Gestational Disorders Research Articles

Epidemiology of sleep disorders in pregnant subjects: A questionnaire based survey

Introduction There are several changes which occur during the pregnant state that can impact directly or indirectly on breathing. A questionnaire based survey of sleep disorders amongst pregnant subjects attending a tertiary care hospital in New Delhi. Material & Methods The study was based on a questionnaire. It contained, besides personal identification of the subject, a set of 35 questions. In addition it also had the Epworth Sleep Questionnaire. A validated questionnaire for anxiety and depression was also used. Details of present pregnancy (parity, gravida, last menstrual period, expected date of delivery and period of gestation) was also recorded. The total number of pregnant subjects interviewed was 325. They were selected randomly from those attending the ante-natal clinic of Safdarjang Hospital & Vardhman Mahavir Medical College, New Delhi. Observations The overall prevalence of snoring was 13.5%. It correlated positively with depression (p<0.075) and gestation period (p<0.016). The overall prevalence of SDB was 9.5%. It correlated positively with gestation period (p<0.042) BMI (p<0.05) and disorders of initiation & maintenance of sleep (DIMS) (p<0.005) and depression (p<0.021). The overall prevalence of DIMS was 47.6%. The prevalence of DIMS was maximum in the third trimester; and it showed a positive correlation with rising gestation period. The overall prevalence of Restless Leg Syndrome (RLS) was 15.7%. It was most prevalent in age group 21-25 years (p<0.045). It showed rising trend with increase in gestation period (p<0.049), increasing parity (p<0.071) and decreasing hemoglobin concentration (p<0.047). The overall prevalence of depression was 11.4%. It correlated positively with increasing parity (p<0.045). The overall prevalence of anxiety was 18.1%. It correlated negatively with increasing age (p<0.057) & BMI (p<0.067) and positively with increasing gestation period (p<0.099). The overall prevalence of excessive daytime sleepiness (EDS) was 30.5%. It correlated negatively, with

Gestational trophoblastic neoplasia and disorders of thyroid function

Pregnancy is associated with physiological changes in thyroid function that can make the diagnosis of hyperthyroidism difficult. Many symptoms of normal pregnancy mimic the symptoms of hyperthyroidism.

P57kip2 immunohistochemical expression and ultrastructural findings of gestational trophoblastic disease and related disorders

Gestational trophoblastic disease (GTD) is a unique spectrum of diseases ranging from complete hydatidiform mole (CHM), partial hydatidiform mole (PHM), and invasive mole (IM) to choriocarcinoma (CC). Placental site trophoblastic tumor (PSTT) and epithelioid trophoblastic tumor (ETT) have been classified as related disorders. Mesenchymal dysplasia (MD) may be misdiagnosed as PHM; however, it is said to have a quite different histogenesis from PHM. P57kip2 is the protein product of a paternally imprinted or maternal gene that inhibits cyclin-dependent kinases (CDK), thus serving to inhibit cell proliferation and to suppress tumor growth. Its lack of expression in trophoblastic disease plays a role in its abnormal proliferation and differentiation. In this study, P57kip2 immunostaining was absent in the trophoblastic layers of CHM and was positive in the trophoblast layer of nonmolar villi and MD. Ultrastructure of complete molar cystic villi showed tree-like branching of microvillous processes and intracytoplasmic lacunae without capillaries in the stroma, whereas MD contained many newly formed blood vessels and collagen. Also, large lacunae with microvilli and polymorphic nuclei of syncytiotrophoblast cells with well-developed organelles were observed in IM. Lung ETT following CHM and normal deliveries showed two types of large mononuclear cells and binuclear cells with abundant organelles and bundles of intermediate-type filaments in the stroma.

