16.04.2 Glucocorticoids

Another major treatment for inflammatory bowel disease is the glucocorticoids. In addition to inhibiting the production of prostaglandins and leukotrienes by inhibiting phospholipase A₂, glucocorticoids have inhibitory effects on other components of inflammation, such as histamine, cytokines, and adhesion molecules (Figure 16.7). Adhesion molecules are required for white blood cells to adhere to the site of inflammation. Prednisone is an example of a glucocorticoid, which inhibits all these components of inflammation. Oral prednisone is the standard treatment for acute severe exacerbations of inflammatory bowel disease. Indeed, prednisone gives remission in most patients with ulcerative colitis and active Crohn’s disease.

Figure 16.7 Components of inflammation inhibited by glucocorticoids (Copyright QUT, Sheila Doggrell)

The main problem with glucocorticoids, such as prednisone, is systemic circulation leads to increasing and more severe side effects with time. Thus only short courses of treatment should be used. With prolonged systemic treatment, prednisone causes the side effects of hypertension, hyperglycemia, an increased susceptibility to infection, osteoporosis, myopathy, behavioural disturbances, cataracts and more! Clearly, it is best to avoid long treatment with prednisone. Thus, prednisone is reserved for acute severe exacerbations of inflammatory bowel disease.

An alternative approach, if long term treatment with glucocorticoids is necessary is to use a glucocorticoid with extensive first pass liver metabolism to avoid some of the systemic side effects e.g. budesonide.

The weak glucocorticoid hydocorticosterone is used in enemas for a local effect in inflammation limited to the rectum (proctitis).