Systemic Corticosteroid Therapy

Prednisone and other systemic corticosteroids suppress inflammation by entering cells, binding cytoplasmic glucocorticoid receptors, and changing gene transcription. The result is less cytokine production, less leukocyte migration into tissues, and reduced capillary permeability. Swelling, pain, wheezing, rash, and autoimmune tissue injury may improve quickly because the inflammatory response has been turned down. That same effect creates the central safety problem: corticosteroids can blunt the visible signs of infection while impairing the immune response needed to control it. A patient may have less redness or fever yet be developing pneumonia, a urinary infection, or sepsis. Systemic corticosteroids also mimic cortisol. Cortisol helps maintain vascular tone, glucose availability, and the physiologic response to stress. Exogenous corticosteroids signal the hypothalamic-pituitary-adrenal axis to reduce endogenous cortisol production. After prolonged therapy, abruptly removing the drug can leave the patient without enough cortisol for routine function or acute stress.