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Oral corticosteroids in the management of chronic

rhinosinusitis with and without nasal polyps: Risks and

benefits

David M. Poetker, M.D., M.A.

ABSTRACT

Background:

Oral steroids are synthetic mimics of adrenal cortex hormones and are considered a staple in the management of chronic rhinosinusitis due

to their anti-inflammatory effects. Despite their common use, many providers are not familiar with the potential risks of the drugs.

Methods:

Literature review.

Results:

An overview of the existing data on the risks of oral steroids is presented as well as a review of the malpractice lawsuits with regard to oral steroid

use and a discussion of the data that support the use of oral steroids in patients with chronic rhinosinusitis with and those without nasal polyps.

Conclusion:

It is essential for providers to be aware of the potential complications of a medication, the medical jurisprudence of the drugs, and the data

that support their use.

(Am J Rhinol Allergy 29, 339–342, 2015; doi: 10.2500/ajra.2015.29.4223)

O

ral steroids are a mainstay of treatment in the management of

sinonasal inflammatory disease, are commonly used, and are

considered by many rhinologists to constitute a key component of

“maximal” medical therapy.

1

Their anti-inflammatory effects to treat

the inflammation associated with chronic rhinosinusitis (CRS) as well

as their antifibroblast effects to reduce postoperative scar formation

are the most common reasons for their widespread use.

2

Despite their

common use, many providers are not familiar with the potential risks

of the drugs.

The objectives of this review were to present an overview of the

existing data on the risks of oral steroids. This was not intended to be

an exhaustive review because other articles exist that specifically

outline those risks.

3

We plan to discuss what is known about specific

risks, review the lawsuits regarding oral steroid use, and finally,

discuss the data that support the use of oral steroids in patients with

CRS, with and without nasal polyps.

COMPLICATIONS OF STEROID USE

Morphologic Changes

Redistribution of adipose tissue, a common effect associated with

prolonged oral steroids, is known as “corticosteroid-induced lipodys-

trophy” or “cushingoid” changes, and includes truncal obesity, facial

adipose tissue (moon facies), and dorsocervical adipose tissue (buf-

falo hump).

4

The rate and incidence is variable but has been reported

to occur in 15% of patients in 3 months, with daily doses equivalent

to 10–30 mg of prednisone.

4

Higher doses and longer durations of

corticosteroids seem to increase the frequency of adipose tissue re-

distribution.

5

The risk is reportedly higher in women, patients 50

years of age, and patients with either a high initial body mass index

or a high calorie intake.

5

Hyperglycemia

Steroids increase blood sugars by stimulating proteolysis, promot-

ing gluconeogenesis, and inhibiting glucose uptake.

6

In addition,

steroids cause an insulin resistance by decreasing the ability of adi-

pocytes and hepatocytes to bind insulin. This effect can occur within

hours of beginning therapy but seems to decrease with prolonged

use.

6

Synthetic steroids are many times more potent than natural

steroids at decreasing carbohydrate tolerance.

6

Upon cessation of the

steroids, the inhibition of glucose uptake and metabolism usually

returns to normal.

6

Despite their common use, the degree of hyper-

glycemia caused by steroids has not been clearly established.

Infection

Although steroids increase circulating neutrophils by enhanced

release from bone marrow and reduced migration from blood vessels,

the number of lymphocytes, monocytes, basophils, and eosinophils

decrease due to a migration from the vascular bed to lymphoid

tissue.

7

Steroids can impair neutrophil function by reducing their

adherence to vascular endothelium and their bactericidal activity;

inhibit antigen-presenting cells by limiting chemotaxis, phagocytosis,

and the release of cytokines; decrease the expression of inflammatory

mediators; and may inhibit B-cell production of immunoglobulins.

7,8

Interestingly, steroid administration on an alternate day schedule has

been shown to reduce their negative impact on leukocyte function.

8

Two large meta-analyses found that the rate of infections were

significantly higher in patients treated with steroids.

9,10

Further re-

view found that patients who received a daily dose of 10 mg per

day or a cumulative dose of 700 mg of prednisone did not have an

increased rate of infectious complications.

10

Although the disease

processes for which the patients are being treated may themselves be

independent risk factors for infection, close review of the included

studies identified few patients with diseases known to increase risk

for infection.

9,10

Additional studies demonstrated that patients treated

with glucocorticoids are at increased risk for developing invasive

fungal infections, pneumocystosis, and viral infections, especially in

patients who have undergone bone marrow transplantation.

4,11–15

Wound Healing

Steroids inhibit the natural wound healing process by decreasing

the influx of macrophages, which may decrease phagocytosis as well

as growth factor and/or cytokine production.

16–19

Steroids can also

delay reepithelialization, decrease the fibroblast response, slow cap-

illary proliferation, and inhibit collagen synthesis and wound matu-

ration.

16,18,20

From the Division of Otolaryngology, Department of Surgery, Zablocki VA Medical

Center, Milwaukee, Wisconsin

D. Poetker is a speaker for Intersect ENT and a consultant for GlaxoSmithKline

Presented at the North American Rhinology and Allergy Conference, Boca Raton,

Florida, February 7, 2015

Address correspondence to David M. Poetker, M.D., Division of Rhinology and Sinus

Surgery, Department of Otolaryngology and Communication Sciences, Medical College

of Wisconsin, 9200 W Wisconsin Avenue, Milwaukee, WI 53226

E-mail address:

dpoetker@mcw.edu

Copyright

©

2015, OceanSide Publications, Inc., U.S.A.

American Journal of Rhinology & Allergy

Reprinted by permission of Am J Rhinol Allergy. 2015; 29(5):339-342.

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