A patient with lupus on corticosteroids develops fever and hypotension. Which factors increase risk of severe infection? Select all that apply.

Patients with systemic lupus erythematosus on long-term corticosteroid therapy face multiple compounding risks for severe infection. Immunosuppression is the most direct mechanism: corticosteroids reduce lymphocyte proliferation, impair neutrophil function, and diminish antibody production, leaving the patient unable to mount an effective defense against pathogens. A masked inflammatory response is equally dangerous because corticosteroids blunt the fever, redness, and pain that normally signal infection; by the time obvious symptoms appear, the infection may already be severe, as in this scenario where fever and hypotension suggest septic shock. Hyperglycemia, a well-documented adverse effect of corticosteroid therapy, impairs neutrophil chemotaxis and phagocytosis and promotes bacterial growth, independently increasing infection severity and risk of poor outcomes. Steroid-induced hypertension does not increase infection risk and is actually the opposite of what this patient is exhibiting; that option is a distractor. Disease exacerbation refers to the lupus flare itself, not a risk factor for infection, and the clinical picture here (fever and hypotension) points more strongly toward sepsis than a primary lupus flare, making it an incorrect choice.