Association between maternal-fetal HLA-DR relationships and fetal growth.

PROBLEM: To determine whether maternal-fetal human leukocyte antigen (HLA) antigenic relationships are associated with differential fetal growth in weight. METHOD: A cohort of 659 primigravid women were enrolled in this study in the prepartum period and their neonates were subsequently examined. Anthropometric, maternal cigarette smoking behavior, health, pregnancy, and delivery data were collected; serogenetic typing was conducted on maternal and cord bloods to determine maternal and neonatal HLA antigenic phenotypes. Women and their neonates were assigned to one of the four different types of maternal-fetal relationships existing at each of the HLA-A, B, DR, and DQ loci. Birthweights were treated quantitatively and qualitatively (neonates classified as growth-retarded or normal). RESULTS: After controlling for other factors influencing birthweight (e.g., smoking, maternal body size), significantly lower birthweight trends (P < .01) were found when neonates expressed a single HLA-DR antigen and their mothers expressed a second HLA-DR antigen that was foreign (allogeneic) to their neonate. CONCLUSION: Our findings supports the hypothesis that lack of maternal immune exposure to fetal HLA antigens is associated with a slowing of fetal growth. However, in this situation slowed fetal growth is most likely to occur when the fetus is potentially exposed to maternal HLA-DR alloantigens. We believe this sheds new light on immunologic events at the maternal-fetal interface influencing fetal growth. We present one possible explanation to account for this finding.

Adenosine administration for neonatal SVT.

Adenosine is a purine nucleoside that impairs conduction through the AV node and is thus effective in terminating tachycardias involving the AV node. Gaining acceptance as the drug of choice for neonatal supraventricular tachycardia (SVT), it is given IV as a rapid bolus with an initial dose of 0.05 mg/kg and can be increased in increments of 0.05 mg/kg every one to two minutes until termination of SVT (to a maximum of 0.25 mg/kg). Because of its half-life of 0.6 to 10 seconds, adenosine will not prevent reinitiation of SVT, therefore other medications should be considered if prophylaxis is required. An advantage of the short half-life is the transient nature of adverse effects, which can include flushing, nondistressing alterations in respiratory pattern, irritability, sinus bradycardia, and varying degrees of AV block. Administration to critically ill infants, including those requiring mechanical ventilation, has been reported. The infant's blood pressure, electrocardiogram, respiratory status, and capillary refill should be monitored before, during, and after adenosine administration.

Maternal-fetal HLA-DR relationships and pregnancy-induced hypertension.

OBJECTIVE: Some studies have found an increased prevalence of pregnancy-induced hypertension among women sharing HLA antigens with their spouses or fetuses, thus supporting the hypothesis that maternal sensitization to fetal HLA alloantigens reduces the risk for pregnancy-induced hypertension. However, not all studies have confirmed these findings. No investigators have examined the four different types of maternal-fetal HLA relationships in their studies of pregnancy-induced hypertension. Our goal was to examine such associations to test further the HLA-allosensitization hypothesis. METHODS: We conducted a cohort study of pregnancy-induced hypertension among 683 nulliparous women. Women and their neonates were typed for HLA-A, -B, -DR, and -DQ antigens using serologic techniques to establish maternal-fetal relationships. RESULTS: We found an increased prevalence of pregnancy-induced hypertension when the fetus, but not the mother, was potentially exposed to HLA-DR alloantigens (maternal allogenicity) compared with the other three conditions combined (P < .003). Controlling for confounding factors, the increased prevalence of pregnancy-induced hypertension persisted in situations of maternal HLA-DR allogenicity (P < .007). CONCLUSIONS: Based upon our observations and other immunologic studies of pregnancy-induced hypertensive and uncomplicated pregnancies, we conclude that a maternal humoral response against fetal anti-HLA-DR immunoglobulin (IgG) antibody may influence the development of pregnancy-induced hypertension. This could occur when an immunocompetent fetus is exposed to maternal HLA-DR alloantigens, maternal exposure to fetal HLA-DR alloantigens alloantigens, maternal exposure to fetal HLA-DR alloantigens is not possible, and fetal IgG antibody bears paternally inherited markers allogeneic to the mother.