Glucocorticoid-induced hyperglycemia is a frequent problem. In the general clinical practice, it may generate hospital admissions, their prolongation and repeated emergency visits without obtaining an adequate solution to the problem. Even so, this problem continues to be undervalued in terms of diagnosis, and especially, treatment. The diversity of preparations and dosing schedules of corticosteroids, and above all, the low level of involvement by the professionals who prescribe steroids and the absence of clinical studies and specific recommendations for diagnosis and treatment, contribute to this. In this paper we review the pathophysiology of glucocorticoid-induced hyperglycemia and propose some strategies for their management, based on the clinical situation and the predictable pattern of hyperglycemia according to the type and schedule of glucocorticoids administration.
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http://dx.doi.org/10.1016/j.rce.2010.03.006 | DOI Listing |
Indian J Clin Biochem
January 2025
College of Nursing, Al-Kitab University, Kirkuk, Iraq.
Adrenal insufficiency (AI) is a serious disorder characterized by the adrenal glucocorticoid deficiency. Regardless of the etiology, AI patients need long-term replacement therapy for glucocorticoids and, in some cases, for mineralocorticoids. The replacement therapy cannot completely mirror the physiological secretion patterns, and therefore, glucocorticoid excess is a common sequela in AI patients.
View Article and Find Full Text PDFAnn Endocrinol (Paris)
December 2024
University of Lille, CHU de Lille, Inserm U1190, EGID, Institut Pasteur de Lille, 59000 Lille, France. Electronic address:
Introduction: Glucocorticoid-induced diabetes (GCID) is a prevalent health issue, generally attributed to insulin resistance. High doses of dexamethasone (DEX) are known to inhibit glucose-stimulated insulin secretion (GSIS), but the effects of lower doses, commonly used in chronic therapy, and equipotent doses of other glucocorticoids (GCs) such as hydrocortisone (HC) and prednisone (PRED) remain underexplored. This study aimed to investigate these effects in vitro, and explore variations between patients.
View Article and Find Full Text PDFDiabet Med
December 2024
Diabetes Trials Unit, Oxford Centre for Diabetes, Endocrinology and Metabolism, and NIHR Oxford Biomedical Research Centre, University of Oxford, Oxford, UK.
Introduction: In people living with chronic obstructive pulmonary disease (COPD), we aimed to estimate: (1) the prevalence of glucocorticoid-induced hyperglycaemia (GIH); (2) whether the prevalence of GIH varies by age, baseline diabetes status, treatment duration, ascertainment of glycaemia, definition of hyperglycaemia, study design and year of publication; and (3) the relative risk (RR) of new-onset hyperglycaemia in exposed vs non-exposed to systemic glucocorticoids.
Methods: We searched electronic databases until 9 November 2023 for randomised controlled trials and observational studies including adults diagnosed with COPD, with or without diabetes at baseline, using systemic glucocorticoids equivalent to prednisolone ≥5 mg/day for ≥3 days if exposed. Hyperglycaemia was defined as a blood glucose above a study-specific cut-off.
Eur J Endocrinol
November 2024
Department of Internal Medicine I, Division of Endocrinology and Diabetes, University Hospital, University of Würzburg, 97080 Würzburg, Germany.
Objective: Cushing's syndrome (CS) results in increased cardiovascular (CV) morbidity and mortality. Subtype-specific differences and possible reversibility after biochemical cure are not well investigated.
Design: Prospective cohort study evaluating the CV status in different forms of endogenous cortisol excess.
Sci Rep
November 2024
School of Basic Medical Sciences, Guangxi Medical University, Nanning City, People's Republic of China.
Retinal ganglion cells (RGCs) are among the first neurons to undergo apoptosis in diabetic retinopathy (DR), with their relationship to endoplasmic reticulum stress (ERS)-induced apoptosis still unclear. While glucocorticoid-induced transcript 1 (GLCCI1) has been shown to inhibit apoptosis, its role in ERS-induced apoptosis and its mechanisms in DR remain unclarified. Our findings indicated that GLCCI1 is predominantly localized in the ganglion cell layer and is downregulated in DR.
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