The effects of betamethasone on maternal cellular resistance to infection.
Antenatal administration of glucocorticoids is often used to facilitate fetal lung maturation in cases of prematurity; however, the effects of betamethasone on maternal immune function have not been established. Therefore maternal immune function was assessed with the use of in vitro techniques. Transient and incomplete suppression of the proliferative response to the T-cell mitogen phytohemagglutinin was demonstrated as early as 24 hours after administration of betamethasone. The magnitude and duration of suppression showed a corresponding increase with advancing gestational age, but these effects were not cumulative and were always short-lived (less than 72 hours). No such suppression of the B-cell mitogen lipopolysaccharide was detected. The nonspecific cellular resistance to infection of maternal monocytes was determined through coincubation with the facultative intracellular pathogen Listeria monocytogenes. Increased phagocytic activity with a normal bactericidal effect was measured in the cell preparations obtained from recipients versus nonrecipients of betamethasone. Taken together, these findings clearly show that both specific and nonspecific immune function are intact in the preterm gravid woman after administration of betamethasone and should allay concerns over its use for reasons of infection control alone.
Cunningham
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Department of Obstetrics and Gynecology, United States Naval Hospital, Portsmouth, VA 23708.
Evans
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D001623:Betamethasone / Q000009:adverse effects*; D005260:Female; D006801:Humans; D007113:Immunity, Innate / Q000187:drug effects*; D007231:Infant, Newborn; D008213:Lymphocyte Activation / Q000187:drug effects; D009894:Opportunistic Infections / Q000276:immunology*; D010587:Phagocytosis / Q000187:drug effects; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000276:immunology*; D012127:Respiratory Distress Syndrome, Newborn / Q000517:prevention & control
D001623:Betamethasone