Long-term outcome of children following maternal human parvovirus B19 infection.

OBJECTIVE: To determine the long-term outcomes of children exposed in utero to maternal parvovirus B19 infection. METHODS: All pregnant women with serologic evidence of recent parvovirus B19 infection and a comparison group with serologic evidence of past infection from January 1988 to December 1994 were sent questionnaires or contacted by phone about the health and development of their children. Information requested included: pregnancy complications, date of delivery, birth weight, sex, birth defects, need for special care, significant health problems, and developmental delays. All women had serology done at either the Centers for Disease Control and Prevention or the virology laboratory of the Connecticut Department of Health. The data were analyzed using descriptive statistics, chi2 analysis with Fisher exact test, or Student t test in appropriate cases. P < .05 was considered significant. RESULTS: Outcome information was obtained from 113 of 117 immunoglobulin-M positive women. The 113 respondents had 103 term singletons, two sets of twins (of which one neonate died of complications of prematurity), one hydropic stillborn, four spontaneous abortions, and one ectopic pregnancy. The mean gestational age at time of exposure was 15.6 weeks. The median age of the liveborn infants in study and comparison groups was 4 years. Eight of the 108 (7.3%) surviving children, one set of twins (exposed at 27 weeks), and six singletons (exposed at 7, 8, 9, 20, 27, and 35 weeks) had developmental delays in speech, language, information processing, and attention. Outcomes were obtained for 99 of 110 patients with past infection; they had 83 liveborn singletons, five sets of twins, two stillborns, and five spontaneous abortions. Seven of the 93 (7.5%) children had developmental delays, similar to the study group. Post-hoc power analysis revealed that 712 infected patients would be needed to find a twofold difference in the risk of abnormal neurologic development; our study had 30% power to find such a difference. CONCLUSION: There is no apparent increase in the frequency of developmental delays in children with exposure in utero to parvovirus, but larger studies are needed.

Calcium channel blockers inhibit the antidipsogenic effect of central injections of zinc in rats.

Previous data from our laboratory have indicated that acute third ventricle injections of Zn2+ elicit a significant antidipsogenic response in rats in three different situations; dehydration, and central angiotensinergic or cholineric stimulation. In the present study we analyzed whether this response depends on voltage-dependent calcium channels. Dehydrated (14 h of water deprivation, overnight) animals received 2-microliters i.c.v. injections of zinc acetate (Zn(Ac)2; 300 pmol/rat) after pretreatment with the voltage-dependent calcium channel blockers gadolinium (Gd3+; 0.03, 3.0 and 30 pmol/rat) or verapamil (VER; 0.027, 0.05 and 0.11 pmol/rat). Both blockers reserved the antidipsogenic effect of third ventricle injections of Zn2+ in a dose-dependent manner. After 120 min, animals pretreated with saline receiving Zn(Ac)2 drank 3.10 +/- 0.57 ml/100 g body weight while those pretreated with Gd3+ at the highest dose displayed a water intake of 5.45 +/- 0.41 ml/100 body weight (P < 0.01). Animals pretreated with the vehicle of VER receiving Zn(Ac)2 drank 3.15 +/- 0.45 ml/100 g while animals pretreated with VER at the highest dose receiving Zn(Ac)2 drank 6.16 +/- 0.62 ml/100 g (P < 0.01). The antidipsogenic effect of Zn(Ac)2 seems to be specific since the metal (same dose and injection procedures) did not modify food intake in rats after 24 h of food deprivation. It is suggested that Zn2+ exerts its antidipsogenic effect by activation of mechanism(s) depending on the functional integrity of voltage-dependent calcium channels.