784

Letters

September 1991 Am J Obstet Gyneco1

ion to long-term neurologic impairment!· 5 More than 75% of histologically evident intraamniotic infection ("chorioamnionitis") and >95% of cases of chronic villitis are clinically silent, we submit that the "usefulness" of the information derived from placental pathologic examination will be minimal if the only outcome variable to be considered is the level of neurologic function at birth. In this discussion we also indirectly addressed the issues raised in the third paragraph. Chronic villitis, hemorrhagic endovillitis, infarcts, and other villous pathologic conditions cannot be definitely assessed by any modality other than placental examination. We stand by our assertion that placental examination may identify the exact cause of poor pregnancy outcome. Finally, we agree that the cost of placental pathologic examination, if the information is not combined with the obstetric clinical data, is indeed unconscionable. Placental pathologic examination cannot be considered to be separate from, or a substitute for, clinical assessment and only achieves its optimal returns when utilized in concert with clinical and laboratory investigations. Our article was born of the realization that the unique benefits we obtained from placental examinations in our institution were derived from our communications and interactions on the obstetrics floor, in the delivery suite, and at morbidity and mortality reviews. We thank Dr. Goldman for his comments. He has permitted us to restate, perhaps more strongly, the need for informed examination of the placenta, informed by clinical information and by collaboration with obstetric colleagues. Carolyn M. Salafia, MD, and Anthony M. Vintzileos, MD

Table I. Maternal herpesvirus serologic results and gender of offspring (N = 2084)

Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, The University of Connecticut Health Center, Farmington, CT 06032

Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, RH-20, University of Washington School of Medicine, Seattle, WA 98195

REFERENCES 1. Salafia CM, Mangam HE, Weigl CA, Foye GJ, Silberman L. Abnormal fetal heart rate pattern and placental inflammation. AM J OBSTET GYNECOL 1989; 160: 140. 2. Fleming AD, Salafia CM, Vintzileos AM, Rodis JF, Campbell WA, Bantham KF. The relationship among umbilical artery velocimetry, fetal biophysical profile, and placental inflammation in preterm premature rupture of the membranes. AM J OBSTET GYNECOL 1991; 164:38-41. 3. Mann LI. Pregnancy events and brain damage. AM J OBSTET GYNECOL 1986; 155:6-9. 4. Remington JS, Klein JO, eds. Infectious diseases of the fetus and newborn infant. 3rd ed. Philadelphia: WB Saunders, 1990:774. 5. Remington JS, Klein JO, eds. Infectious diseases of the fetus and newborn infant. 3rd ed. Philadelphia: WB Saunders, 1990:262.

Maternal genital herpes and gender of offspring To the Editors: In their Letter to the Editors McGregor and Leff (McGregor J A, Leff M. Does maternal genital herpes infection influence fetal gender? AM J OBSTET GYNECOL 1990;162:1346-7) suggest that there is a decreased proportion of male infants born to mothers with a history of genital herpes complicating pregnancy. This caused us to review the data from our co-

Herpesvirus types 1 and 2

Male 234 (50.6%) 503 (50.9%) 169 (53.7%) 162 (50.8%) Female 228 (49.4%) 485 (49.1 %) 146 (46.3%) 157 (49.2%) X'

= 0.87; p =

.83.

Table II. Maternal herpesvirus history and gender of offspring (N = 2041) Infants

Male 943 (51.7%) Female 880 (48.3%)

Herpesvirus before Herpesvirus during pregnancy pregnancy

86 (48%) 93 (52%)

21 (53.8%) 18 (46.2%)

x = 0.97; P = 0.61. 2

hort of pregnant women with symptomatic and asymptomatic genital herpes at the University of Washington. Among women with herpesvirus type 2 type-specific antibodies, as detected by Western blot analysis, we demonstrated a normal malelfemale ratio of their offspring (Table I). Similarly, in this same cohort, when we calculated the percentage of male infants on the basis of the clinical history rather than serologic results, again there was no alteration in the normal male/female ratio among offspring (Table II). Zane Brown, MD, and Larry Corey, MD

Reply To the Editors: My colleagues and I are pleased that Brown and Corey have answered our question in their uniquely well-described population. As noted in our letter, others have described fetal and newborn gender differences among women with proven or possible perinatal infectious processes in a variety of settings; male gender consistently predisposes to perinatal infection in studies going back decades. 1-3 MacGillivray and Davey' noted convincingly higher rates of pre term birth and premature rupture of membranes among South African women giving birth to male infants. Conversely, in a recent analysis of 8758 births at the University of Colorado, similar risks of preterm premature rupture of membranes, clinical chorioamnionitis, and postpartum endometritis were found in women giving birth to male and female infants. 4 These contrasting findings suggest that male gender-linked predispositions to perinatal infection are most likely to be expressed in women at high risk for reproductive tract infections before or during pregnancy. Controlled studies of possible interactions of reproductive tract infection, fetal gender, and the pathologic character-