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38 (2014) 131–132
Available online at www.sciencedirect.com
www.elsevier.com/locate/semperi
Ischemic placental disease: A unifying concept for preeclampsia, intrauterine growth restriction, and placental abruption Ischemic placental disease is a syndrome that involves preeclampsia, intrauterine growth restriction, and placental abruption.1 The pathophysiological mechanisms leading to these complications may be uteroplacental ischemia and placental insufficiency beginning as early as the stages of placental implantation.2–9 Given that these obstetrical conditions may share the same biologic pathways,10 it is plausible that they represent differing clinical manifestations of the same disease process at advancing gestational ages.11,12 Epidemiologic data demonstrates that there is a greater overlap in the occurrence of these obstetrical complications at preterm than term deliveries,13 and ischemic placental
disease is implicated in greater than 50% of all iatrogenic preterm deliveries.1,14 These observations suggest that ischemic placental disease may be more homogeneous in preterm than term gestations. The consequences of ischemic placental disease on the long-term health of the mother and newborn remain less well understood. We conceptualize ischemic placental disease primarily as the culmination of two processes: inadequate placental attachment or premature placental detachment (Fig.).15 Each of these pathways share similar and overlapping mechanisms leading to ischemic placental disease—abnormal extracellular matrix remodeling, thrombosis and coagulation defects,
Fig – Conceptual model for ischemic placental disease. (Reproduced and modified from Ananth and Kinzler,15 with permission from the publisher of UpToDate.)
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inflammation, infection, and angiogenesis. Further elaboration of the mechanisms underlying ischemic placental disease will provide an unprecedented opportunity to identify interventions that predict and prevent these conditions. This collection highlights the similarity of epidemiologic and clinical risk factors, pathophysiological mechanisms, and prediction and prevention strategies for preeclampsia, intrauterine growth restriction, and placental abruption. This series is organized in three broad sections: (i) epidemiology and pathophysiology of ischemic placental disease; (ii) short- and long-term maternal consequences, perinatal morbidity and mortality, and neurodevelopmental outcomes in relation to ischemic placental disease; and (iii) prediction and prevention of ischemic placental disease. Methodological innovation, clarity, and simplicity are the cornerstone for research if progress is to be made in understanding disease etiologies. This series presents data highlighting the similarities and differences in the pathophysiology, epidemiology and risk factors, and short- and longterm consequences of these obstetrical complications on both the mother and the fetus, as well as, prediction and prevention of these conditions. Upon reviewing the articles in this series, two questions spring to mind: Should preeclampsia, IUGR, and placental abruption be studied separately? Should they be combined and examined as a syndrome? Any effort to understand the etiologic underpinnings of a disease or complication should consider, among others, the heterogeneity in the phenotypic classification of the outcome being examined. Progress in epidemiology is often guided by corroboration of findings, and the accumulating data converging on a single theme will pave the way for new research innovation. In that regard, the most apt responses to the two important questions are “yes” and “yes”!
r e f e r e n c e s
1. Ananth CV, Vintzileos AM. Maternal–fetal conditions necessitating a medical intervention resulting in preterm birth. Am J Obstet Gynecol. 2006;195:1557–1563. 2. Srinivas SK, Edlow AG, Neff PM, Sammel MD, Andrela CM, Elovitz MA. Rethinking IUGR in preeclampsia: dependent or independent of maternal hypertension? J Perinatol. 2009;29: 680–684.
