Comprehensive morphological study of free radical processes in chronic chorioamnionitis on the background of iron deficiency anemia in pregnancy.

OBJECTIVE: Aim: To establish the features of free radical processes in the endotheliocytes of the chorionic plate of the placenta in chronic chorioamnionitis against the background of iron deficiency anemia of pregnant women using both chemiluminescent and histochemical methods of research. PATIENTS AND METHODS: Materials and Methods: 82 placentas from parturients at 37 - 40 weeks of gestation were studied. Including, for comparison, the placenta during physiological pregnancy and the observation of iron deficiency anemia of pregnant women without inflammation of the placenta. The number of observations in specific study groups is given in the tables. To achieve the objective and solve the tasks set in this study, there were carried out the following histochemical, chemiluminescent, morphometric and statistical methods of material processing. RESULTS: Results: In case of chorionamnionitis against the background of anemia in pregnancy, the R/B ratio (R/B - ratio between amino- (blue) and carboxyl (red) groups of proteins)) in the method with bromophenol blue according to Mikel Calvo was 1.56±0.021, indicators of chemiluminescence of nitroperoxides were 133±4.5, relative optical density units of histochemical staining using the method according to A. Yasuma and T. Ichikawa was - 0.224±0.0015. CONCLUSION: Conclusions: With chronic chorioamnionitis, the intensity of the glow of nitroperoxides, the average indicators of the R/B ratio, and the optical density of histochemical staining for free amino groups of proteins are increased compared to placentas of physiological pregnancy and anemia of pregnant women. Comorbid i anemia of pregnant women causes increasing of the intensity of the glow of nitroperoxides, the average values of the R/B ratio, and the optical density of histochemical staining for free amino groups of proteins comparing to placentas with inflammation without anemia. The key factor in the formation of morphological features of chronic chorioamnionitis with comorbid anemia is the intensification of free radical processes, which is reflected by the increase in the concentration of nitroperoxides in the center of inflammation, with the subsequent intensification of the processes of oxidative modification of proteins, which is followed by the increasing activity of the processes of limited proteolysis.

[Deforming endonasal mass during pregnancy]. / Deformierende endonasale Raumforderung während der Schwangerschaft.

This article presents the case of a 33-year-old woman who consulted the authors' ENT clinic in the 39th week of pregnancy with recurrent epistaxis. A livid endonasal mass was found on the left side, subtotally displacing the nose and leading to deformation of the external nose. External biopsy provided no indications of malignancy. Postpartum CT of the paranasal sinuses revealed a mass destroying the cartilaginous nasal septum. Endoscopic resection of the finding was performed with preservation of the clinically sound nasal septal cartilage. Histopathological examination revealed a capillary hemangioma, which was classified as granuloma gravidarum due to its occurrence during pregnancy.

How I manage pregnancy in carriers of hemophilia and patients with von Willebrand disease.

Women with inherited bleeding disorders, including carriers of hemophilia A and B, or with von Willebrand disease, have an increased risk of bleeding during pregnancy and delivery. The unborn child may also be affected by the bleeding disorder for which specific measures have to be considered. This requires a multidisciplinary approach, with a team that includes a hematologist, a pediatric hematologist, a clinical geneticist, an obstetrician-perinatologist, and an anesthesiologist. An optimal approach includes prepregnancy genetic counseling, prenatal diagnostic procedures, and a treatment plan for delivery for both the mother and child. Recent retrospective studies show that even if strict guidelines are followed, these women are still at risk of postpartum bleeding. This occurs even if coagulation factor levels are normalized, either due to the pregnancy-induced rise of factor levels or by infusion of coagulation factor concentrates at the time of delivery. In this article, we describe our current diagnostic and clinical management of pregnancy and delivery in women with inherited bleeding disorders. We also briefly discuss possible interventions to improve the outcome of current strategies by increasing target factor levels during and after delivery.

How I treat lymphoma in pregnancy.

Lymphomas afflict all age groups of people, with certain types demonstrating a female predilection in adolescents and young adults. A proportion of lymphomas that are diagnosed in this population demographic occur in the setting of pregnancy. Most of these behave aggressively at presentation and require immediate or urgent therapy. Treatment must consider both maternal and fetal health, and management approaches are therefore influenced by gestational age at diagnosis and treatment and timing of delivery. Although there is a paucity of literature on how to treat these patients, limited retrospective reports demonstrate generally good outcomes and highlight the necessity of an experienced multidisciplinary team approach to management.

