The placental component and obstetric outcome in severe preeclampsia with and without HELLP syndrome. (November 2016)

• Record Type: Journal Article
• Authors: Weiner, Eran; Schreiber, Letizia; Grinstein, Ehud; Feldstein, Ohad; Rymer-Haskel, Noa; Bar, Jacob; Kovo, Michal
• Is Part Of: Placenta. Volume 47(2016:Nov.)
• Page Start: 99
• Page End: 104
• Publication Date: 2016-11
• Subjects: Placental histopathology -- Malperfusion lesions -- Severe preeclampsia -- HELLP syndrome -- Neonatal outcome -- Small for gestational age -- Placental weight; HELLP hemolysis elevated liver enzymes and low platelet -- SGA small for gestational age -- NICU neonatal intensive care unit -- MIR maternal inflammatory response -- FIR fetal inflammatory response; Placenta -- Periodicals; Reproduction -- Periodicals; Placenta -- Periodicals; Placenta -- Périodiques; Reproduction -- Périodiques; 612.63
• DOI: 10.1016/j.placenta.2016.09.012
• Languages: English
• ISSNs: 0143-4004

Abstract

Abstract: Objective: We aimed to compare obstetric outcome and placental-histopathology in pregnancies complicated by preeclampsia with severe features with and without HELLP syndrome. Methods: Labor, maternal characteristics, neonatal outcome and placental histopathology of pregnancies complicated with severe preeclampsia during 2008–2015 were reviewed. Results were compared between those without signs of HELLP syndrome (severe preeclampsia group) and those with concomitant HELLP syndrome (HELLP group). Placental lesions were classified to maternal vascular lesions consistent with malperfusion, fetal vascular lesions consistent with fetal thrombo-occlusive disease, and inflammatory lesions. Small-for-gestational-age (SGA) was defined as birth-weight ≤10th% and ≤5th%. Composite adverse neonatal outcome was defined as one or more early neonatal complications. Results: Compared to the severe preeclampsia group (n = 223), the HELLP group (n = 64) was characterized by earlier gestational-age, 34.1 ± 2.7 vs. 35.3 ± 3.4 weeks, p = 0.010, higher rates of multiple pregnancies (p = 0.024), and thrombophilia (p = 0.028). Placentas in the HELLP group had higher rates of vascular and villous lesions consistent with maternal malperfusion (p = 0.023, p = 0.037 respectively). By multivariate logistic regression analysis models, vascular and villous lesions of maternal malperfusion were independently associated with HELLP syndrome (aOR 1.9, aOR 1.8, respectively). SGA was also more common in the HELLP group, both below the 10th percentile (p = 0.044) and the 5th percentile (p = 0.016). Composite adverse neonatal outcome did not differ between the groups. Conclusion: Severe preeclampsia and HELLP syndrome have similar placental histopathologic findings. However, HELLP syndrome is associated with higher rates of placental maternal vascular supply lesions and SGA suggesting that the two clinical presentations share a common etiopathogenesis, with higher placental dysfunction in HELLP syndrome. Highlights: Obstetric outcome and placental histopathology in severe preeclampsia ± HELLP syndrome were compared. HELLP had an earlier gestational age and higher rates of multiple pregnancies, and thrombophilia. Placentas in HELLP had higher rates of vascular and villous lesions consistent with maternal malperfusion. These lesions were associated with HELLP syndrome independent of all background factors. SGA was more common in the HELLP group, both below the 10th and 5th percentiles.