Hypertension in pregnancy

Hypertension is the most common medical problem encountered during pregnancy, complicating 2-3% of pregnancies. Hypertensive disorders during pregnancy are classified into 4 categories: chronic hypertension, pre-eclampsia/eclampsia, pre-eclampsia superimposed on chronic hypertension, and gestational hypertension. A relative paucity of investigative data, as well as the frequent difficulty in making an etiological diagnosis, may lead to problems in its management. This case report analyses current concepts regarding the hypertensive disorders of gestation, focusing on chronic hypertension. Chronic hypertension is defined as blood pressure exceeding 140/90 mmHg before pregnancy or before 20 weeks gestation. Hypertensive disorders in pregnancy may cause maternal and fetal morbidity and remain a leading source of maternal mortality. A prompt diagnosis is needed also because hypertension may be an indicator of pre-eclampsia, a condition which can evolve into serious complications. Maintaining blood pressure below 140/90 mmHg is recommended, although treatment should be determined on an individual basis. Many anti-hypertensive agents appear to be safe for use during pregnancy: methildopa has been the most studied of the anti-hypertensive drugs and has the best safety record. Labetalol, idralazine and nifedipine also have been found to be safe; ACE-inhibitors are absolutely contraindicated, because they are associated with intrauterine growth retardation.

Gestation linked radical oxygen species fluxes and vitamins and trace mineral deficiencies in the ruminant

In mammals, radical oxygen species (ROS) are essential factors of cell replication, differentiation and growth (oxidative signal), notably during gestation, but are also potentially damaging agents. In Women, ROS play a role in remodeling of uterine tissues, implantation of the embryo, settlement of the villi and development of blood vessels characteristic of gestation. The body stores of vitamins and minerals of gestating females are used to keep ROS fluxes at a level corresponding to oxidative signals and to prevent an imbalance between their production and scavenging (oxidative stress), which would be detrimental to the mother and fetus. There is some evidence that, although based on different regulatory mechanisms, most of the effects of ROS reported in humans also occur in pregnant ruminant females, some of which have been actually reported. Many vitamins and trace elements have dual effects in the organism of mammals: (a) they are involved in the control of metabolic pathways or/and gene expression, (b) but most of the time they also display ROS trapping activity or their deficiencies induce high rates of ROS production. Deficiencies induce different disorders of gestation and can be induced by different kinds of stress. An example is given, corresponding to the decreased contents of cobalt of forages, when exposed to sustained heavy rains, so that the supply of vitamins B12 to the organism of the ruminant that grazes them is reduced and failure of gestation is induced. Outdoor exposure of ruminants to adverse climatic conditions by itself can increase the vitamin and trace element requirements. Adaptation of production systems taking into account these interactions between gestation and sources of stress or change of the quality of feeding stuffs as well as further developments of knowledge in that field is necessary to promote sustainable agricultural practices.

Pregnancy as the prodrome to vascular dysfunction and cardiovascular risk

In previously apparently healthy women, glucose intolerance and high blood pressure during pregnancy are common and frequently occur together. This article reviews the role of these gestational disorders as markers of vascular dysfunction and its pathophysiology. Mechanisms include alterations to function of large arteries and resistance vessels and to capillary blood flow. Much of the vessel pathology is seen in both gestational diabetes and hypertension. In women who have had transient diabetes during pregnancy and later redeveloped overt diabetes, cardiovascular risk is already elevated nearly fourfold before diagnosis, which is almost as high as the average risk after a clinical diagnosis of diabetes is made. This key finding suggests that vascular risk in such women is at least partly independent of overt hyperglycemia.