Pregnancy-associated venous insufficiency course with placental and systemic oxidative stress.

The development of lower extremity venous insufficiency (VI) during pregnancy has been associated with placental damage. VI is associated with increased oxidative stress in venous wall. We have investigated potential disturbance/dysregulation of the production of reactive oxygen species (ROS) in placenta and its eventual systemic effects through the measurement of malondialdehyde (MDA) plasma levels in women with VI. A total of 62 women with VI and 52 healthy controls (HCs) were studied. Levels of nicotinamide adenine dinucleotide phosphate-oxidase 1 (NOX1), 2 (NOX2), inducible nitric oxide synthase (iNOS), endothelial (eNOS), poly(ADP-ribose) polymerase PARP (PARP) and ERK were measured in placental tissue with immunohistochemistry and RT-qPCR. Plasma and placental levels of MDA were determined by colorimetry at the two study times of 32 weeks of gestation and post-partum. Protein and gene expression levels of NOX1, NOX2, iNOS, PARP and ERK were significantly increased in placentas of VI. eNOS activity was low in both study groups, and there were no significant differences in gene or protein expression levels. Women with VI showed a significant elevation of plasma MDA levels at 32 weeks of gestation, and these levels remained elevated at 32 weeks post-partum. The MDA levels were significantly higher in placentas of women with VI. Placental damage that was found in the women with VI was characterized by overexpression of oxidative stress markers NOX1, NOX2, and iNOS, as well as PARP and ERK. Pregnant women with VI showed systemic increases in oxidative stress markers such as plasma MDA levels. The foetuses of women with VI had a significant decrease in their venous pH as compared to those from HC women. The situation of oxidative stress and cellular damage created in the placenta is in coexpression with the production of a pH acidification.

Inherited Thrombophilia and Pregnancy Complications: Should We Test?

Recurrent miscarriages and pregnancy-related complications cause significant stress to couples looking for successful pregnancy outcome as well as to health care professionals. There is conflicting evidence with respect to the presence and the strength of associations between inherited thrombophilia and these complications. A complete thrombophilia screen is expensive, and no proven effective treatment for women with recurrent miscarriage and inherited thrombophilia is currently available. Based on the concept of microvascular thrombosis of the placenta, women with recurrent miscarriage and placenta-related complications frequently get treated with antithrombotic therapy. In this narrative review, the authors explore the evolving understanding and evidence of inherited thrombophilia in recurrent miscarriages and other pregnancy complications, and whether antithrombotic treatment would modify pregnancy outcome in women with inherited thrombophilia. Finally, they provide some personal recommendations based on available evidence for clinical practice. In summary, inherited thrombophilia testing is not required outside a clinical trial for women with recurrent pregnancy losses or late pregnancy complications. The presence of thrombophilia markers does not generally indicate additional therapy during pregnancy, even if a heritable thrombophilic defect is found in women with recurrent miscarriages or late pregnancy complications.

Thrombocytopenia in pregnancy.

Thrombocytopenia develops in 5% to 10% of women during pregnancy or in the immediate postpartum period. A low platelet count is often an incidental feature, but it might also provide a biomarker of a coexisting systemic or gestational disorder and a potential reason for a maternal intervention or treatment that might pose harm to the fetus. This chapter reflects our approach to these issues with an emphasis on advances made over the past 5 to 10 years in understanding and managing the more common causes of thrombocytopenia in pregnancy. Recent trends in the management of immune thrombocytopenia translate into more women contemplating pregnancy while on treatment with thrombopoietin receptor agonists, rituximab, or mycophenylate, which pose known or unknown risks to the fetus. New criteria to diagnose preeclampsia, judicious reliance on measurement of ADAMTS13 to make management decisions in suspected thrombotic thrombocytopenic purpura, new evidence supporting the efficacy and safety of anticomplement therapy for atypical hemolytic uremic syndrome during pregnancy, and implications of thrombotic microangiopathies for subsequent pregnancies are evolving rapidly. The goals of the chapter are to help the hematology consultant work through the differential diagnosis of thrombocytopenia in pregnancy based on trimester of presentation, severity of thrombocytopenia, and coincident clinical and laboratory manifestations, and to provide guidance for dealing with some of the more common and difficult diagnostic and management decisions.

