Sara Iqbal

Predictors of fetal growth in maternal HIV disease

We sought to determine predictors of fetal growth restriction in maternal HIV disease. Pregnant HIV-positive women on antiretroviral therapy were monitored with serial viral load and CD4 counts. Individualized growth potential (GP) percentile was calculated for birth weight (BW). BW <10th GP percentile defined fetal growth restriction (FGR). Multiple medical and social factors, CD4 count, viral load, and antiretroviral therapy were tested for impact on fetal growth using chi-square and multiple regression analysis. Two hundred eleven women were studied. CD4 count <200 in the first trimester was strongly associated with FGR (odds ratio 8.75, 95% confidence interval 2.88 to 26.52). Maternal age ( P = 0.02) and smoking ( P = 0.03) were independent cofactors for FGR (Nagelkerke R(2) = 0.33). No other factors demonstrated an independent effect. Severity of maternal HIV disease as indicated by the CD4 count, rather than placental exposure to viral load, predicts FGR. Smoking has an independent detrimental effect on fetal growth.

Protease inhibitor therapy and fetal growth potential in HIV-positive women

Our objective was to test if protease inhibitors (PIs) increase the incidence of fetal growth restriction (FGR). Human immunodeficiency (HIV)-seropositive women were studied. At birth the neonatal weight percentile was assigned by predicted growth potential (GP), accounting for race, parity, weight, height, gestational age, birthweight, and gender (Gardosi, 1992). FGR was defined as GP < 10% percentile. Maternal age, CD4 count, viral load, weight gain, prenatal care, tobacco, alcohol, substance abuse, and PI use were related to FGR using chi-square and multiple regression analysis. Ninety-three of 191 women received PI. In these, FGR occurred in 27 (29%) compared with 15 (15.3%) in the non-PI group ( P = 0.02). Maternal CD4 count ( P < 0.0001) was the primary determinant, and smoking ( P = 0.037) was an independent cofactor for FGR (Nagelkerke r2 = 0.24). Twenty-six of 82 (31.7%) smokers had FGR, versus 16 of 109 (14.7%) of nonsmokers (odds ratio, 2.69; 95% confidence interval, 1.33 to 5.46; P = 0.005). After exclusion of the CD4 count, PI became a cofactor for FGR ( P = 0.021 and Nagelkerke r2 = 0.104). We concluded that maternal HIV status and smoking determine the risk for FGR. Although PIs increase the risk for FGR, this effect appears to depend on maternal disease severity.