CATALYST identified hypercortisolism in 24% of patients with difficult-to-control type 2 diabetes. How should this finding influence current diagnostic protocols for endocrinologists and primary care physicians managing diabetes?

A 2.01% HbA1c reduction was observed in the 900mg Korlym group. How significant is this change relative to existing diabetes therapies, and what does it tell us about the role of cortisol in glycemic dysregulation?

Korlym led to significant reductions in body weight and waist circumference. Are these changes mechanistically tied to cortisol blockade, and could this be a unique advantage in managing patients with central obesity and insulin resistance?

The study reports glycemic improvements despite reductions or discontinuation of glucose-lowering medications. How do you interpret this finding in terms of treatment simplification and cost-effectiveness?

Only about a third of patients received the 900mg dose, yet this subgroup saw the greatest benefit. Do you see this informing a future dose-response strategy, and what considerations should guide individual dose titration in clinical practice?

Fatigue, depression, and metabolic disturbances are common to both type 2 diabetes and hypercortisolism. How can clinicians better distinguish between the two, especially in patients with multiple comorbidities?

Hypokalemia, fatigue, and nausea were the most reported adverse events. Were these side effects consistent with expectations for GR antagonism, and what monitoring protocols would you recommend to safely implement Korlym in this population?

Given the trial’s size and rigor, how might CATALYST shape future screening guidelines or reimbursement decisions for hypercortisolism diagnostics in metabolic clinics? Could it potentially justify routine dexamethasone suppression testing in certain diabetic subpopulations?