Glucocorticoid induced adrenal insufficiencyBMJ 2021; 374 doi: https://doi.org/10.1136/bmj.n1380 (Published 12 July 2021) Cite this as: BMJ 2021;374:n1380
- 1Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK
- 2Division of Endocrinology, Metabolism and Nutrition, Department of Internal Medicine, Mayo Clinic, Rochester, MN 55905, USA
- Correspondence to: I Bancos
Synthetic glucocorticoids are widely used for their anti-inflammatory and immunosuppressive actions. A possible unwanted effect of glucocorticoid treatment is suppression of the hypothalamic-pituitary-adrenal axis, which can lead to adrenal insufficiency. Factors affecting the risk of glucocorticoid induced adrenal insufficiency (GI-AI) include the duration of glucocorticoid therapy, mode of administration, glucocorticoid dose and potency, concomitant drugs that interfere with glucocorticoid metabolism, and individual susceptibility. Patients with exogenous glucocorticoid use may develop features of Cushing’s syndrome and, subsequently, glucocorticoid withdrawal syndrome when the treatment is tapered down. Symptoms of glucocorticoid withdrawal can overlap with those of the underlying disorder, as well as of GI-AI. A careful approach to the glucocorticoid taper and appropriate patient counseling are needed to assure a successful taper. Glucocorticoid therapy should not be completely stopped until recovery of adrenal function is achieved. In this review, we discuss the factors affecting the risk of GI-AI, propose a regimen for the glucocorticoid taper, and make suggestions for assessment of adrenal function recovery. We also describe current gaps in the management of patients with GI-AI and make suggestions for an approach to the glucocorticoid withdrawal syndrome, chronic management of glucocorticoid therapy, and education on GI-AI for patients and providers.
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Contributors: IB and AP conceptualized and performed the literature review for this manuscript. AP and IB drafted the manuscript. IB and AP contributed to the critical revision of the article. AP and IB gave final approval of the version to be published. IB is the guarantor.
Funding: AP is a Diabetes UK Sir George Alberti research training fellow (grant reference number 18/0005782). This research was supported by the Catalyst Award for Advancing in Academics from the Mayo Clinic (to IB) and the National Institute of Diabetes and Digestive and Kidney Diseases of the NIH under award K23DK121888 (to IB). The views expressed are those of the authors and not necessarily those of the NIH. The funders of the study had no role in the conceptualization, writing, and decision to publish the manuscript. All researchers were independent from funders.
Competing interests: We have read and understood the BMJ policy on declaration of interests and declare the following interests: IB is a consultant to CinCor, Corcept, Sparrow Pharmaceutics, Strongbridge, and HRA Pharma, outside this work. IB has received research support from HRA Pharma for an investigator initiated study outside this work.
Patient and public involvement: Patients or the public were not involved in the design, conduct, reporting, or dissemination plans for this work.
Provenance and peer review: Commissioned; externally peer reviewed.