Maternal Obesity, Metabolism, and Pregnancy Outcomes

About one third of all pregnant women in the United States are obese. Maternal obesity at conception alters gestational metabolic adjustments and affects placental, embryonic, and fetal growth and development. Neural tube defects and other developmental anomalies are more common in infants born to obese women; these defects have been linked to poor glycemic control. Preeclampsia, a gestational disorder occurring more frequently in obese women, appears to be due to a subclinical inflammatory state that impairs early placentation and development of its blood supply. Fetal growth and development during the last half of pregnancy depends on maternal metabolic adjustments dictated by placental hormones and the subsequent oxygen and nutrient supply. Maternal obesity affects these metabolic adjustments as well. Basal metabolic rates are significantly higher in obese women, and maternal fat gain is lower, possibly in response to altered leptin function. The usual increase in insulin resistance seen in late pregnancy is enhanced in obese mothers, causing marked postprandial increases in glucose, lipids, and amino acids and excessive fetal exposure to fuel sources, which in turn increases fetal size, fat stores, and risk for disease postnatally. Impaired glucose tolerance, gestational diabetes, and hyperlipidemia are more common among obese mothers. To date, little attention has been given to the role of diet among obese women in preventing these problems. However, studies of women with impaired glucose tolerance show that replacing refined carbohydrates and saturated fat with complex, low-glycemic carbohydrates and polyunsaturated fatty acids improves metabolic homeostasis and pregnancy outcomes. Thus, current dietary guidelines regarding the amount and type of carbohydrates and fat for nonpregnant women seem appropriate for pregnant women as well.

Development of the metabolic syndrome along the female biological life-path

Development of the metabolic syndrome along the female biological life-path

Serum Lipid Levels at 28–32 Weeks Gestation and Hypertensive Disorders

Background: The etiology and pathogenesis of hypertensive disorders complicating pregnancy are poorly understood, and the definition of these disorders is controversial. Methods: In a prospective study, 470 primigravida women between 28 and 32 weeks of pregnancy were evaluated for serum levels of total cholesterol, low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol, and triglyceride. Afterward, they were observed for any symptoms of preeclampsia and gestational hypertension until 40 weeks of gestational age. We than compared the serum lipid levels among women with preeclampsia and gestational hypertension with those of matched women with normal pregnancies. Results: The numbers of patients developing preeclampsia and gestational hypertension were 25 (5.3%) and 32 (6.8%), respectively. At the beginning of the study, the mean values of serum triglyceride levels between women who later experienced preeclampsia or gestational hypertension and those who did not differed significantly (p < 0.0001, p < 0.03). Conclusion: Although many cases of gestational hypertension represent latent essential hypertension based on the lipid levels, some of these women display true pregnancy-induced hypertension or nonproteinuric preeclampsia.

Hiperglicemia materna diária diagnosticada pelo perfil glicêmico: um problema de saúde pública materno e perinatal

This is both a synthesis and a review of the major research findings, with the aim of validating Rudge's group IB. In this group of pregnants, screening for gestational diabetes was positive while the diagnosis was negative (normal 100 g-oral glucose tolerance test 100 g-OGTT). Nonetheless, the variations in glucose levels observed throughout the day, and confirmed by the glycemic profile (GP), characterized diurnal hyperglycemia, which accounts for maternal and adverse perinatal outcome. The description of this group is unique for both the establishment of the diagnosis during gestation and the follow-up of both the mother and the infant. These pregnancies have been erroneously classified as low risk and have not been diagnosed or treated. The IB group corresponds to 13.8% of the pregnant women screened in our service. This rate, added to the 7% of pregnancies complicated by diabetes, increase the occurrence of hyperglycemic disorders during gestation to up to 20.0%. In Rudge's group IB: a) perinatal mortality rate is 41‰, which is similar to that observed among diabetic pregnant women and 10 times higher than that found among non-diabetics; b) the observed placental abnormalities (both morphological and functional) differed from those seen in non-diabetic and diabetic pregnant women, indicating an adjustment to maintain functional activities that facilitated the passage of glucose to the fetus and explained fetal macrosomia (53.8% in non-treated pregnancies); c) maternal for hypertension, obesity and hyperglycemia was high and seemed to reproduce a model of metabolic syndrome, favoring the potential for future diabetes; d) 10 years after the index-pregnancy, type 2 diabetes was confirmed in 16.7% of the women in group IB. The authors suggest the development of multicentric studies in order to identify biomarkers specific for Rudge's group IB and establish protocols for the diagnosis of gestational hyperglycemic disorders using the combination GP + 100g-GTT as a standard. This procedure may cause an impact on the morbidity/mortality rate among pregnancies complicated by diurnal hyperglycemia.

