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Preeclampsia is predicted by elevated second trimester human chorionic gonadotropin values
SPO A b s t r a c t s
Volume 172, N u m b e r 1, Part 2 Am .l Obstet Gynecol
406 PRETERM PREECLAMPSIA HAS MAJOR PATHOLOGY DISTINCT FROM UTEROPLACENTAL INSUFFICIENCY. ~;M Salafia x, JC Pezzullo x, AM Vintzileos, VK Miniorx, R Romero. Div Anat Path, UCOnnHealth Ctr, Farmington CT; MFM, RW ,Johnson Med Sch/St Peters Med Ctr, New Brunswick, NJ; Perinatology ResearchBranch, NICHD,Bethesda,MD. OBJECTIVE: To compare the incidence of chronic inflammatory and placental vasoeeclusivelesions in preeclampsia(PE} v. spontaneousdelivery at<32 weeks. STUDY DESIGN: Review of maternal and neonatal charts of singleton livebom non-anomalousinfants born at 22-32 weeks gestation identified 65 PE, and 312 non-PE spontaneous prernaturity (spontaneous premature membrane rupture, (N=166), preterm labor, intact membranes (N=146). Histologic.features scored numerically included lesions of uteroplacental insufficiency (UPI) (e.g., decidual vascular pathology, related ischemle villous damage, decidual hemosiderosis), chronic inflammation and plasma cell infiltrates in decidua and/or placenta, decidual thrombosis, perivillous fibrin deposition and placental vaso-occlusive lesions (avascular villi, fetal stem vessel thrombosis, "hemorrhagic endovascuritis').Contingencytable analysesconsideredp
407 DOES
P L A C E N T A L ' P A T H O L O G Y IN P R E E C L A M P S I A CORRELATE TO MATERNAL HYPERTENSION OR NEONATAL BIRTHWEIGHT P E R C E N T I L E ? Rodis JF, " Sanders M*, Ernst L*, Fast A', Borgida A, Campbell WA. UConn Health Center, Farmington, CT. OBJECTIVE: Correlation of placental pathology in preeclamptie pregnancies with severity of maternal hypertension (HTN) and birthweight percentiles. STUDY DESIGN: Charts on all preeclamptics delivered between 1/89 - 6/94 were reviewed. Only singleton primiparas with no evidence of hypertension before 20 weeks gestation and no other medical or obstetrical complications were included. Placentas were reviewed by a single pathologist who was blinded as to the severity of hypertension or the fetal growth status; all slides were reviewed and graded for acute and chronic inflammation of the membranes and cord, villi and basal plate. Decidual vessels were counted and specific abnormalities were quantified. Small-for-gestational-age (SGA) was defined as <10th percentile for gestaUonal age and sex. Severe HTN was defined as BP >160/110. Data were analyzed by Chi-square with p<.05 considered significant*. RESULTS: Eighty-one primiparas with preeclampsia were identified in whom pathology slides were available in 80. Mean gastational age at delivery was 32.4 weeks and mean birthweight was 1642 gm. n= 14 66 47 33 Path Flndlnu SGA AGA I Severe HTN Non-severe HTN Abn. Decid. vessels% 92.9 58.7* i 57.8 75.0 Fibnnoid necrosis% 14.3 36.5 I 66.7 53.1 Accel. Maturation% 28.6 36.4 38.3 30.3 AbruptJon% 14.3 24.2 27.7 15.2 vinitis% 78.6 37.9* 44.7 42.4 CONCLUSIONS: Placental pathology in preeclamptic pregnancies is frequently abnormal. Placentas of preeclamptics with SGA infants were significantly more likely to exhibit abnormal decidual vessels and villitis. While patients with severe HTN were more likely to have abruption, in general placental pathology did not correlate with severity of maternal hypertension.
