Prevalence

UP TO 10% OF PATIENTS WITH DIFFICULT-TO-CONTROL T2D MAY HAVE UNDERLYING HYPERCORTISOLISM1-3

The physiologic drivers of hyperglycemia due to chronic endogenous hypercortisolism are different than hyperglycemia due to type 2 diabetes (T2D).4-6

Hyperglycemia due to hypercortisolism

  • Excess cortisol—usually caused by an adenoma on the adrenal (adrenocorticotropic hormone-independent) or pituitary gland or an ectopic tumor (both considered adrenocorticotropic hormone-dependent)—may be the cause of hyperglycemia in patients with difficult-to-control T2D5,7
  • Excess cortisol causes6:
    • Exacerbated gluconeogenesis and hepatic glucose output
    • Insulin resistance
    • β-cell dysfunction

THE FOLLOWING PATIENTS HAVE AN INCREASED RISK OF BEING DIAGNOSED WITH HYPERCORTISOLISM8

About 3.5 times icon.

~3.5x increased risk in patients with advanced T2D* (n=2283)†

About 2.0 times icon.

~2.0x increased risk in patients who require insulin (n=1400)‡

About 2.0 times icon.

~2.0x increased risk in patients with T2D + hypertension (n=2184)

Advanced T2D defined as the prevalence of microvascular/macrovascular complications or insulin treatment plus hypertension or hypertension treated with 2 or more medications.8

†DerSimonian and Laird (DSL) method (OR, 3.47; 95% confidence interval [CI], 2.12-5.67; P<0.0001) and Hartung-Knapp-Sidik-Jonkman (HKSJ) method (OR, 3.60; 95% CI, 2.03-6.41; P=0.004).8

‡DSL method (OR, 2.29; 95% CI,1.07-4.91; P=0.034) and HKSJ method (OR, 2.50; 95% CI, 0.30-21.01; P=0.205).8

DSL method (OR, 1.92; 95% CI, 1.05-3.50; P=0.034) and HKSJ method (OR, 2.13; 95% CI, 0.81-5.65; P=0.100).8

Heartbeat icon.

Left untreated, hypercortisolism can lead to increased mortality

VIEW DATA
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How to screen for hypercortisolism in patients with T2D

VIEW SCREENING
Test tubes icon.

Additional tests may be needed to identify hypercortisolism

HOW TO EVALUATE

References

1. Chiodini I, Torlontano M, Scillitani A, et al. Eur J Endocrinol. 2005;153(6):837-844. doi:10.1530/eje.1.02045 2. Catargi B, Rigalleau V, Poussin A, et al. J Clin Endocrinol Metab. 2003;88(12):5808-5813. doi:10.1210/jc.2003-030254 3. Costa DS, Conceição FL, Leite NC, Ferreira MT, Salles GF, Cardoso CR. J Diabetes Complications. 2016;30(6):1032-1038. doi:10.1016/j.jdiacomp.2016.05.006 4. Galicia-Garcia U, Benito-Vicente A, Jebari S, et al. Int J Mol Sci. 2020;21(17):6275. doi:10.3390/ijms21176275 5. Scaroni C, Zilio M, Foti M, Boscaro M. Endocr Rev. 2017;38(3):189-219. doi:10.1210/er.2016-1105 6. Barbot M, Ceccato F, Scaroni C. Front Endocrinol (Lausanne). 2018;9:284. doi:10.3389/fendo.2018.00284 7. Guaraldi F, Salvatori R. J Am Board Fam Med. 2012;25(2):199-208. doi:10.3122/jabfm.2012.02.110227 8. Aresta C, Soranna D, Giovanelli L, et al. Endocr Pract. 2021;27(12):1216-1224. doi:10.1016/j.eprac.2021.07.014