A National Estimate of the Elective Primary Cesarean Delivery Rate

We describe national trends for elective primary cesarean delivery from 1994 to 2001, with attention to changes in indications. We used data from the Healthcare Cost and Utilization Project Nationwide Inpatient Sample. Cesarean deliveries were identified by International Classification of Diseases, 9th Revision, Clinical Modification procedure and diagnostic codes; V codes identified all types of deliveries for denominators. Twelve indications for elective primary cesarean delivery were targeted. International Classification of Diseases, 9th Revision, Clinical Modification coding changes were also evaluated. After excluding women who had labored and previous cesarean deliveries, elective primary cesarean deliveries rose from 19.7% of all cesarean deliveries in 1994 to 28.3% in 2001, an increase of approximately 43.6%. The use of the identified indications for elective primary cesarean delivery increased for codes representing malpresentation, antepartum bleeding, hypertension and severe hypertension, macrosomia, unengaged head, preterm gestation, and maternal soft tissue disorders. Coding for herpes, multiple gestation, other uterine scar, and congenital central nervous system remained the same. Additionally, a new 1998 code for fetal heart rate abnormalities was rapidly adopted during the study period. A national estimate of the elective primary cesarean delivery rate shows a rising trend. Additionally, coded indications for these procedures are shifting. Further examination into the use and clinical implications of indications through national surveillance for elective primary cesarean delivery is important for future obstetric practice. A revision of the terminology classification used to identify indications for cesarean delivery procedures would aid in this effort. III.

Correlations between serum assays of human chorionic gonadotrophin (hCG) and human placental lactogen (hPL) and pre-eclampsia or intrauterine growth restriction (IUGR) among nulliparas younger than 38 years

Objective: To study the relation between serum human chorionic gonadotrophin (hCG) levels measured at 15–18 weeks and gestational disorders, assess their correlation with the artery uteroplacental Doppler (AUD) at 24 weeks among nulliparas, and assess the predictivity of the hCG/hPL (human placental lactogen) ratio for pre-eclampsia. Study Design: Retrospective study of two groups of women younger than 38 years old: one with an elevated serum hCG level (2 MoM (multiples of the median) or more) and a normal fetal karyotype (group A), and the other with a lower hCG level (group B). Within each group, we studied the nulliparas separately (respectively groups AO and BO). We analyzed the double screening, elevated hCG levels with abnormal AUD, for the predicting of hypertensive disorders. Results: Elevated hCG levels were significantly ( p<0.05) more prevalent among women who developed gestational diabetes (groups A and AO) and among nulliparas with pregnancy-induced hypertension and pre-eclampsia (AO). Among nulliparas, the combination of the hCG assay and a subsequent Doppler increased the positive predictive value (PPV) of the assay from 19 to 75%, without reducing its negative predictive value (NPV) for gestational vascular disorders. The hCG/hPL ratio did not improve the predictivity of the hCG assay alone for pre-eclampsia. Conclusions: An hCG level of 2 MoM or more at 15–18 weeks identifies a group of women at risk of gestational vascular disorders; it therefore ought to lead to an AUD at 24 weeks. This double screening should be able to define a population of women at risk of developing a hypertensive disorder, who could thus benefit from a preventive treatment, as aspirin.

Further Evidence of Relation Between Prenatal Famine and Major Affective Disorder

OBJECTIVE: In a previous study, the authors demonstrated an association between prenatal famine in middle to late gestation and major affective disorders requiring hospitalization. In this study, they sought to examine the association by using newly identified cases from the Dutch birth cohort used previously to examine the gender specificity of the association and to assess whether this relation is present for both unipolar and bipolar affective disorders. METHOD: The authors compared the risk of major affective disorder requiring hospitalization in birth cohorts who were and were not exposed, in each trimester of gestation, to famine during the Dutch Hunger Winter of 1944–1945. These cases of major affective disorder requiring hospitalization were newly ascertained from a national psychiatric registry. A larger data set from this registry was used for analysis by gender and diagnostic subtype. RESULTS: For the newly ascertained cases, the risk of developing major affective disorder requiring hospitaliza...