408
IMMUNOLOGIC ALTERATION OF NITABUCH'S MEMBRANET CLINICAL SEQUELAlg. J. Balducci, P. We're, R. Aline, M. pajarillo, W. Dupren, R.V. Cumminp. Dept. of OblGyu, Lehigh Valley Hospital, Allentown, PA, Lehigh University, Allentown, PA. OBJECTIVE: Our hypothesls is that preecinmpgin hi an immunologic disease process similar to a gratt versus host reaction evklencod by antigen Antibody complexes with fibrin deposition being greatly increased at the maternal fetal inteafaco (Nitabuch's layer) in precelamptio patients. STUDY DESIGN: A prospective study of patients at the Lehigh Valley Hospital was conducted betweea July 1993 end April 1994. Group l consisted of 11 primigravid patients meeting the criteria cousig.ent with the diagnosis of preeclampsin. Group 2 (control group) were 11 prlmigravid patients that had an anenmplicated prenatal course. Immediately utter delivery, placental specimerm were obtained, luted, and procomed to be studied by u blinded ob=¢rver by GAME Immanoflnorew.enen techaique. The rcmaioing specimen was sent to a blinded GYN pathologist for evaluation and measurement of Nitebueh's Membrane by light micruseopy. RESULTS: Light microcopy - An av=~ge of 3 mensuremenr~ of the width of Nitebuch's Membren©in each specimen revealed no signilrw-aatdiffexenen between the control group end etudy group (.1839 mm vesitm .1555 ram). lmmanoflunresenco - GAMEimmanofloare, senco revealed that the mesa width of Nitebuch's Membrane was significantly grcat~ in the study group versus the control group (157.48 versus 63.80, p=.006). CONCLUSION: Evaluation of the materuel-fetal interface reveals the deposition of antigen antibody complexes, the physiology of which m y be similar to nephropathiea as seen in systemic disease proceaw~. This data suggests that entigen eat=body complexes with fibrin deposition cause an increased placental reaistenco which may lead to meny of the sequelae of pre¢clampsin, such su elevated S/D ratios, olignhydramnios, end subsequent intrauterine growth retardation. Similar events may likely take place in the kidney add other organs of the preeclamptic patient.
409 PREECLAMPSIA IS PREDICTED BY ELEVATED
SECOND TRIMESTER HUMAN CHORIONIC GONADOTROPIN VALUES. HS MillerX, TD MelendezX, R WeinX, M O'Harax, KA AquaX, R LapinskiX, CJ Lockwood. Depts. of OB/Gyn, U. Arizona, Tucson, AZ and the Mount Sinai School of Medicine, New York, NY. OBJECTIVE: Preeclampsia (PE) is typically preceded by inadequate endovascular trophoblast invasion. This process may be mediated by enhanced deeidual cell protease inhibitor expression resulting from increased placental human chorionie gonadotropin (hCG) production. Therefore, we assessed the value of elevated second trimester hCG values in the prediction of PE. METHODS: We retrospectively compared obstetrical and neonatal variables as well as weight and diabetes-adjusted bCG and maternal serum alpha-fetoprotein (MSAFP)values obtained at 15 to 20 weeks in 51 patients developing mild and severe PE defined by ACOG criteria. Similar data were obtained in 84 consecutive patients with uncomplicated pregnancies. RESULTS: There were no differences in maternal age, race, parity, gestational age (GA) at draw (16.8 vs. 16.7 weeks), fetal sex or Apgar scores between PE patients and controls. Patients with PE had significantly increased maternal weight, neonatal birth weights, GA at delivery, prevalence of low birth weight, and neonatal intensive care unit admissions when compared with controls. The mean (+SD) hCG value in multiples of the median (MUM) was significantly higher among patients with PE (1.41 + 0.84) (p< 0.02) and severe PE (1.89+ 0.99) (p< 0.03) compared with controls (1.08+0.66). Birth weight was inversely correlated with hCG values (R=0.18; p=0.04). Receiver Operating Characteristic curve analysis indicated that a hCG cutoff of 1.15 MUM detected 56% and 80% of patients developing PE and severe PE, respectively, with a specificity of 71.4%. No differences in MSAFP values were noted among the groups. CONCLUSIONS: Elevated second trimester hCG values ere predictive of PE, and are particularly predictive of severe PE.
