Abstract
Glucocorticoids (GCs) are widely used due to their anti-inflammatory and immunosuppressive effects. As many as 1–3% of the population are currently on GC treatment. Prolonged therapy with GCs is associated with an increased risk of GC-induced adrenal insufficiency (AI). AI is a rare and often underdiagnosed clinical condition characterized by deficient GC production by the adrenal cortex. AI can be life-threatening; therefore, it is essential to know how to diagnose and treat this disorder. Not only oral but also inhalation, topical, nasal, intra-articular and intravenous administration of GCs may lead to adrenal suppression. Moreover, recent studies have proven that short-term (<4 weeks), as well as low-dose (<5 mg prednisone equivalent per day) GC treatment can also suppress the hypothalamic–pituitary–adrenal axis. Chronic therapy with GCs is the most common cause of AI. GC-induced AI remains challenging for clinicians in everyday patient care. Properly conducted GC withdrawal is crucial in preventing GC-induced AI; however, adrenal suppression may occur despite following recommended GC tapering regimens. A suspicion of GC-induced AI requires careful diagnostic workup and prompt introduction of a GC replacement treatment. The present review provides a summary of current knowledge on the management of GC-induced AI, including diagnostic methods, treatment schedules, and GC withdrawal regimens in adults.
Highlights
Adrenal glands are composed of the adrenal medulla and adrenal cortex
The adrenal cortex consists of three layers: zona glomerulosa, fasciculata, and reticularis, which produce mineralocorticoids, glucocorticoids (GCs) (11-deoxycorticosterone, corticosterone, and cortisol), and androgens (mostly dehydroepiandrosterone (DHEA), DHEA sulfate (DHEA-S), and androstenedione), respectively
adrenocorticotropic hormone (ACTH) triggers the release of cortisol and adrenal androgens by binding to the melanocortin-2 receptor on the cells of the zona fasciculata and zona reticularis of the adrenal cortex [1]
Summary
Adrenal glands are composed of the adrenal medulla and adrenal cortex. The medulla is responsible for the secretion of adrenaline, noradrenaline, and dopamine. The reason for secondary AI is impaired secretion of ACTH, either due to pituitary conditions or due to decreased hypothalamic secretion of CRH It is most commonly caused by chronic therapy with GCs (GC-induced AI) [2]. Recent studies have shown that the treatment with an IV methylprednisolone administered every week protocol (cumulative dose of 4.5 g) does not cause GC-induced AI [24,25,26,27] It was, proven that this therapy affects adrenal function, causing more severe impairment of DHEA-S secretion than that of cortisol [25]. Proven that this therapy affects adrenal function, causing more severe impairment of DHEA-S secretion than that of cortisol [25] This subject requires further investigation, as the possibility of the HPA axis suppression in patients receiving IV GCs has not been sufficiently investigated
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