Author: Lauren Aversman, PharmD Candidate 2016
Clinical review: Kelly Cochran, PharmD, BCPS
Corticosteroids are used to treat or control a wide range of health conditions, specifically for their anti-inflammatory properties. By reducing inflammation, the associated tissue damage and pain can also be reduced, helping you to effectively manage the signs and symptoms of multiple disease states such as arthritis, asthma, or even multiple sclerosis. However, there are other indications aside from the anti-inflammatory effects. Corticosteroids can also affect the immune system, decreasing our body’s immune response. Our immune system is thought to help us fight infection and prevent us from becoming sick; however, when our body has an unnatural response and starts attacking its own cells, we need an immune suppressant to help control our body’s fighting power. Corticosteroids are capable of this type of action, and therefore are often times also referred to as immune suppressants.1
There are different classifications of corticosteroids, including glucocorticoids and mineralocorticoids, both of which are secreted by the adrenal glands, located on top of the kidneys. Although these are naturally produced in our bodies, levels that exceed our natural production are necessary in order to see the anti-inflammatory or immunosuppressive effects.2 Each type is similar, but they do have distinct differences. In addition to the anti-inflammatory and immunosuppressive effects, glucocorticoids mimic cortisol, a natural hormone produced by our body, essential for the utilization of carbohydrates, fat and protein as well as aiding in our normal response to stress.3 Like all medications, corticosteroids do not come without their risk for side effects. Common side effects seen with short term use of oral corticosteroids include elevated pressure in the eyes (glaucoma), fluid retention, elevated blood pressure, mood swings and weight gain. With longer term use, you may also experience high blood sugar, increased risk of infection, thinning bones (osteoporosis), and thin skin or easy bruising. The severity and type of side effects seen is dependent on the total daily dose and can also differ among each individual. When discontinuing after prolonged use (>3 weeks), a tapered dosing schedule may be necessary to slowly reverse adrenal gland suppression.4 Common medications that are classified as glucocorticoids include prednisone, methylprednisolone, dexamethasone, and hydrocortisone.
Mineralocorticoids also play a role in anti-inflammatory and immunosuppressive therapy, but more importantly, they mimic aldosterone. Aldosterone is another hormone secreted by the adrenal glands, which plays a critical role in the regulation of sodium and water transport.2 Fludrocortisone has the highest mineralocorticoid potency, and can be used for replacement therapy if the adrenal gland does not produce enough hormones naturally (Addison’s disease) or in individuals with orthostatic hypotension.5
Orthostatic hypotension, sometimes referred to as postural hypotension, is defined as a drop in systolic pressure by 20 mmHg or a drop in diastolic pressure by 10 mmHg when an individual goes from a lying or seated position to a standing position.6 This drop in blood pressure is only temporary because your body senses to increase the pressure to ensure proper blood flow back to your brain; however, it can cause the individual to become dizzy, lightheaded, or even pass out. With the use of fludrocortisone, higher levels of sodium are retained in the body, which causes an increase in water retention, resulting in higher blood volume and higher blood pressure in hopes to eliminate the low pressure after someone abruptly changes their postural position.2
As you can see, all corticosteroids can have similar effects, but it’s their subcategory of glucocorticoid or mineralocorticoid that can differentiate between their distinct mechanisms of action. Corticosteroids will continue to be a mainstay in treatment regimens for individuals suffering from chronic inflammation, auto-immune disorders, and many other disease states.
Citations:
- Katzung B, ed. Basic and Clinical Pharmacology. 10th San Franciso, CA: McGraw-Hill Companies Inc; 2007.
- Fuller P, Young M. Mechanisms of Mineralocorticoid Action. American Heart Association Web Site. http://hyper.ahajournals.org/content/46/6/1227.full. Published Oct 18, 2005. Accessed July 21, 2015.
- Velden V H. Glucocorticoids: Mechanisms of Action and Anti-inflammatory Potential in Asthma, Mediators of Inflammation. U.S. National Library of Medicine. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1781857/. Accessed July 21, 2015.
- Neiman L. Pharmcologic Use of Glucocorticoids. Up To Date Web site. http://www.uptodate.com/contents/pharmacologic-use-of-glucocorticoids. Accessed July 28, 2015.
- Corticosteroids Systemic Equivalencies. Lexicomp Online. Lexicomp Web Site. http://online.lexi.com/lco/action/doc/retrieve/docid/patch_f/4144. Accessed July 21, 2015.
- NINDS Orthostatic Hypotension Information Page. National Institute of Neurological Disorders and Stroke. http://www.ninds.nih.gov/disorders/orthostatic_hypotension/orthostatic_hypotension.htm. Updated September 30, 2011. Access July 28, 2015.