Abstract

Ritodrine hydrochloride, a beta 2 adrenergic receptor agonist, is used for prevention of preterm birth. Maternal cardiac arrhythmias, pulmonary edema, rhabdomyolysis, parotitis, granulocytopenia, acute generalized exanthematous pustulosis, nausea, vomiting, and elevated blood glucose are the main adverse reactions induced by ritodrine hydrochloride in the pregnant woman. The possible mechanisms of the above-mentioned adverse reactions may be associated with ritodrine hydrochloride inducing electrolyte imbalance, hypokalemia, changes of pulmonary capillary wedge pressure, muscular transient ischemia due to hypokalemia, hypersecretion of salivary amylase, bone marrow suppression, and promoting of glycogenolysis. The mechanism of acute generalized exanthematous pustulosis induced by ritodrine hydrochloride is yet unknown. Fetal over growth, fetal tachycardia, and neonates transient neutrophil reduction may be the main adverse reactions induced by ritodrine hydrochloride in the fetuses. The possible mechanisms may be associated with fetal insulin hypersecretion which is due to maternal hyperglycemia induced by ritodrine hydrochloride, immune-mediated toxic reactions through placental barrier, as well as changes in placental blood flow. The maternal heart rate, blood glucose, routine blood tests, liver and kidney function should be checked regularly when the pregnant woman is receiving ritodrine hydrochloride. Once the adverse reactions occured, ritodrine hydrochloride should be discontinued and the symptomatic treatment should be given. In infants whose mother received ritodrine hydrochloride, cardiac function should be evaluated by echocardiography when necessary, blood glucose should be checked, and breast-feeding or formula feeding should be started as early as possible. Key words: Ritodrine; Premature birth

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