Calcium Supplementation to Prevent Hypertensive Disorders of Pregnancy

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Calcium Supplementation to Prevent Hypertensive Disorders of Pregnancy
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  342 Citations from the Literature disorders of pregnancy (gestational hypertension and preeclampsia) and to determine the value of urinary calcium levels as a predictor of the response. Methods. We studied 1194 nulliparous women who were in the 20th week of gestation at the beginning of the study. The women were randomly assigned to receive 2 g per day of elemental calcium in the form of calcium carbonate (593 women) or placebo (601 women). Urinary excretion of calcium and creatinine was measured before calcium supplementation was begun. The women were followed to the end of their pregnancies, and the incidence of hypertensive disorders of pregnancy was determined. Results. The rates of hypertensive disorders of pregnancy were lower in the calcium group than in the placebo group (9.8 vs. 14.8 ; odds ratio, 0.63; 95 confidence interval, 0.44-0.90). The risk of these disorders was lower at all times during gestation, par- ticularly after the 28th week of gestation (P = 0.01 by life-table analysis), in the calcium group than in the placebo group and the risk of both gestational hypertension and preeclampsia was also lower in the calcium group. Among the women who had low ratios of urinary calcium to urinary creatinine (0.62 mmol/mmol) during the 20th week of gestation, those in the calcium group had a lower risk of hypertensive disorders of pregnancy (odds ratio, 0.56; 95 confidence interval, 0.29- 1.09) and less of an increase in diastolic and systolic blood pressure than the placebo group. The pattern of response was similar among the women who had a high ratio of urinary calcium to urinary creatinine during the 20th week of gestation, but the differences were smaller. Conclusions. Pregnant women who receive calcium supplementation after the 20th week of pregnancy have a reduced risk of hypertensive disorders of pregnancy. Amniotic fluid contains tissue factor a potent initiator of coagulation Lockwood CJ; Bach R; Guha A; Zhou X; Miller WA; Nemer- son Y Division of Maternal-Fetal Medicine Department of Obstetrics Gynecology and Reproductive Science Mount Sinai School of Medicine 1 Gustave L. Levy Place New York NY 10029-6574. USA AM J OBSTET GYNECOL 1991 165/5 I (1335-1341) A primary clinical manifestation of amniotic fluid embolism is coagulopathy. Prior studies have identified a poorly characterized yet potent procoagulant property in amniotic fluid that increases with gestational age. One possible source of procoagulant activity is tissue factor, a primary biologic in- itiator of coagulation. We used sensitive immunoassays and functional assays to identify substantial quantities of tissue fac- tor antigen ans tissue factor-specific procoagulant activity in amniotic fluid, which increased with gestational age. Moreover, tissue factor accounted for virtually all of the coagulant poten- tial of amniotic fluid. Amniotic tissue factor appeared intact and membrane bound and, when reconstituted into synthetic microvesicles of .ptimal phospholipid content, displayed near- ly full activity. Calcium chelation and sonication experiments suggested that the presence of inhibitors and the physical con- figuration of membrane-bound tissue factor in amniotic fluid might explain the modest reduction in tissue factor pro- coagulant activity relative to total antigen levels observed in vivo. We postulate that the substantial quantities of functional- ly active tissue factor in amniotic fluid account for the coagula- tion changes accompanying amniotic fluid embolism and could indirectly contribute to the characteristic hemodynamic derangements of amniotic fluid embolism. Fetal lateral ventricle choroid plexus cysts: The dilemma of amnioceatesis Achiron R; Barkai G; Bat-Miriam Katznelson M; Mashiach S Department of Obstetrics and Gynecology Chaim Sheba Medical Center Tel Aviv University Sackler School of Medicine. Tel Hashomer 52621. ISR OBSTET GYNECOL 1991 7815 1(815-818) Although lateral ventricle choroid plexus cysts in the second- trimester fetus have been considered a benign developmental phenomenon of no clinical significance, an association with trisomy 18 has been suggested. We designed a prospective study to determine whether karyotype analysis is indicated when such cysts are encountered on prenatal sonogram. During a 20-month period, 5408 low-risk pregnant women were exam- ined sonographically in the second trimester to evaluate the prevalence of fetal lateral ventricle choroid plexus cysts and the incidence of ultrasonographic anomalies associated with such cysts in fetuses with trisomy 18 referred from cytogenetic laboratories. Thirty cases of fetal lateral ventricle choroid plexus cysts (0.6 ) were detected during the study period; 28 newborns were normal and two had trisomy 18. One of the af- fected infants had other associated ultrasonographic abnor- malities suggesting aneuploidy, whereas no detectable abnormalities could be found in the other. Three other preg- nant women were referred to us from the cytogenetics services because fetal karyotype revealed trisomy 18; in all three cases lateral ventricle choroid plexus cysts and other sonographic ab- normalities were observed. In total, we scanned five fetuses with trisomy 18, of which all had lateral ventricle choroid plexus cysts and four had associated detectable anomalies. We could not find any association between cyst size, number, or laterality and trisomy 18. In addition to the five cases of trisomy 18 described, we found 33 other fetuses reported with trisomy 18 in the second trimester; of this total, 25 (66 ) had lateral ventricle choroid plexus cysts and 30 had no other detectable abnormalities. Statistical analysis of a hypothetical sample that would produce the total 38 trisomy 18 fetuses revealed a calculated risk of about I for trisomy 18 in a fetus with lateral ventricle choroid plexus cysts and no other sonographic abnormalities. Thus, the finding of choroid plexus cysts on routine second-trimester ultrasound examination war- rants chromosomal analysis. Int J Gynecol Obstet 38
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