Transient, profound thrombocytopenia in a premature infant: Is this a ranitidine-induced immune reaction?

Abstract

Case Report: A female infant was delivered at 31-weeks gestation for suspected chorioamnionitis. Maternal antenatal dexamethasone had been given one hour prior to delivery to hasten foetal lung maturation. From day 11 to 19, the infant received ranitidine for gastric hyperacidity (pH <4). On day 16, her blood culture was positive for Staphylococcus epidermidis and her C-reactive protein (CRP) was slightly elevated. She was treated with vancomycin and cefotaxime. On day 19, when she had become clinically well, profound thrombocytopenia (8 x 109/L), eosinophilia (3 x 109/L) and borderline neutropenia (1 x 109/L) occurred in the presence of highly elevated CRP (132 mg/L). For this she received multiple platelet transfusions. Ranitidine was ceased on day 19. On day 20, leukopenia and neutropenia had resolved when the last dose of cefotaxime was given. Eosinophil count normalised by day 21 and platelet count by day 25. Discussion: This phenomenon was similar to that reported in ranitidine-treated adults during acute illness. Although premature infants are generally thought to be incapable of drug-induced allergic reactions, the foetal immune system can be activated by intrauterine infections. Glucocorticoid therapy during mid to late gestation could heighten the immune sensitivity in premature infants. This infant's antenatal history and postnatal events could possibly have predisposed her to hypersensitivity to antigenic stimulation.