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3. Karumanchi SA, Lindheimer MD. Advances in the understanding of eclampsia. Curr Hypertens Rep. 2008;10:305–312. 4. Redman CW, Sargent IL. Latest advances in understanding preeclampsia. Science. 2005;308:1592–1594. 5. Redman CW, Sargent IL. Placental stress and pre-eclampsia: a revised view. Placenta. 2009;30(suppl A):S38–S42. 6. Roberts JM, Cooper DW. Pathogenesis and genetics of preeclampsia. Lancet. 2001;357:53–56. 7. Sibai BM. Maternal and uteroplacental hemodynamics for the classification and prediction of preeclampsia. Hypertension. 2008;52:805–806. 8. Christianson RE. Gross differences observed in the placentas of smokers and nonsmokers. Am J Epidemiol. 1979;110:178–187. 9. Signore C, Mills JL, Qian C, Yu KF, Rana S, Karumanchi SA, et al. Circulating soluble endoglin and placental abruption. Prenat Diagn. 2008;28:852–858. 10. Ness RB, Roberts JM. Heterogeneous causes constituting the single syndrome of preeclampsia: a hypothesis and its implications. Am J Obstet Gynecol. 1996;175:1365–1370. 11. Ness RB, Sibai BM. Shared and disparate components of the pathophysiologies of fetal growth restriction and preeclampsia. Am J Obstet Gynecol. 2006;195:40–49. 12. Villar J, Carroli G, Wojdyla D, Abalos E, Giordano D, Ba'aqeel H, et al. Preeclampsia, gestational hypertension and intrauterine growth restriction, related or independent conditions? Am J Obstet Gynecol. 2006;194:921–931. 13. Ananth CV, Smulian JC, Vintzileos AM. Ischemic placental disease: maternal versus fetal clinical presentations by gestational age. J Matern Fetal Neonatal Med. 2010;23:887–893. 14. Ananth CV, Vintzileos AM. Medically indicated preterm birth: recognizing the importance of the problem. Clin Perinatol. 2008;35:53–67. 15. Ananth CV, Kinzler WL. Placental Abruption: Clinical Features and Diagnosis. Philadelphia, PA: UpToDate, Wolters Kluwer Health; 2014. Available at: http://www.uptodate.com/contents/ placental-abruption-clinical-features-and-diagnosis.
Cande V. Ananth, PhD, MPHa,b,n Department of Obstetrics and Gynecology, College of Physicians and Surgeons, Columbia University, 622 West 168th Street, New York, NY b Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY E-mail: [email protected]
a
http://dx.doi.org/10.1053/j.semperi.2014.03.001 0146-0005/& 2014 Elsevier Inc. All rights reserved.
Correspondence address: Department of Obstetrics and Gynecology, College of Physicians and Surgeons, Columbia University Medical Center, 622 W 168th St, New York, NY 10032.
M I N A R S I N
P
E R I N A T O L O G Y
38 (2014) 131–132
Available online at www.sciencedirect.com
www.elsevier.com/locate/semperi
Ischemic placental disease: A unifying concept for preeclampsia, intrauterine growth restriction, and placental abruption Ischemic placental disease is a syndrome that involves preeclampsia, intrauterine growth restriction, and placental abruption.1 The pathophysiological mechanisms leading to these complications may be uteroplacental ischemia and placental insufficiency beginning as early as the stages of placental implantation.2–9 Given that these obstetrical conditions may share the same biologic pathways,10 it is plausible that they represent differing clinical manifestations of the same disease process at advancing gestational ages.11,12 Epidemiologic data demonstrates that there is a greater overlap in the occurrence of these obstetrical complications at preterm than term deliveries,13 and ischemic placental
disease is implicated in greater than 50% of all iatrogenic preterm deliveries.1,14 These observations suggest that ischemic placental disease may be more homogeneous in preterm than term gestations. The consequences of ischemic placental disease on the long-term health of the mother and newborn remain less well understood. We conceptualize ischemic placental disease primarily as the culmination of two processes: inadequate placental attachment or premature placental detachment (Fig.).15 Each of these pathways share similar and overlapping mechanisms leading to ischemic placental disease—abnormal extracellular matrix remodeling, thrombosis and coagulation defects,
Fig – Conceptual model for ischemic placental disease. (Reproduced and modified from Ananth and Kinzler,15 with permission from the publisher of UpToDate.)
