Clinical Consequences

INCREASED CARDIOVASCULAR MORTALITY

A prospective study of people with endogenous hypercortisolism* revealed that medical treatment of comorbidities, like type 2 diabetes (T2D), without directly treating the underlying hypercortisolism does not reduce cardiovascular risk. This long-term follow up (15 years) compared cardiovascular survival in people with nonfunctioning adenomas (NFA; n=471), people who received medications optimized for comorbidities (OM; n=118), and people who received surgery (n=29).1,2

Optimized Medications For Comorbidities May Not Reduce Cardiovascular Risk

People with hypercortisolism who received only optimized medications (OM) for comorbidities had a 2.6x increased risk for cardiovascular mortality compared to people with nonfunctioning adenoma (NFA).1

Cumulative Cardiovascular Survival In People During Follow-up1

Chart depicting a 2.6x greater cardiovascular mortality risk for patients with hypercortisolism.

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

Pharmacological therapy optimized to reduce altered metabolic and cardiovascular parameters (eg, T2D and hypertension).1

More Cardiovascular Disease*

In the CATALYST study, people with hypercortisolism (DST >1.8 μg/dL) had significantly more cardiovascular disease compared to people who did not have hypercortisolism (DST ≤1.8 μg/dL)3,4

Cardiac Disorders Overall

Chart depicting worsening cardiac disorders in patients with hypercortisolism.

Coronary Artery Disease

Chart depicting worsening coronary artery disease in patients with hypercortisolism.Chart depicting worsening coronary artery disease in patients with hypercortisolism.

Atrial fibrillation

 Chart depicting worsening atrial fibrillation in patients with hypercortisolism. Chart depicting worsening atrial fibrillation in patients with hypercortisolism.

Congestive Cardiac Failure

 Chart depicting worsening congestive cardiac failure in patients with hypercortisolism. Chart depicting worsening congestive cardiac failure in patients with hypercortisolism.

CATALYST was a phase 4, two-part, multicenter trial. Part one (screening phase) primary endpoint was to determine the prevalence of hypercortisolism in people 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.2,3

Worsening Symptoms

A systematic review and meta-analysis of 32 studies with over 4,000 people with adrenal incidentalomas found that people with hypercortisolism experienced worsening T2D and hypertension compared to people with nonfunctioning adenomas.5

Worsening T2d And Hypertension

Patients with hypercortisolism experienced worsening comorbidities compared to patients with nonfunctioning adenomas.5

Worsening Comorbid Conditions

 Chart depicting worsening comorbid conditions in patients with hypercortisolism.
 24 percent.

Nearly 1 in 4 people with difficult-to-control T2D had endogenous hypercortisolism3

UNCOVER PREVALENCE

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

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References

1. Petramala L, Olmati F, Concistrè A, et al. Endocrine. 2020;70(1):150-163. doi:10.1007/s12020-020-02297-2 2. DeFronzo RA, Auchus RJ, Bancos I, et al. BMJ Open. 2024;14(7):e081121. doi:10.1136/bmjopen-2023-081121 3. Buse JB, Kahn SE, Aroda VR, et al. Prevalence of hypercortisolism in patients with difficult-to-control type 2 diabetes: updated results from CATALYST part 1 [symposium]. Presented by Fonseca, V. at the 22nd World Congress Insulin Resistance Diabetes & Cardiovascular Disease; December 12-14, 2024; Los Angeles, CA. 4. Fonseca V, Aroda VR, Budoff M, et al. Prevalence of hypercortisolism in patients with difficult-to-control type 2 diabetes and cardiovascular disease: results from CATALYST. Poster 0046 presentation at: World Congress Insulin Resistance, Diabetes, & Cardiovascular Disease. Los Angeles, CA, December 12–14, 2024. 5. Elhassan YS, Alahdab F, Prete A, et al. Ann Intern Med. 2019;171(2):107-116. doi:10.7326/M18-3630