TY - JOUR
T1 - Protease inhibitor therapy and fetal growth potential in HIV-positive women
AU - Iqbal, Sara
AU - Kriebs, Jan
AU - Harman, Christopher
AU - Gungor, Sadettin
AU - Alger, Lindsay
AU - Turan, Ozhan
AU - Kopelman, Jerome
AU - Malinow, Andrew
AU - Baschat, Ahmet A.
PY - 2008/9/26
Y1 - 2008/9/26
N2 - 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.
AB - 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.
KW - Antiretroviral therapy
KW - Fetal growth restriction
KW - HIV
KW - Pregnancy
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U2 - 10.1055/s-2008-1078757
DO - 10.1055/s-2008-1078757
M3 - Article
C2 - 18509788
AN - SCOPUS:52249117650
SN - 0735-1631
VL - 25
SP - 335
EP - 339
JO - American journal of perinatology
JF - American journal of perinatology
IS - 6
ER -