By Michael Spinner
Corticosteroids are commonly prescribed medications used to suppress an overactive and unwanted immune response. This may include suppression of an immune response to innocuous, environmental antigens (allergies or asthma), self-antigens (autoimmunity), and foreign, transplanted antigens (allograft rejection).
While beneficial in reducing inflammation in these conditions, there are numerous pathologic side effects of corticosteroids, which should temper their use when possible. Remember the major side effects of corticosteroids with the mnemonic CUSHINGOID:
U – Ulcers
S – Striae, Skin thinning
H – Hypertension, Hirsutism
I – Immunosuppression, Infections
N – Necrosis of femoral heads
G – Glucose elevation
O – Osteoporosis, Obesity
I – Impaired wound healing
D – Depression/mood changes
These numerous side effects of corticosteroids are a reflection of their diverse physiologic effects on numerous organ systems. From a cardiovascular and renal standpoint, corticosteroids have some mineralocorticoid activity, often leading to hypertension from salt and fluid retention.
From an endocrine and metabolic standpoint, corticosteroids promote glucose production from amino acid breakdown and oppose the actions of insulin, often leading to hyperglycemia or steroid-induced diabetes. Over time, diversion of amino acids to glucose may also lead to muscle wasting, while fat redistribution often results in truncal obesity, including the classic “moon face” and “buffalo hump.”
Potent suppression of innate and adaptive immune responses may be desirable in mitigating allergic and autoimmune disease, but also heightens susceptibility to infection, often with opportunistic pathogens.
Recognition of the potential side effects of corticosteroids may help physicians anticipate and ideally prevent their occurrence (e.g. GI prophylaxis with proton pump inhibitors or H2 blockers to prevent peptic ulcers, or titration of blood pressure meds or insulin to correct for hypertension or hyperglycemia). Fortunately, the development of various “steroid-sparing” agents over the past few decades (e.g. calcineurin inhibitors for allograft rejection or specific cytokine inhibitors for autoimmune disease) has helped to reduce prolonged exposure to high-dose corticosteroids and minimize these pathologic side effects.