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Carnitine deficiency as a cause of lipid storage myopathy originates from a defect of carnitine transport into muscle cells.1 Secondary carnitine deficiency with lipid storage myopathy2 can be a result of genetic defects of intermediary metabolism, especially mitochondrial respiratory chain defects, defects of β-oxidation enzymes, or drug therapy—for example, valproate or pivampicillin. A transient systemic carnitine deficiency regularly occurs during pregnancy even in healthy women. At delivery, decreased plasma carnitine concentrations are in the same range as in patients with inborn carnitine deficiency.3
We report a 24 year old woman in good health without any previous episodes of muscle weakness or metabolic crises who experienced a slowly progressive weakness of proximal muscles after delivery. The pregnancy and delivery had been uneventful other than the necessity for a caesarean section due to placental insufficiency. She did not receive any medication during pregnancy or after delivery with the exception of the nitrous oxide-oxygen-isoflurane anaesthesia in combination with vecuronium bromide, suxamethonium chloride, codeine, and fentanyl. Atropine and theophylline were given during the first hours after the section.
The muscular weakness was first noticed three months after delivery and increased to a so far stable deficit with only slight fluctuations within the …