Recent in vitro investigations have demonstrated that corticosteroids
in combination with interleukin-4 induce the synthesis of IgE. Cortico
steroids are increasingly being used to treat the inflammatory compone
nt of asthma, This has raised concern over the potential in vivo effec
ts of corticosteroids on IgE production and the correlation of IgE-enh
ancing effects with clinical effects on asthma. In this study 10 patie
nts with asthma were given a 7-day course of 20 mg of prednisone, admi
nistered orally two times a day. All of the patients had a rise in ser
um IgE levels after the course of prednisone (p = 0.005). Detection of
specific IgE to pollen and perennial allergens demonstrated that the
rise in serum IgE was polyclonal. Peripheral blood mononuclear cells f
rom patients treated with prednisone produced increased levels of IgE
in vitro when exogenous IL-4 was added to their cultures. Peripheral b
lood mononuclear cells obtained from patients before and after adminis
tration of prednisone revealed a significant decrease in interferon-ga
mma synthesis (p = 0.005), but not in interleukin-4 (p = 0.6), after t
he course of prednisone. These findings were paralleled by a significa
nt decrease in the frequency of interferon-gamma (p = 0.03), bur not i
nterleukin-4 (p = 1.0) expressing cells. Despite the increase in IgE s
ynthesis, there was a significant increase in forced expiratory volume
in 1 second after the course of prednisone (p = 0.01). These data sug
gest that the observed rise in IgE production associated with predniso
ne treatment is not clinically deleterious bur reflects the immunomodu
latory effects of corticosteroids on T lymphocytes.