Adverse effects of corticosteroids

Introduction

Systemic corticosteroid treatment inevitably results in adverse effects if the dose and/or duration of treatment are sufficient, because most are dose-related biological effects of the hormone. A summary of the major adverse effects of systemic corticosteroid treatment is given in Table 6.1. More information about some of these effects and strategies for minimising them are discussed below.

Corticosteroids injected into joints or soft tissues are commonly associated with mild, transient adverse effects 

Corticosteroids applied topically can also cause adverse effects 

Important complications of corticosteroids (Table 6.1)

Glucocorticoid

Mineralocorticoid

avascular necrosis of the femoral and humeral head dermatological effects (eg skin atrophy, purpura and ecchymoses, striae, hirsutism) gastrointestinal effects (eg dyspepsia, risk factor for peptic ulceration, gastrointestinal bleeding) growth retardation immunosuppression, risk of infections metabolic effects (eg diabetes, hypertriglyceridaemia) myopathy ocular effects, particularly increased intraocular pressure and cataracts osteoporosis pituitary-adrenal suppression  psychological disturbances (eg euphoria, depression, paranoid psychosis) weight gain and redistribution of fat

hypertension hypokalaemic alkalosis sodium-retaining effects

Avascular necrosis

Avascular or ischaemic necrosis can affect a variety of bones, but most commonly involves the proximal femur. It is an infrequent and idiosyncratic adverse effect of corticosteroid treatment, and occurs more commonly following exposure to doses in excess of 20 mg/day prednis(ol)one. The time between corticosteroid exposure and the development of avascular necrosis is variable, and can be up to many years, which makes diagnosis difficult. Both the pathogenesis and treatment of this condition remain controversial.

Avascular necrosis should be considered in the differential diagnosis of hip and groin pain especially in patients who have been on high-dose and/or long-term corticosteroids at any time.

Bone density loss

Osteoporosis is a risk for patients on continuous glucocorticoid therapy in doses greater than the equivalent of prednisolone 5 to 7.5 mg per day. The risk of osteoporosis becomes greater at higher glucocorticoid doses. Loss of bone mineral density occurs rapidly after corticosteroids are commenced and may exacerbate the osteoporosis associated with some rheumatological diseases, such as ankylosing spondylitis, and inflammatory bowel disease .

If corticosteroid therapy is expected to last for longer than a month, strategies to minimise bone density loss should begin as soon as treatment with corticosteroids starts.

The key issues are:

• weight-bearing exercise where possible

• adequate calcium intake

• measurement and addition of vitamin D if indicated

• monitoring bone densitometry from initiation of long-term glucocorticoid therapy

• bisphosphonate therapy as indicated.

For further discussion and detail,

Hyperglycaemia

Hyperglycaemia frequently accompanies treatment with high-dose corticosteroids. While oral hypoglycaemic agents can often control this, insulin may be necessary. Regimens using intermediate-acting insulin at lunchtime may be most successful in controlling the hyperglycaemia, which is commonly worse in the evening.

Blood glucose levels should be closely monitored in diabetic patients on long-term corticosteroid therapy.

Infections

High-dose corticosteroids increase the risk of contracting many types of infection, and may mask the early symptoms of infection, resulting in later diagnosis, delay in treatment, and more severe clinical consequences. Reactivation of Mycobacterium tuberculosis (TB) infection occurs with such frequency that prior to commencing immunosuppressive treatment with corticosteroids, screening for active or latent TB should be considered . Prophylaxis for Pneumocystis jiroveci (carinii) infection should be considered in patients who are at risk and on high-dose oral corticosteroids long term 

Use of steroid-sparing drugs

Drugs from other classes may be used to allow a reduction of the corticosteroid dose. For example, in rheumatology, use of disease-modifying antirheumatic drugs (DMARDs) and NSAIDs often allows a lower corticosteroid dose to be used.