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inflammation, infection, and angiogenesis. Further elaboration of the mechanisms underlying ischemic placental disease will provide an unprecedented opportunity to identify interventions that predict and prevent these conditions. This collection highlights the similarity of epidemiologic and clinical risk factors, pathophysiological mechanisms, and prediction and prevention strategies for preeclampsia, intrauterine growth restriction, and placental abruption. This series is organized in three broad sections: (i) epidemiology and pathophysiology of ischemic placental disease; (ii) short- and long-term maternal consequences, perinatal morbidity and mortality, and neurodevelopmental outcomes in relation to ischemic placental disease; and (iii) prediction and prevention of ischemic placental disease. Methodological innovation, clarity, and simplicity are the cornerstone for research if progress is to be made in understanding disease etiologies. This series presents data highlighting the similarities and differences in the pathophysiology, epidemiology and risk factors, and short- and longterm consequences of these obstetrical complications on both the mother and the fetus, as well as, prediction and prevention of these conditions. Upon reviewing the articles in this series, two questions spring to mind: Should preeclampsia, IUGR, and placental abruption be studied separately? Should they be combined and examined as a syndrome? Any effort to understand the etiologic underpinnings of a disease or complication should consider, among others, the heterogeneity in the phenotypic classification of the outcome being examined. Progress in epidemiology is often guided by corroboration of findings, and the accumulating data converging on a single theme will pave the way for new research innovation. In that regard, the most apt responses to the two important questions are “yes” and “yes”!
r e f e r e n c e s
1. Ananth CV, Vintzileos AM. Maternal–fetal conditions necessitating a medical intervention resulting in preterm birth. Am J Obstet Gynecol. 2006;195:1557–1563. 2. Srinivas SK, Edlow AG, Neff PM, Sammel MD, Andrela CM, Elovitz MA. Rethinking IUGR in preeclampsia: dependent or independent of maternal hypertension? J Perinatol. 2009;29: 680–684.
n
38 (2014) 131–132
3. Karumanchi SA, Lindheimer MD. Advances in the understanding of eclampsia. Curr Hypertens Rep. 2008;10:305–312. 4. Redman CW, Sargent IL. Latest advances in understanding preeclampsia. Science. 2005;308:1592–1594. 5. Redman CW, Sargent IL. Placental stress and pre-eclampsia: a revised view. Placenta. 2009;30(suppl A):S38–S42. 6. Roberts JM, Cooper DW. Pathogenesis and genetics of preeclampsia. Lancet. 2001;357:53–56. 7. Sibai BM. Maternal and uteroplacental hemodynamics for the classification and prediction of preeclampsia. Hypertension. 2008;52:805–806. 8. Christianson RE. Gross differences observed in the placentas of smokers and nonsmokers. Am J Epidemiol. 1979;110:178–187. 9. Signore C, Mills JL, Qian C, Yu KF, Rana S, Karumanchi SA, et al. Circulating soluble endoglin and placental abruption. Prenat Diagn. 2008;28:852–858. 10. Ness RB, Roberts JM. Heterogeneous causes constituting the single syndrome of preeclampsia: a hypothesis and its implications. Am J Obstet Gynecol. 1996;175:1365–1370. 11. Ness RB, Sibai BM. Shared and disparate components of the pathophysiologies of fetal growth restriction and preeclampsia. Am J Obstet Gynecol. 2006;195:40–49. 12. Villar J, Carroli G, Wojdyla D, Abalos E, Giordano D, Ba'aqeel H, et al. Preeclampsia, gestational hypertension and intrauterine growth restriction, related or independent conditions? Am J Obstet Gynecol. 2006;194:921–931. 13. Ananth CV, Smulian JC, Vintzileos AM. Ischemic placental disease: maternal versus fetal clinical presentations by gestational age. J Matern Fetal Neonatal Med. 2010;23:887–893. 14. Ananth CV, Vintzileos AM. Medically indicated preterm birth: recognizing the importance of the problem. Clin Perinatol. 2008;35:53–67. 15. Ananth CV, Kinzler WL. Placental Abruption: Clinical Features and Diagnosis. Philadelphia, PA: UpToDate, Wolters Kluwer Health; 2014. Available at: http://www.uptodate.com/contents/ placental-abruption-clinical-features-and-diagnosis.
Cande V. Ananth, PhD, MPHa,b,n Department of Obstetrics and Gynecology, College of Physicians and Surgeons, Columbia University, 622 West 168th Street, New York, NY b Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY E-mail: [email protected]
a
http://dx.doi.org/10.1053/j.semperi.2014.03.001 0146-0005/& 2014 Elsevier Inc. All rights reserved.
Correspondence address: Department of Obstetrics and Gynecology, College of Physicians and Surgeons, Columbia University Medical Center, 622 W 168th St, New York, NY 10032.
