Platelet aggregation and prostaglandin formation was evaluated in 20 control mother-neonate pairs (Grp I), and in 13 pairs where maternal DM was present (Grps II and III). Grp I control mothers demonstrated normal platelet aggregation with their infants showing the physiological impairment in aggregation that occurs in the neonate. Using platelet Malonyldialdehyde (MDA) as an indicator of platelet prostaglandin formation, Grp I mothers and infants demonstrated normal values of 3.20 ± 0.31 (1

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... and 2.46 ± 0.61 n moles MDA per 109 plts respectively. In the 13 patient pairs, 8/13 diabetic mothers (Grp II) showed platelet hyperaggregability and platelet MDA was increased to 3.92 ±; 0.22. All Grp II infants also manifested platelet hyperfunction and increased MDA formation (p<.005) to 3.37 t 0.67.2/8 Grp II neonates restudied on the fourth day of life no longer demonstrated the hyperfunction present at birth. 5/13 diabetic others (Grp III) showed normal platelet aggregation and MDA formation (3.18 ± 0.17) and their infants showed normal neonatal aggregation and MDA formation (2.27 ± 0.67). In tne acuic with DM platelet hyperfunction and increased prostaglandin formation is present, mese findings appear to be transmitted to the offsprings of such mothers as well. Platelet hpperfunction was not correlated with either neonatal blood sugar or blood viscosity measurements. Platelet hyperfunetion may be the etiologic factor in the increased incidence of both arterial and venous thrombosis that occurs in the infant of the diabetic mother.