Not all hyperglycaemia in hospitalised pneumonia is created equal.

Community-acquired pneumonia (CAP) remains a major cause of hospitalisation and mortality worldwide. Corticosteroid therapy reduces 30-day mortality in hospitalised patients with CAP but nearly doubles the risk of hyperglycaemia. It may appear that hyperglycaemia can arise from distinct mechanisms: "inflammation-mediated hyperglycaemia," which signals disease severity and predicts worse outcomes, and "corticosteroid-induced hyperglycaemia," a side effect of beneficial treatment that may appear not to increase mortality risk. Evidence from COVID-19 cohorts supports this distinction, showing that hyperglycaemia following corticosteroid use correlates with disease severity and longer hospital stays but not with increased mortality. Early glycaemic control reduces complications such as healthcare-associated infections in the context of hyperglycaemia due to inflammatory mediators and in the absence of corticosteroids, yet its role in corticosteroid-induced hyperglycaemia remains unclear. The lack of a standardised definition of hyperglycaemia further complicates research and clinical management. Understanding the differential impacts and optimal glucose targets for these potential hyperglycaemia subtypes is critical. Future research should focus on evaluating the effects of glucose control on outcomes in corticosteroid-associated hyperglycaemia, determining optimal glycaemic thresholds and evaluating suitable therapeutic management strategies in this clinical context.