xposure during the first trimester,78 during the second trimester, 16 during the third trimester, and 4 unknown). The occurrence
of major birth defects (excluding fetal deaths and induced abortions without reported defectsand all spontaneous pregnancy losses) during first-trimester exposure to sumatriptan was 4.2%(20/478 [95% CI: 2.6% to 6.5%]) and during any trimester of exposure was 4.2% (24/576 [95%CI: 2.7% to 6.2%]). The sample size in this study had 80% power to detect at least a 1.73- to1.91-fold increase in the rate of major malformations. The number of exposed pregnancyoutcomes accumulated during the registry was insufficient to support definitive conclusionsabout overall malformation risk or for making comparisons of the frequencies of specific birthdefects. Of the 20 infants with reported birth defects after exposure to sumatriptan in the firsttrimester, 4 infants had ventricular septal defects, including one infant who was exposed to both
sumatriptan and naratriptan, and 3 infants had pyloric stenosis. No other birth defect wasreported for more than 2 infants in this group.
In a study using data from the Swedish Medical Birth Register, live births to women whoreported using triptans or ergots during pregnancy were compared with those of women who didnot. Of the 2,257 births with first-trimester exposure to sumatriptan, 107 infants were born withmalformations (relative risk 0.99 [95% CI: 0.91 to 1.21]). A study using linked data from theMedical Birth Registry of Norway to the Norwegian Prescription Database compared pregnancyoutcomes in women who redeemed prescriptions for triptans during pregnancy, as well as amigraine disease comparison group who redeemed prescriptions for sumatriptan beforepregnancy only, compared with a population control group. Of the 415 women who redeemed prescriptions for sumatriptan during the first trimester, 15 had infants with major congenital
malformations (OR 1.16 [95% CI: 0.69 to 1.94]) while for the 364 women who redeemed
prescriptions for sumatriptan before, but not during, pregnancy, 20 had infants with major
congenital malformations (OR 1.83 [95% CI: 1.17 to 2.88]), each compared with the population
comparison group. Additional smaller observational studies eva luating use of sumatriptan during
pregnancy have not suggested an increased risk of teratogenicity.
Animal Data
Oral administration of sumatriptan to pregnant rats during the period of organogenesis resultedin an increased incidence of fetal blood vessel (cervicothoracic and umbilical) abnormalities.
The highest no-effect dose for embryofetal developmental toxicity in rats was 60 mg/kg/day.
Oral administration of sumatriptan to pregnant rabbits during the period of organogenesisresulted in increased incidences of embryolethality and fetal cervicothoracic vascular andskeletal abnormalities. Intravenous administration of sumatriptan to pregnant rabbits during theperiod of organogenesis resulted in an increased incidence of embryolethality. The highest oraland intravenous no-effect doses for developmental toxicity in rabbits were 15 and 0.75mg/kg/day, respectively.
Oral administration of sumatriptan to rats prior to and throughout gestation resulted inembryofetal toxicity (decreased body weight, decreased ossification, increased incidence ofskeletal abnormalities). The highest no-effect dose was 50 mg/kg/day. In offspring of pregnantrats treated orally with sumatriptan during or |
