Glucocorticoid therapy and adrenal suppression

Abstract

Introduction. Adrenal insufficiency results from the inadequate adrenocortical conjunction. Adrenal insufficiency can be primary, secondary and tertiary one. The most common cause of adrenal suppression is the effect of exogenous therapy with glucocorticoids. Glucocorticoids. Corticosteroids are used in treatment of endocrine and non-endocrine diseases. They are applied as a substitution therapy in the patients with primary and secondary adrenal insufficiency. Due to their immunosuppressive and anti-inflammatory characteristics, they are used to treat a wide range of diseases. They are usually divided according to the length and size of the effect i.e. how they are applied. Adrenal Insufficiency. Glucocorticoid therapy may lead to a number of adverse effects such as a disorder in glucose metabolism, osteoporosis or frequent infections. Adrenal suppression is the most common complication resulting from corticosteroid application. The function of the hypothalamus-pituitary-adrenal axis may be inhibited for months after the treatment cessation. There are several predictors of potential glucocorticoid-induced adrenal suppression. Diagnosing Adrenal Insufficiency. The most frequent symptoms and signs of adrenal insufficiency are fatigue, nausea and vomiting, hyponatremia, hyperpigmentation or hypotension. Algorithm for the diagnosis of adrenal insufficiency must be followed in clinical practice. Reduction in Glucocorticoid Therapy. Reduction or complete cessation of the therapy is indicated when the maximum therapeutic benefit has been achieved or when considerable side effects, such as diabetes mellitus, severe hypertension, osteoporosis i.e. adrenal insufficiency, develop. Conclusion. Numerous synthetic glucocorticoids have been developed to be used in everyday clinical practice and they can be administered systemically or locally. A lot of side effects are associated with chronic administration of glucocorticoids. In order to avoid complications, it is recommended to administer intermediate-acting glucocorticoids every second day. In addition, the patients must be monitored carefully and glucocorticoid therapy should be discontinued gradually to prevent adrenal insufficiency or reactivation of the disease under therapy.

Mechanisms of a Sustained Anti‐inflammatory Drug Response in Alveolar Macrophages Unraveled with Mathematical Modeling

“…Glucocorticoids act through the glucocorticoid receptor (GR) and inhibit the release of cytokines from macrophages, e.g., through inhibition of transcription, changes in mRNA stability, changes in protein translation, and/or posttranslational processing. The synthetic glucocortocoid dexamethasone (dexa) is 30 times more potent than the endocrine glucocorticoid cortisol in inhibiting cytokine production 10 . There are two main hypotheses for the mechanisms of action of dexa ( Figure , box to the right): hypothesis A, new synthesis of the protein IB that binds to NF‐B and thereby hinders the inflammatory response; 11,12 and hypothesis B, a physical association between activated GR and the NF‐B subunit p65/RelA that reduces the activity of NF‐B 13,14 .…”

Nutritional aspects of neurological diseases

“…Kortikosteroidi (CS) jesu sintetički proizvedeni hormoni nadbubrežne žlezde, koji poboljšavaju stanje imunološkog odgovora. Koriste se za postizanje brzog kliničkog poboljšanja budući da imaju snažno antiinflamatorno, imunosupresivno dejstvo (81).…”

High Performance Liquid Chromatography (HPLC) with Fluorescence Detection for Quantification of Steroids in Clinical, Pharmaceutical, and Environmental Samples: A Review

“…Naturally secreted steroids are classified into steroid hormones (sex hormones, mineralo- and glucocorticoids, and anabolic steroids) and cholesterol. These compounds travel the bloodstream bound specifically or non-specifically to plasma proteins, such as albumin and binding globulins [ 1 ]. Steroids are key players in many biological, physiological, and pathological events, which are mediated after binding to their cognate tissue receptors.…”