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Volume 172, N u m b e r 1, Part 2 Am .l Obstet Gynecol
406 PRETERM PREECLAMPSIA HAS MAJOR PATHOLOGY DISTINCT FROM UTEROPLACENTAL INSUFFICIENCY. ~;M Salafia x, JC Pezzullo x, AM Vintzileos, VK Miniorx, R Romero. Div Anat Path, UCOnnHealth Ctr, Farmington CT; MFM, RW ,Johnson Med Sch/St Peters Med Ctr, New Brunswick, NJ; Perinatology ResearchBranch, NICHD,Bethesda,MD. OBJECTIVE: To compare the incidence of chronic inflammatory and placental vasoeeclusivelesions in preeclampsia(PE} v. spontaneousdelivery at<32 weeks. STUDY DESIGN: Review of maternal and neonatal charts of singleton livebom non-anomalousinfants born at 22-32 weeks gestation identified 65 PE, and 312 non-PE spontaneous prernaturity (spontaneous premature membrane rupture, (N=166), preterm labor, intact membranes (N=146). Histologic.features scored numerically included lesions of uteroplacental insufficiency (UPI) (e.g., decidual vascular pathology, related ischemle villous damage, decidual hemosiderosis), chronic inflammation and plasma cell infiltrates in decidua and/or placenta, decidual thrombosis, perivillous fibrin deposition and placental vaso-occlusive lesions (avascular villi, fetal stem vessel thrombosis, "hemorrhagic endovascuritis').Contingencytable analysesconsideredp
407 DOES
P L A C E N T A L ' P A T H O L O G Y IN P R E E C L A M P S I A CORRELATE TO MATERNAL HYPERTENSION OR NEONATAL BIRTHWEIGHT P E R C E N T I L E ? Rodis JF, " Sanders M*, Ernst L*, Fast A', Borgida A, Campbell WA. UConn Health Center, Farmington, CT. OBJECTIVE: Correlation of placental pathology in preeclamptie pregnancies with severity of maternal hypertension (HTN) and birthweight percentiles. STUDY DESIGN: Charts on all preeclamptics delivered between 1/89 - 6/94 were reviewed. Only singleton primiparas with no evidence of hypertension before 20 weeks gestation and no other medical or obstetrical complications were included. Placentas were reviewed by a single pathologist who was blinded as to the severity of hypertension or the fetal growth status; all slides were reviewed and graded for acute and chronic inflammation of the membranes and cord, villi and basal plate. Decidual vessels were counted and specific abnormalities were quantified. Small-for-gestational-age (SGA) was defined as <10th percentile for gestaUonal age and sex. Severe HTN was defined as BP >160/110. Data were analyzed by Chi-square with p<.05 considered significant*. RESULTS: Eighty-one primiparas with preeclampsia were identified in whom pathology slides were available in 80. Mean gastational age at delivery was 32.4 weeks and mean birthweight was 1642 gm. n= 14 66 47 33 Path Flndlnu SGA AGA I Severe HTN Non-severe HTN Abn. Decid. vessels% 92.9 58.7* i 57.8 75.0 Fibnnoid necrosis% 14.3 36.5 I 66.7 53.1 Accel. Maturation% 28.6 36.4 38.3 30.3 AbruptJon% 14.3 24.2 27.7 15.2 vinitis% 78.6 37.9* 44.7 42.4 CONCLUSIONS: Placental pathology in preeclamptic pregnancies is frequently abnormal. Placentas of preeclamptics with SGA infants were significantly more likely to exhibit abnormal decidual vessels and villitis. While patients with severe HTN were more likely to have abruption, in general placental pathology did not correlate with severity of maternal hypertension.