Further evidence of relation between prenatal famine and major affective disorder.

In a previous study, the authors demonstrated an association between prenatal famine in middle to late gestation and major affective disorders requiring hospitalization. In this study, they sought to examine the association by using newly identified cases from the Dutch birth cohort used previously to examine the gender specificity of the association and to assess whether this relation is present for both unipolar and bipolar affective disorders. The authors compared the risk of major affective disorder requiring hospitalization in birth cohorts who were and were not exposed, in each trimester of gestation, to famine during the Dutch Hunger Winter of 1944-1945. These cases of major affective disorder requiring hospitalization were newly ascertained from a national psychiatric registry. A larger data set from this registry was used for analysis by gender and diagnostic subtype. For the newly ascertained cases, the risk of developing major affective disorder requiring hospitalization was increased for subjects with exposure to famine in the second trimester and was increased significantly for subjects with exposure in the third trimester, relative to unexposed subjects. For the cases from the entire period of ascertainment, the risk of developing affective disorder was significantly increased for those exposed to famine during the second and the third trimesters of gestation. The effects were demonstrated for men and women and for unipolar and bipolar affective disorders. These results provide support for the authors' previous findings on the association between middle to late gestational famine and affective disorder.

Pathology of the Placenta. 2nd ed.

Yale University School of Medicine, New Haven, Connecticut, U.S.A. The increased interest in explaining and avoiding poor fetal outcome by gynecologists and pediatricians, and the interest by researchers in “nonrejection” of the fetoplacental unit has led to a great increase in the number of texts addressing various aspects of the biology of the placenta. The second edition of Pathology of the Placenta is one of the series of Contemporary Issues in Surgical Pathology. Each of the book's 16 chapters is written by an author who is an expert in that area, including a chapter on the umbilical cord by the late Dr. Heifetz. This edition begins with a brief chapter that provides an overview of the placental pathology and the justification for examination of the placenta. The following three chapters address gross examination of the placenta and provide anatomic, histologic, and embryologic overviews. The next four chapters are organized anatomically and discuss the pathology of the umbilical cord, placental membranes, placental parenchyma, and decidua and maternal vasculature. The writing in these chapters is concise, with emphasis on clinicopathologic correlations. The subsequent chapters deal with individual categories of disease—multiple gestation, gestational trophoblastic disease, placental neoplasms, and infectious disorders of the placenta. The chapter on multiple gestation provides a comprehensive “heuristic table” for effective placental examination that features more than 30 questions that might be raised by multiple gestations. It also addresses briefly interval delivery, molar twinning, sexual discordance in monozygotic twins, and supertwin placentation. The chapter on molar gestations discusses, in addition to clinicopathologic aspects, the genetics of molar gestations and applications of molecular investigations to this disease. Brief discussions of gestational trophoblastic diseases and nontrophoblastic placental neoplasms follow. The chapter on infectious disorders of the placenta is perhaps too brief. The chapter on molecular pathology is one of the major strengths of this text and sets this book apart from other placental pathology texts. It addresses newer developments in placental pathology such as confined placental mosaicism and genomic imprinting. The role of emerging molecular techniques is discussed. The book ends with chapters on ultrasound and pathologic correlations, and medicolegal aspects of the placenta. The information content of this book is of high quality. The quality of illustrations is generally superior, as is the paper used. Unfortunately and perhaps predictably in a book of this type, there is a lack of in-depth coverage. However, the extensive bibliography of most of the chapters offsets this shortcoming. There is some repetition from chapter to chapter, largely because gross evaluation is discussed in the second chapter as well as in the chapter that addresses that anatomic structure specifically. The largest area of repetition is the first chapter, which provides brief summaries on lesions discussed in later chapters, with duplication of photographs, and does little to add to the overall substance of the book. This book is not as comprehensive or as inclusive as the editors suggest. Some abnormalities are completely overlooked, such as storage disorders affecting the placenta. In addition, complex maternal disorders are not served well by this division of chapters (e.g., lupus anticoagulant or diabetes). This makes the book a “hard to use at the microscope” text, especially because the index does not reference these entities either. In spite of these shortcomings, this is a useful and timely book, considering the increasing interest in this organ. It will serve a wide range of students, physicians, and scientists beginning their training in the area of placental pathology. It is a good textbook for the student or resident. It is well written, flows quite easily from chapter to chapter, and is concise. Pathology of the Placenta is a useful reference book (in the areas that it covers) for the more advanced placental pathologist with its large bibliography and up-to-date references especially with respect to molecular aspects and recent developments in the understanding of placental function.

