Glucocorticoids in IBD

Glucocorticoids in IBD

It is assumed that the anti-inflammatory properties of steroids are responsible for their therapeutic efficacy. Glucocorticoids act by binding to a glucocorticoid receptor which binds to a glucocorticoid-binding element (GRE) on DNA. Binding of this complex to the DNA results in inhibition of transcription of specific genes. For inflammatory bowel diseases, the following activities of glucocorticoids are important:

  1. Decreased production of cytokines, interleukins, and TNF
  2. Decreased influx of leukocytes
  3. Decreased activity of mononuclear cells and proliferation of T and B cells

Glucocorticosteroids are typically employed in IBD when 5-ASA products are inadequate. This may be in the case of acute attacks, when patients are significantly ill and can require intravenous administration. The majority of patients with severe ulcerative colitis will have a response in 7 to 10 days. However, due to the serious adverse events associated with long-term use of systemic glucocorticosteroids, chronic administration is usually avoided. When used chronically, glucocorticosteroid adverse effects can be minimized either with topical hydrocortisone enemas or foams, or with budesonide. When budesonide is given orally, more than 90% of this corticosteroid is eliminated via the liver's first-pass effect. However, despite these precautions, the side effects of glucocorticosteroids still correlate with the dose and duration of administration.


Appropriate utilization of corticosteroids for inflammatory bowel disease includes all the following EXCEPT: