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Letters to the Editor Indian Pediatrics 2002; 39: 101-102 |
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Antenatal Carbamazepine Use Associated with d-TGA and ASD |
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"Fetal anticonvulsant syndrome" refers to a group of phenotypic abnormalities in the fetus associated with the use of various anti-convulsants during pregnancy(1). Congenital heart diseases have been described with the use of anticonvulsants(2), but usually consist of acyanotic diseases like ventricular septal defects. We describe a hitherto unreported possble association of d-TGA with the maternal use of Carbamazepine. A 20-day-old male child was brought to the emergency with history of bluish discoloration of hands and feet since birth, and swelling of feet since last 5 days. Mother was a known epileptic for the last 2.5 years and was on 800 mg of Carbamazepine monotherapy (in two divided doses) till 6 months of pregnancy after which the drug was stopped. The child weighed 3.0 kg and had an occipito frontal circumference of 32.5 cm (between –2 and –3 SD). He also had micrognathia, peripheral and central cyanosis, pedal edema, sweating over the forehead, tachycardia, single S2 and ejection systolic murmur. Chest examinaltion revealed basal crepts bilaterally. Initial impression was of a cyanotic congenital heart disease with conges-tive cardiac failure with increased blood flow. Chest radiograph showed pulmonary plethora and cardiomegaly. Two dimensional echo-cardiography revealed d-TGA with small atrial septal defect and intact interventricular septum, no pulmonary stenosis. The child was started on decongestive therapy with lasix and digoxin and showed improvement in clinical status. He was subsequently referred for definitive surgery. Carbamazepine has been used as a primary drug in the treatment of all types of seizures, except absence seizures. Carbamazepine has been shown to be associated with major malformations(2-5). However in none of the studies reviewed was Carbamazepine mono-therapy associated with any congenital heart disease other than a ventricular septal defect(5). Our index case had history of mono-therapy with Carbamazepine in the mother till 6 months gestation. This child had small OFC between –2SD and –3SD and micrognathia, both known associations of antenatal Carba-mazepine therapy(5). Also there was d-TGA with atrial septal defect. It would seem that this too would be related to teratogenic effects of Carbamazepine administration. The metabolic basis behind "fetal anticonvulsant syndrome" has been suggested to be an inhibition of the enzyme epoxide hydrolase that results in the accumulation of teratogenic epoxide intermediaries of these antiepileptic drugs(2). It would be prudent to record in literature an association between the various drugs and the malformation, though it is clear that a single case does not make the association casual. This case adds to the clinical profile of "fetal anticonvulsant syndrome". Gaurav Gupta, |
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