Gynäkologie und Geburtshilfe
Offener Zugang

Abstrakt

Mütterliche mitochondriale Enzephalomyopathie, Laktatazidose und Schlaganfall-ähnliche Episoden-Syndrom und neonatale Magnesiumtoxizität: Ein Fallbericht

Bénédicte Le Tinier, Kuntheavy Ing Lorenzini, Arnaud Joal and Begoña Martinez De Tejada

Introduction: Mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) syndrome is a progressive disorder associated with neurologic, cardiac, neuromuscular, hepatic, metabolic and gastrointestinal dysfunction, including potential anesthetic and obstetrical complications. Increased susceptibility to drugs in patient with MELAS syndrome can be due to drug-induced mitochondrial toxicity and/or decreased elimination. We present here a case of severe neonatal magnesium sulfate toxicity in the context of MELAS syndrome.

Case presentation: A 43-year-old, gravida 5, para-5 (4 prior vaginal deliveries and the current cesarean section) woman with asymptomatic MELAS syndrome (carrier of the genetic variant NC_012920.1: m3243A>G in 20% of the mitochondrial DNA) was given intravenous magnesium sulfate for preeclampsia shortly before an emergency cesarean section at 33 weeks. The newborn presented a severe toxic effect characterized by cardio-respiratory arrest. Genetic evaluation revealed that he carried the same maternal mutation, but at a higher rate (80%). There was no other risk factor for cardio-respiratory arrest other than the potential interaction between the maternal/ neonatal mitochondrial disease and the medication, thus potentially leading to the risk of overdose.

Conclusion: The cause of the severe toxicity is uncertain, but it may have resulted from magnesium accumulation in the mother and/or the newborn due the presence of the MELAS syndrome in the neonate. A close assessment of potential severe drug toxicity in mothers and neonates with MELAS syndrome is warranted.