Role of the IGF system in trophoblast invasion and pre-eclampsia.

Insulin-like growth factor-II (IGF-II) and IGF binding protein-1 (IGFBP-1) appear to play an important role in paracrine interactions at the maternal-fetal interface in human pregnancy. Patterns of expression of IGF-II and IGFBP-1 at the decidual-trophoblast interface suggest paracrine interactions occur between the IGF-II-expressing invading cytotrophoblast and maternal decidua-derived IGFBP-1. Autocrine/paracrine actions of trophoblast-derived IGF-II may be important in invasion, and for both trophoblast and decidual function. The actions of IGFBP-1 in binding IGF, and as an integrin ligand, suggest it may have multiple roles in the interactions between the invading trophoblast and the maternal decidua. Abundant decidual IGFBP-1 may interact with the IGF-II-expressing, protease-secreting trophoblast to modulate invasion. In-vitro studies of trophoblast-decidual cell interactions in invasion, and clinical observations in a gestational disorder with shallow placental invasion such as pre-eclampsia, have provided new insights into the possible role(s) of IGFBP-1 in trophoblast invasion. The precise mechanisms underlying IGF and IGFBP-1 action at the decidual-trophoblast interface remain to be elucidated. The potential predictive value of serum IGFBP-1 concentrations in pre-eclampsia also remains to be established.

Paracrine regulation of human placenta: control of hormonogenesis

There is much evidence indicating that the human placenta plays a very important role in modulating the endocrinology of pregnancy. Placental tissue produces cytokines, hormones and growth factors that are essential in the regulation of the feto-maternal unit. The production of these substances is regulated by a network of interactions within and between intra-uterine through paracrine and/or autocrine mechanisms. Communication between the gestational intra-uterine tissues is critical for successful pregnancy, from the earliest stage of implantation until the expulsive phase of delivery. This is confirmed by the demonstration that the human placenta directly controls the release of substances such as hCG, hPL, steroid hormones and prostoglandins. Furthermore, there is evidence that intra-uterine tissues also can regulate ACTH release and have effects on the hypothalamus–pituitary–gonadal axis and the hypothalamus–pituitary–adrenal axis. The set of data reported in this article confirms that the placenta must be considered an organ that is essential for the initiation, maintenance and successful conclusion of pregnancy and that an imbalance between the complex network of placental regulating systems may cause serious gestational disorders.

Determining the time before birth when ischemia and hypoxemia initiated cerebral palsy

To test the hypothesis that lymphocyte and normoblast counts in neonatal blood can be used to identify the time that ischemia and hypoxemia produced cerebral palsy. Blood lymphocyte and normoblast counts were analyzed at intervals after birth in 16 neonates for whom we knew the time when antenatal ischemic and hypoxemic brain damage began. These counts were compared with counts from normal newborns, infants with low Apgar scores and no cerebral palsy, and infants with cerebral palsy caused by developmental and other early gestational disorders. Lymphocyte counts increased to more than 10,000/mm3 and normoblast counts to 2000/mm3 or more within 2 hours after the brain-damaging ischemia and hypoxemia began. Lymphocyte counts returned to normal levels 24 hours after the damaging event took place, and normoblast counts in 24-36 hours. Normal neonates had a mean +/- one standard deviation lymphocyte count of 4430 +/- 1418/mm3 and a normoblast count of 560 +/- 771/mm3. Following the changing counts of lymphocytes and normoblasts in neonates' blood may accurately identify the time before birth when brain-damaging ischemia and hypoxemia began.

