Clinical Consequences

In the CATALYST study, patients with endogenous hypercortisolism had significantly more cardiovascular disease than patients without hypercortisolism1

More Cardiovascular Disease1*

In the CATALYST study, patients with hypercortisolism (post-DST cortisol >1.8 μg/dL) had significantly more cardiovascular disease compared to patients who did not have hypercortisolism (post-DST cortisol ≤1.8 μg/dL)1

Heart Disorders Overall

Comparison of cardiac disorder rates by post-DST cortisol: 20.9 percent for less than or equal to 1.8 mcg per dL versus 33.3 percent for greater than 1.8 mcg per dL; p-value less than 0.0001.

Coronary Artery Disease

Comparison of coronary artery disease rates by post-DST cortisol: 9.8 percent for less than or equal to 1.8 mcg per dL versus 16.7 percent for greater than 1.8 mcg per dL; p-value 0.003.Comparison of coronary artery disease rates by post-DST cortisol: 9.8 percent for less than or equal to 1.8 mcg per dL versus 16.7 percent for greater than 1.8 mcg per dL; p-value 0.003.

Atrial fibrillation

Comparison of atrial fibrillation rates by post-DST cortisol: 3.0 percent for less than or equal to 1.8 mcg per dL versus 8.3 percent for greater than 1.8 mcg per dL; p-value 0.0004.Comparison of atrial fibrillation rates by post-DST cortisol: 3.0 percent for less than or equal to 1.8 mcg per dL versus 8.3 percent for greater than 1.8 mcg per dL; p-value 0.0004.

Congestive Heart Failure

Comparison of congestive cardiac failure rates by post-DST cortisol: 1.4 percent for less than or equal to 1.8 mcg per dL versus 6.7 percent for greater than 1.8 mcg per dL; p-value less than 0.0001.Comparison of congestive cardiac failure rates by post-DST cortisol: 1.4 percent for less than or equal to 1.8 mcg per dL versus 6.7 percent for greater than 1.8 mcg per dL; p-value less than 0.0001.

CATALYST was a phase 4, two-part, multicenter trial. Part one (screening phase) primary endpoint was to determine the prevalence of hypercortisolism in patients with difficult-to-control type 2 diabetes (N=1057). Participants were screened with a 1-mg DST. Hypercortisolism defined as cortisol >1.8 μg/dL with dexamethasone ≥140 ng/dL.1,2

†P-value from a simple logistic regression model is used separately for each variable for assessing a possible association of the variable with hypercortisolism.1

Hypercortisolism can lead to worsening TYPE 2 DIABETES (T2D) and hypertension

A systematic review and meta-analysis of 32 studies with adrenal incidentalomas found that patients with hypercortisolism experienced worsening T2D and hypertension compared to patients with nonfunctioning adenomas.3

WORSENING OF COMORBIDITIES

Patients with hypercortisolism experienced worsening comorbidities compared to patients with nonfunctioning adenomas.3

Worsening Comorbid Conditions

Comparison of worsening comorbid conditions in nonfunctioning adenoma versus mild autonomous cortisol excess: for type 2 diabetes, 0 percent versus 9.2 percent; for hypertension, 4.8 percent versus 13.4 percent.

Left untreated, endogenous hypercortisolism can lead to increased cardiovascular morbidity and mortality

INCREASED CARDIOVASCULAR MORTALITY

A prospective study of patients with endogenous hypercortisolism* revealed that when providing medical treatment for comorbidities, like T2D and/or hypertension, directly treating the underlying hypercortisolism can reduce cardiovascular risk. This long-term follow-up (15 years) compared cardiovascular survival in patients with nonfunctioning adenomas (NFA; n=471), patients who received medications optimized for comorbidities† (OM; n=118), and patients who received surgery (n=29).2,4

Optimized Medications For Comorbidities May Not Reduce Cardiovascular Risk

Patients with hypercortisolism who received only optimized medications (OM) for comorbidities† had a 2.6x increased risk for cardiovascular mortality compared to patients with nonfunctioning adenoma (NFA).4

Cumulative Cardiovascular Survival In Patients During Follow-up1

Cumulative CV survival by group: Risk ratio 2.64 for OM vs NFA, 1.54 for surgery vs NFA, 1.72 for OM vs surgery; log-rank p < 0.001.

Dexamethasone suppression test (DST) cortisol >1.8 µg/dL (or >50 nmol/L) plus 1 abnormal hormonal test of hypothalamic-pituitary-adrenal axis.4

†Pharmacological therapy optimized to reduce altered metabolic and cardiovascular parameters (eg, T2D and hypertension).4

Despite receiving optimized medications for comorbidities, including T2D and hypertension, after 3 years, patients with hypercortisolism experienced no significant improvements.4

Twenty-four percent.

Nearly 1 in 4 patients with difficult-to-control T2D had endogenous hypercortisolism1

UNCOVER PREVALENCE

The 1-mg dexamethasone suppression test detects all etiologies of hypercortisolism2

VIEW SCREENING

Discuss the research with a Corcept representative

CONTACT A REP

References

1. Buse JB, Kahn SE, Aroda VR, et al. Diabetes Care. 2025;48(00):1-9. doi:10.2337/dc24-2841 2. DeFronzo RA, Auchus RJ, Bancos I, et al. BMJ Open. 2024;14(7):e081121. doi:10.1136/bmjopen-2023-081121 3. Elhassan YS, Alahdab F, Prete A, et al. Ann Intern Med. 2019;171(2):107-116. doi:10.7326/M18-3630 4. Petramala L, Olmati F, Concistrè A, et al. Endocrine. 2020;70(1):150-163. doi:10.1007/s12020-020-02297-2