408
IMMUNOLOGIC ALTERATION OF NITABUCH'S MEMBRANET CLINICAL SEQUELAlg. J. Balducci, P. We're, R. Aline, M. pajarillo, W. Dupren, R.V. Cumminp. Dept. of OblGyu, Lehigh Valley Hospital, Allentown, PA, Lehigh University, Allentown, PA. OBJECTIVE: Our hypothesls is that preecinmpgin hi an immunologic disease process similar to a gratt versus host reaction evklencod by antigen Antibody complexes with fibrin deposition being greatly increased at the maternal fetal inteafaco (Nitabuch's layer) in precelamptio patients. STUDY DESIGN: A prospective study of patients at the Lehigh Valley Hospital was conducted betweea July 1993 end April 1994. Group l consisted of 11 primigravid patients meeting the criteria cousig.ent with the diagnosis of preeclampsin. Group 2 (control group) were 11 prlmigravid patients that had an anenmplicated prenatal course. Immediately utter delivery, placental specimerm were obtained, luted, and procomed to be studied by u blinded ob=¢rver by GAME Immanoflnorew.enen techaique. The rcmaioing specimen was sent to a blinded GYN pathologist for evaluation and measurement of Nitebueh's Membrane by light micruseopy. RESULTS: Light microcopy - An av=~ge of 3 mensuremenr~ of the width of Nitebuch's Membren©in each specimen revealed no signilrw-aatdiffexenen between the control group end etudy group (.1839 mm vesitm .1555 ram). lmmanoflunresenco - GAMEimmanofloare, senco revealed that the mesa width of Nitebuch's Membrane was significantly grcat~ in the study group versus the control group (157.48 versus 63.80, p=.006). CONCLUSION: Evaluation of the materuel-fetal interface reveals the deposition of antigen antibody complexes, the physiology of which m y be similar to nephropathiea as seen in systemic disease proceaw~. This data suggests that entigen eat=body complexes with fibrin deposition cause an increased placental reaistenco which may lead to meny of the sequelae of pre¢clampsin, such su elevated S/D ratios, olignhydramnios, end subsequent intrauterine growth retardation. Similar events may likely take place in the kidney add other organs of the preeclamptic patient.
409 PREECLAMPSIA IS PREDICTED BY ELEVATED
SECOND TRIMESTER HUMAN CHORIONIC GONADOTROPIN VALUES. HS MillerX, TD MelendezX, R WeinX, M O'Harax, KA AquaX, R LapinskiX, CJ Lockwood. Depts. of OB/Gyn, U. Arizona, Tucson, AZ and the Mount Sinai School of Medicine, New York, NY. OBJECTIVE: Preeclampsia (PE) is typically preceded by inadequate endovascular trophoblast invasion. This process may be mediated by enhanced deeidual cell protease inhibitor expression resulting from increased placental human chorionie gonadotropin (hCG) production. Therefore, we assessed the value of elevated second trimester hCG values in the prediction of PE. METHODS: We retrospectively compared obstetrical and neonatal variables as well as weight and diabetes-adjusted bCG and maternal serum alpha-fetoprotein (MSAFP)values obtained at 15 to 20 weeks in 51 patients developing mild and severe PE defined by ACOG criteria. Similar data were obtained in 84 consecutive patients with uncomplicated pregnancies. RESULTS: There were no differences in maternal age, race, parity, gestational age (GA) at draw (16.8 vs. 16.7 weeks), fetal sex or Apgar scores between PE patients and controls. Patients with PE had significantly increased maternal weight, neonatal birth weights, GA at delivery, prevalence of low birth weight, and neonatal intensive care unit admissions when compared with controls. The mean (+SD) hCG value in multiples of the median (MUM) was significantly higher among patients with PE (1.41 + 0.84) (p< 0.02) and severe PE (1.89+ 0.99) (p< 0.03) compared with controls (1.08+0.66). Birth weight was inversely correlated with hCG values (R=0.18; p=0.04). Receiver Operating Characteristic curve analysis indicated that a hCG cutoff of 1.15 MUM detected 56% and 80% of patients developing PE and severe PE, respectively, with a specificity of 71.4%. No differences in MSAFP values were noted among the groups. CONCLUSIONS: Elevated second trimester hCG values ere predictive of PE, and are particularly predictive of severe PE.
373