Altered rheological properties of red and white cells during normal gestation

Beside plasma viscosity and the functional state of the vessel wall, placental perfusion is determined by the concentration and behaviour of the blood cells. In order to evaluate the contribution of erythrocytes to placental flow in late pregnancy, we applied a new filtration technique allowing to analyze the passages of erythrocytes through a single pore. As a parameter of decreased deformability in late pregnancy, we found a significant increase in transit time (22.69 +/1.60 ms vs 24.03 +/2.40 ms; pore size 4.1 pm; hydrostatic pressure 100 Pa) correlating with the mean cell volume (r=0.763). Due to their size and rigidity, their property to adhere to altered endothelium and to release radicals and mediators, granulocytes were the second point of interest to investigate in late pregnancy. Granulocytes were more adherent in vitro when stimulated with PMA, FMLP or in the absence of these mediators. This was shown for BSAand fibronectincoated wells (BSA: PMA 72.6% vs 67.2%, FMLP 43.4% vs 36.1%, unstimulated 26.5% vs 15.4%; fibronectin: PMA 71.6% vs 66.7%, FMLP 44.7% vs 31.1 %, unstimulated 25.7% vs 18.2%). Transit times of granulocytes through 8 pm pores were significantly shorter in the pregnant group at 400 Pa (5.02 +/0.50 ms vs 5.49 +/0.74 ms), nearly identical at 200 Pa (9.34 +/1.79 ms vs 9.57 +/1.65 ms) and impossible to measure at 100 Pa (frequent obstruction). Luminol-enhanced whole blood chemiluminescence of unstimulated granulocytes was decreased in the pregnant group (0.19 counts/ce11l2s vs 0.33 counts/cell12s) but exceeded values of the control group when stimulated with PMA or FMLP (PMA: 20.13 counts/cell/2s vs 15.90 counts/cell/2s; FMLP: 2.35 counts/cell/2s vs 1.94 counts/cell/2s). Our results may indicate that in times of insufficient placental flow, as it is seen in hypertension-related gestational disorders, a decreased erythrocyte deformability as well as an enhanced adhesivity and chemiluminescence of activated granulocytes may perpetuate and aggravate placental malperfusion.

THE SYNDROME OF PREECLAMPSIA

Preeclampsia has traditionally been viewed as one of several forms of hypertension complicating pregnancy. More recently, the multisystem nature of this unique gestational disorder has been emphasized. Pathophysiologic events, including abnormal placentation and heightened vascular reactivity, may occur weeks or months prior to clinical recognition of the disease. Although most frequently presenting as hypertension and proteinuria, hepatic (abdominal pain and elevation of transaminases) and hematologic (intravascular hemolysis and thrombocytopenia) involvement may be important features of the disease. Current theories suggest that multiorgan dysfunction may be caused by widespread vascular endothelial dysfunction, vasospasm, and variable activation of coagulation mechanisms. Pending delivery, which is the only definitive therapy for preeclampsia, maternal complications of intracerebral hemorrhage and eclampsia may be prevented with judicious use of antihypertensive medication (e.g., hydralazine) and magnesium sulfate, respectively. Finally, data from a number of small trials suggest that low-dose aspirin (60-100 mg/d) may reduce the incidence of preeclampsia in patients at high risk without adversely affecting the fetus or newborn; however, it is recommended that aspirin not be used as a routine prophylactic intervention until publication of results of several ongoing large multicenter trials, which will help to more fully clarify the benefits and risks of this approach.