Which immune change is associated with infection risk in hypercortisolism?

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Multiple Choice

Which immune change is associated with infection risk in hypercortisolism?

Explanation:
Excess cortisol suppresses the immune system by hitting adaptive immunity, especially lymphocytes. This creates lymphopenia because glucocorticoids reduce lymphocyte production, promote their redistribution, and can trigger lymphocyte apoptosis, leading to weakened T-cell–mediated responses and lower IL-2 signaling. That weakened cell‑mediated immunity is what increases infection risk in hypercortisolism. Cortisol can also raise neutrophil counts through demargination, which might seem protective, but the critical vulnerability comes from the reduced lymphocytes. Changes in red blood cells or platelets aren’t the primary drivers of infection risk in this context.

Excess cortisol suppresses the immune system by hitting adaptive immunity, especially lymphocytes. This creates lymphopenia because glucocorticoids reduce lymphocyte production, promote their redistribution, and can trigger lymphocyte apoptosis, leading to weakened T-cell–mediated responses and lower IL-2 signaling. That weakened cell‑mediated immunity is what increases infection risk in hypercortisolism. Cortisol can also raise neutrophil counts through demargination, which might seem protective, but the critical vulnerability comes from the reduced lymphocytes. Changes in red blood cells or platelets aren’t the primary drivers of infection risk in this context.

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