Steroid diabetes or steroid-induced diabetes is characterized as an unusual rise in blood sugar that is linked to the use of glucocorticoids in a patient who may or may not have had diabetes mellitus in the past.[1]
Causes
Steroid diabetes is caused by the use of glucocorticoids.[1]
Risk factors
Traditional risk factors for type 2 diabetes, such as advanced age, a family history of the disease, a high body mass index, and impaired glucose tolerance, are also suggested risk factors for steroid-induced diabetes, in addition to cumulative dosage and length of steroid course.[2]
Glycemic control can be impacted by other immunosuppressive medications through different mechanisms, which could complicate the effects of glucocorticoid therapy.[1] By inhibiting the production of insulin, calcineurin inhibitors, especially tacrolimus, are used in transplant patients, which increases their risk of developing glucose intolerance.[2] Diabetes was linked to the concurrent use of mycophenalate mofetil in patients with lupus receiving high-dose steroid therapy; this could be explained by decreased insulin secretion due to elevated beta cell stress.[3][4]
There is an inverse correlation between serum magnesium levels and glycemic control, according to several studies.[5]
Although chronic hepatitis C virus (HCV) infection is thought to be a separate risk factor for the development of diabetes in both the general population and liver transplant recipients, liver disease is known to exacerbate impaired glucose tolerance.[6][7]
Diagnosis
The American Diabetes Association defines the following criteria for the diagnosis of diabetes: a HbA1c of 6.5%, an 8-hour fasting blood glucose of 7.0 mmol/L (126 mg/dL), a 2-hour oral glucose tolerance test (OGTT) of ≥ 11.1 mmol/L (200 mg/dL), or in patients exhibiting hyperglycemic symptoms, a random plasma glucose of ≥ 11.1 mmol/L (200 mg/dL).[8]
Treatment
Like with all forms of diabetes, lifestyle modification, including exercise and dietary counseling to offer options that might lessen post-prandial hyperglycemia, is the first step toward improving glycemic control.[1]
Current guidelines may not adequately address this because the initiation of glucocorticoids can result in post-prandial hyperglycemia and the tapering of glucocorticoids can normalize glycemic control. The most accommodating option for patients is still basal bolus insulin therapy, which consists of three parts: basal insulin, prandial insulin, and supplemental correction factor insulin.[1]
References
- ^ a b c d e Hwang, Jessica L.; Weiss, Roy E. (2014). "Steroid-induced diabetes: a clinical and molecular approach to understanding and treatment". Diabetes/Metabolism Research and Reviews. 30 (2). Wiley: 96–102. doi:10.1002/dmrr.2486. ISSN 1520-7552. PMC 4112077. PMID 24123849.
- ^ a b Kim, Seo Yun; Yoo, Chul-Gyu; Lee, Chun Taeg; Chung, Hee Soon; Kim, Young Whan; Han, Sung Koo; Shim, Young-Soo; Yim, Jae-Joon (2011). "Incidence and Risk Factors of Steroid-induced Diabetes in Patients with Respiratory Disease". Journal of Korean Medical Science. 26 (2). Korean Academy of Medical Sciences: 264–267. doi:10.3346/jkms.2011.26.2.264. ISSN 1011-8934. PMC 3031012. PMID 21286019.
- ^ Ha, YJ; Lee, K-H; Jung, SJ; Lee, S-W; Lee, S-K; Park, Y-B (June 9, 2011). "Glucocorticoid-induced diabetes mellitus in patients with systemic lupus erythematosus treated with high-dose glucocorticoid therapy". Lupus. 20 (10). SAGE Publications: 1027–1034. doi:10.1177/0961203311402246. ISSN 0961-2033. PMID 21659423. S2CID 6767818.
- ^ MAZZANTINI, MAURIZIO; TORRE, CLAUDIA; MICCOLI, MARIO; BAGGIANI, ANGELO; TALARICO, ROSARIA; BOMBARDIERI, STEFANO; DI MUNNO, OMBRETTA (January 15, 2012). "Adverse Events During Longterm Low-dose Glucocorticoid Treatment of Polymyalgia Rheumatica: A Retrospective Study". The Journal of Rheumatology. 39 (3): 552–557. doi:10.3899/jrheum.110851. ISSN 0315-162X. PMID 22247343.
- ^ Van Laecke, S.; Van Biesen, W.; Verbeke, F.; De Bacquer, D.; Peeters, P.; Vanholder, R. (2009). "Posttransplantation Hypomagnesemia and Its Relation with Immunosuppression as Predictors of New-Onset Diabetes after Transplantation". American Journal of Transplantation. 9 (9). Elsevier BV: 2140–2149. doi:10.1111/j.1600-6143.2009.02752.x. ISSN 1600-6135. PMID 19624560.
- ^ Baid, Seema; Cosimi, A. Benedict; Lin Farrell, Mary; Schoenfeld, David A.; Feng, Sandy; Chung, Raymond T.; Tolkoff-Rubin, Nina; Pascual, Manuel (2001). "Posttransplant Diabetes Mellitus in Liver Transplant Recipients: Risk Factors, Temporal Relationship with Hepatitis C Virus Allograft Hepatitis, and Impact on Mortality1". Transplantation. 72 (6). Ovid Technologies (Wolters Kluwer Health): 1066–1072. doi:10.1097/00007890-200109270-00015. ISSN 0041-1337. PMID 11579302.
- ^ Bahtiyar, Gül; Shin, John J.; Aytaman, Ayse; Sowers, James R.; McFarlane, Samy I. (2004). "Association of diabetes and hepatitis C infection: Epidemiologic evidence and pathophysiologic insights". Current Diabetes Reports. 4 (3). Springer Science and Business Media LLC: 194–198. doi:10.1007/s11892-004-0023-7. ISSN 1534-4827. PMID 15132884. S2CID 45679334.
- ^ "Diagnosis and Classification of Diabetes Mellitus". Diabetes Care. 35 (Supplement_1). American Diabetes Association: S64–S71. December 13, 2011. doi:10.2337/dc12-s064. ISSN 0149-5992. PMC 3632174. PMID 22187472.
Further reading
- Longaker, Lauren; Clements, Jennifer N. (2022). "Evidence-Based Management of Steroid-Induced Hyperglycemia in the Inpatient Setting". ADCES in Practice. 10 (1): 40–45. doi:10.1177/2633559X211056902. ISSN 2633-559X. S2CID 244519159.
- Li, Jia-Xu; Cummins, Carolyn L. (May 18, 2022). "Fresh insights into glucocorticoid-induced diabetes mellitus and new therapeutic directions". Nature Reviews Endocrinology. 18 (9). Springer Science and Business Media LLC: 540–557. doi:10.1038/s41574-022-00683-6. ISSN 1759-5029. PMC 9116713. PMID 35585199.
External links
This page was last edited on 12 February 2024, at 04:37