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Introduction Stress reactions are by no means universal, and the activation of ‘stress hormones’, such as glucocorticoids or corticotropin-releasing hormone (CRH), is not necessarily the mark of a stress response ( 1 ). Some individuals have

therapies ( 1 ). The remaining treatment options include observation or glucocorticoid therapy and each of them can be used as the primary treatment based on clinical scenario. A recent meta-analysis concluded that patients with milder presentation be

Introduction In patients with malignant disease, glucocorticoids are widely used on various indications. High-dose treatment is given as part of chemotherapy regimens and for treating oedema associated with metastatic spinal cord compression

pathway of the stress response ( 1 ). This in turn, has many peripheral effects, such as an increase in circulating glucocorticoids (GCs) ( 2 , 3 ). Chronic stress or prolonged exogenous GC treatment also disrupts the central homeostatic nature of GC

Introduction Polymorphisms of the glucocorticoid receptor (GR) may influence the sensitivity to glucocorticoids by altering the GR expression (e.g. reducing transcription) and influencing transactivation and transrepression of target genes

Introduction Acute adrenal insufficiency , also termed adrenal crisis , is a life-threatening endocrine emergency brought about by a lack of production of the adrenal hormone cortisol, the major glucocorticoid. Identifying patients at risk

and associated metabolic conditions, such as insulin resistance ( 5 ), diabetes ( 6 ), hypercholesterolaemia ( 7 ), statins ( 8 ), abdominal fat ( 9 ), the sympathetic nervous system ( 10 , 11 ), and corticosteroid use ( 12 ). Glucocorticoids are a

profiles in adult patients with 21-hydroxylase deficiency have shown a substantial circadian rhythm highly influenced by glucocorticoid replacement ( 6 ). Most recent clinical guideline from the US Endocrine Society suggests levels of androstenedione and 17

components, and related cardiometabolic risk factors, including measures of obesity, insulin resistance, and glucose intolerance ( 3 , 4 , 5 , 6 , 7 ). Cortisol may not be the only glucocorticoid involved in metabolic syndrome as humans also produce

the sympathetic–adrenal–medullary axis, which subsequently release glucocorticoids and catecholamines, respectively. The HPA and SNS axes are the two major pathways through which stress is able to modulate immune functions depending on the nature