**14. Immunosuppression and risk of infection**

There are multiple anti-inflammatory and immunosuppressive effects of GCs (**Table 9**) [126]. These mechanisms may predispose patients to infections. The overall risk of infections is 50–60% higher in the patients exposed to GCs. The risk of infections can be related with dose and duration of GCs. Infection rates were not increased in patients given a daily dose of <10 mg or a cumulative dose of <700 mg of prednisone. But the exact dosages and duration that substantially change the benefit-risk ratio for GCs varies by the personal and the underlying risk factors. The risk factors for infections are the underlying disorders (especially rheumatoid arthritis and systemic lupus erythematosus), patient age, lower functional status, and concomitant use of immunosuppressive or biologic therapies. In addition, a low albumin level is strongly associated with the risk of infection, because of direct (i.e. as an etiological factor) or indirect (i.e. by being a marker of the malnutrition-inflammation syndrome) effects. Furthermore, a low albumin level is associated with a higher free glucocorticoid fraction. Due to the inhibition of cytokine release and associated reduction in inflammatory and febrile responses, patients treated with GCs may not be presented with obvious signs and symptoms of infection. Therefore, it may be difficult to detect infections at an early stage. In addition to serious bacterial infections, the increase in risk is much higher for opportunistic infections (e.g. *Pneumocystis jiroveci* pneumonia, herpes zoster tuberculosis, listeriosis, aspergillosis, nontuberculous mycobacterial disease, invasive fungal infections), and in specific populations (e.g. allogeneic bone marrow transplant and solid organ transplant). Reactivation of cytomegalovirus with GCs is a serious problem especially in solid organ transplant recipients [127–131].

### **Lymphocytes**


### **Neutrophils**


### **Other effects**


**Table 9.** Immunosuppressive effects of glucocorticoids (adapted from [126]).
