**12. Gastrointestinal side effects**

Side effects of GCs on the gastrointestinal system include peptic ulcers (PU), upper gastrointestinal bleeding (UGB), and pancreatitis.

until visual loss. Discontinuation of GCs leads to reversal of intraocular hypertension within

Posterior subcapsular cataracts (PSC) induced by GCs appears bilaterally and is distinguishable from the more common types of cataract. Increased glucose levels, caused by an

inhibition of glucose-6-phosphate-dehydrogenase; inhibition of RNA synthesis; loss of ATP; and covalent binding of steroids to lens proteins are the possible mechanisms. These changes are specific for PSC induced by GCs. The risk appears to be both duration and dose-dependent. PSC is more likely to occur at higher doses of GCs. But as with other side effects, lower

CSCR is also associated with systemic GCs. Symptoms are central visual blur and reduced

Exophthalmos and chorioretinopathy rarely occur. Consequently, before treatment with GCs, clinicians should ask about the history of glaucoma, cataracts, and CSCR; and patients with

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

visual acuity. GCs should be used cautiously in patients with a history of CSCR [125].

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a few weeks, but the optic nerve damage is often permanent [122, 123].

doses (<5 mg prednisone per day) have been linked to PSC [123, 124].

risk factors should be referred to ophthalmologic examination.

**14. Immunosuppression and risk of infection**

organ transplant recipients [127–131].

increased gluconeogenesis rate; inhibition of Na<sup>+</sup>

**13.3. Central serous chorioretinopathy (CSCR)**

**13.2. Cataracts**

### **12.1. PU**

There is conflicting evidence related with the risk of PU for patients treated with glucocorticoid monotherapy. In a case-control study, there was no increased risk of PU at any dose or duration of glucocorticoid monotherapy. But in the same study, the combination of GCs with nonsteroidal anti-inflammatory drugs (NSAID), there was a significantly increased risk of peptic ulcer. Treatment with GCs may cause gastric irritation, more than PU [116, 117].
