Corticosteroid binding globulin normal range

Denatured TBG does not bind iodothyronines but can be detected with antibodies that recognize the primary structure of the molecule (23).  In euthyroid adults with normal TBG concentration, about one-third of the molecules carry thyroid hormone, mainly T4.  When fully saturated, it carries about 20 µg of T4/dl of serum.  The biologic half-life is about 5 days, and the volume of distribution is similar to that of albumin (34,35) (Table 1).  TBG is cleared by the liver.  Loss of sialic acid accelerates its removal through interaction with the asialo-glycoprotein receptors reducing the half live by 500-fold (21).  However, it is unknown whether desialylation is a required in the normal pathway of TBG metabolism.

As a glucocorticoid , the lipophilic structure of prednisolone allows for easy passage through the cell membrane where it then binds to its respective glucocorticoid receptor (GCR) located in the cytoplasm. Upon binding, formation of the GC/GCR complex causes dissociation of chaperone proteins from the glucocorticoid receptor enabling the GC/GCR complex to translocate inside the nucleus. This process occurs within 20 minutes of binding. Once inside the nucleus, the homodimer GC/GCR complex binds to specific DNA binding-sites known as glucocorticoid response elements (GREs) resulting in gene expression or inhibition. Complex binding to positive GREs leads to synthesis of anti-inflammatory proteins while binding to negative GREs block the transcription of inflammatory genes. [28]

Human corticosteroid binding globulin (CBG, transcortin), also referred to as SerpinA6, belongs to the serpin superfamily. Corticosteroid binding globulin is a 52 kDa secreted α1-glycoprotein consisting of 405 amino acids. Corticosteroid binding globulin is synthesized and secreted by hepatocytes in the liver and is present in glycocorticoid responsive cells. The concentration of corticosteroid binding globulin is regulated by estrogens. CBG is the major transport protein for progestins and glucocorticoids within the blood. Thus CBG regulates their bioavailability and metabolic clearance and protects them from absorption into cells and degradation by chemicals and enzymes. CBG contains a single steroid binding site with high affinity for cortisol and progesterone. About 80–90% of circulating cortisol is bound to CBG. Albumin bound cortisol is reported to represent 14% and free cortisol 6% of total plasma cortisol under basal conditions. The CBG bound cortisol is considered to be biologically inactive, whereas the unbound cortisol constitutes the active form of cortisol. The active fraction of plasma cortisol will thus depend on the concentration of CBG. Defects in the gene encoding CBG are the cause of corticosteroid binding globulin deficiency (CBG deficiency), a rare disorder characterized by reduced CBG production that results in hypo/ hypertension and muscle fatigue. The plasma concentration of CBG shows little or no diurnal variation and no marked differences are observed in adult subjects according to age, sex or menstrual cycle. In umbilical cord blood, however, CBG is present at half of the normal adult level and prepubertal children have higher levels than adults. Plasma CBG levels increase during pregnancy and are decreased in cirrhosis. Estrogen therapy (. oral hormonal contraception) or implantation during pregnancy cause a very marked increase of the CBG concentration. Decreased levels of CBG are observed in women with polycystic ovary syndrome, hypoproteinemia, Cushing´s syndrome or corticoid treatment and some cases of vitamin B12 deficiency. Extremely low levels of CBG have been reported in patients with septic shock. Measurement of corticosteroid binding globulin is important to the interpretation of cortisol levels. The concentration of unbound cortisol, which is biologically active, can be calculated from the concentration of total cortisol and that of CBG on the basis of mass action.

Mild nasopharyngeal irritation following the use of beclomethasone aqueous nasal spray has been reported in up to 24% of patients treated, including occasional sneezing attacks (about 4%) occurring immediately following use of the spray. In patients experiencing these symptoms, none had to discontinue treatment. The incidence of transient irritation and sneezing was approximately the same in the group of patients who received placebo in these studies, implying that these complaints may be related to vehicle components of the formulation.

Corticosteroid binding globulin normal range

corticosteroid binding globulin normal range

Mild nasopharyngeal irritation following the use of beclomethasone aqueous nasal spray has been reported in up to 24% of patients treated, including occasional sneezing attacks (about 4%) occurring immediately following use of the spray. In patients experiencing these symptoms, none had to discontinue treatment. The incidence of transient irritation and sneezing was approximately the same in the group of patients who received placebo in these studies, implying that these complaints may be related to vehicle components of the formulation.

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