stress upon postnatal development. We further note that in Dom and Sub mice undisturbed by restraint, nearly twice as much corticosterone was found in the serum of Naïve Dom dams, relative to their Sub counterparts on GD15 (Figure 2(A)). Importantly, the concentrations detected represent total corticosterone, without discrimination of the portion bound to corticosteroid-binding globulin (CBG), which attenuates biologic activity of corticosterone. The total serum corticosterone concentrations of Dom dams remained significantly higher than in Sub dams on GD19, albeit corticosterone concentrations were higher on GD 19 than on GD15 among both strains, which is to be anticipated as mice approach parturition (Constantinof et al., 2016). Thus, the lower corticosterone levels of Sub dams (Figure 2(A,B)) may indicate reduced hypothalamo–pituitary–adrenal (HPA) axis recruitment among Sub dams during late gestation.