In pediatric populations (<18 years), secondary adrenocortical insufficiency (ROR: 7.09, 95% CI = 2.6–19.35) was more prevalent, likely due to immature immune-endocrine crosstalk—IL-1β is a critical mediator of stress-induced cortisol release in children, and its inhibition may disrupt this axis [37,38,39]. Here, IL1B is linked to adrenocortical insufficiency.