No abstract

The study attempted to determine if widely used standards of fetal growth have been distorted by the inclusion of infanta with unrecognized growth disorders. 4505 infants of various gestational ages who survived were compared with 1034 of similar gestational ages who died in the perinatal period with disorders not known to affect growth (group A) and with 51 who died after intrapartum accidents (group 8). There were enough infants in the surviving group to compute mean body and placenta measurements starting at 28 weeks of gestation. Group A infants were undergrown at each gestational age compared with the surviving con- .da College of Medicine, Dept. Pediatrics. Cainesville. Polyamine content is correlated with nucleic acid synthesis in rapidly growing tissue and may serve as an indicator of damage by toxina.including teratogens. This report concerns the alterations in embryonic polyamine content after exposure to teratogens. Primagravid Swiss albino mice were injected intraperitoneally on day 9 with diphenylhydantoin (DPH). 88 mg/kg body weight; embryos were recovered on day 11. Pregnant Long-Evans rats were intubated on day 10 and a modified diet was supplemented with 9-methyl pteroylglutamic acid (9-methyl PGA) on days 10-13. Spermidine. spermine and putrescine were quantitated on a Durrum D-500 amino acid analyzer, and are reported as nmoles/mg of embryonic protein. Rat embryos from pregnancies treated with 9-methyl PGA had unaltered polyamines. Mouse embryos whose mothers were exposed to DPH had significant reductions in spermidine and spermine, but putrescine levels remained comparable. Growth during polyamine accumulation is attributed to their stimulation of dihydrofolate reductase, the enzyme antagonized by 9-methyl PGA.Since polyamines were unchanged during this antagonism, they may play no direct role in the reactivation of this enzyme system. Following DPH treatment embryonic DNA was lowered proportionally more than protein content, suggesting a block in DNA synthesis.Folate deficiency has been suggested as the mechanism of DPii teratogenesis. However, the differing polyamine responses to the 9-methyl PGA and DPH teratogenic regimens indicate different mechanisms may exist. H e d i a t r i c s , McGill University, Montreal.It is accepted that vertebral, anal, tracheo-esophageal , renal and radial defects concur nonrandomly (the VATER "association"). Recently, the associ ation has been "extended" to include cardiac. external genital and "other" (usually preaxial) limb anomalies. Despite repeated allusion to the etiologic heterogeneity that must underlie an inconstant association of such breadth, the unlversa1 appeal of classificatory labels has resulted in a growing tendency to exploit the VATER association as a definitive diagnosis for any child with an anorectal anomaly and at least one other defect typical of the association. Since VATER patients are mostly sporadic. indiscriminate use of the VATER diagnosis can lead to faulty genetic counseling. The purpose of this comnunication is to publicise ...