Perinatal Maternal Mortality in Sickle Cell Anemia: Two Case Reports and Review of the Literature.

As outcomes of patients with sickle cell anemia improve and survival into adulthood with good quality of life and expectation of long-term survival becomes more common, challenges have developed, including issues related to reproduction. Pregnancy is frequently complicated in patients with sickle cell anemia with mortality up to 4.0%. Here we report maternal perinatal mortality in two women with sickle cell anemia who died post-partum due to acute chest syndrome (ACS), caused by bone marrow fat embolism and review the literature pertinent to this subject. Patient A was a 28-year-old woman with sickle cell anemia with multiple complications. At 30 weeks' gestation she developed hemolysis associated with poor placental function necessitating delivery by C-section. The fetus was delivered successfully but she died due to multi organ failure after delivery. Autopsy showed pulmonary and amniotic fluid embolization. Patient B was a 37-year-old woman with uncomplicated sickle cell anemia who presented with pre term labor and crisis, then ACS and fetal distress. The infant was delivered successfully but the patient died after cardiovascular collapse. Autopsy results showed fat and bone marrow embolization as the cause of death. Pregnancy continues to be high risk for patients with sickle cell anemia including those with mild disease. Maternal perinatal mortality could be unpredictable due to serious complications of sickle cell disease. More studies to assess maternal perinatal mortality are needed.

Erythroblastosis of the Donor Twin of Twin Anemia-Polycythemia Sequence.

Twin anemia-polycythemia sequence (TAPS) is a group of disorders in monochorionic twins characterized by a large intertwin hemoglobin difference without amniotic fluid discordance. Reticulocyte count is used to diagnose this condition, but little is known about the role of erythroblasts, which are the prior stage of reticulocytes. In the present case of TAPS, the 25-yr-old Japanese mother showed no signs of oligohydramnios or polyhydramnios throughout gestation. The twins were born at 36 weeks and 6 days, weighing 2,648g and 1,994g. The intertwin hemoglobin difference in umbilical cord blood was (21.1－5.0＝) 16.1g/dL and the donor twin showed signs of chronic anemia, including myocardial hypertrophy and pericardial effusion. Erythroblastosis of the donor twin was prolonged (53,088.5, 42,114.8 and 44,217.9/µL on days 0, 1 and 2, respectively). Erythroblastosis, which indicates chronic anemia, is also a good diagnostic indicator of TAPS.

Velamentous Umbilical Cord Insertion and Ruptured Fetal Vessel: A Cause of Fetal-Maternal Hemorrhage: A Case Report.

Background: Fetal hemorrhage is rare but can result in rapid fetal compromise. Abnormally located fetal vessels within the membranes increase the risk for their rupture and subsequent hemorrhage. The classic example of this is vasa previa. Case: We present a case of acute fetal hemorrhage resulting from a ruptured fetal vessel. During induction of labor, significant fetal heart rate deceleration occurred, coinciding with acute vaginal bleeding and amniotomy. A depressed, live female neonate was delivered by emergency cesarean section. Examination of the placenta revealed a velamentous cord insertion and a ruptured fetal vessel coursing through the chorioamniotic membranes. Neonatal resuscitation included red blood cell transfusion for hypotension and low hematocrit. The neonate made a full recovery. Conclusion: Acute fetal hemorrhage from the rupture of aberrant fetal vessels often coincides with rupture of membranes. Identifying ruptured fetal vessels abnormally coursing through the chorioamniotic membranes on examination of the placenta provides supporting evidence for suspected fetal hemorrhage.

[Analysis of risk factors for adverse perinatal outcomes in women with pancytopenia].

OBJECTIVE: To explore the pregnancy outcomes of women with pancytopenia and the risk factors for the adverse perinatal outcomes. METHODS: A total of 106 pregnant women with pancytopenia were admitted to Peking University People's Hospital from Jan. 2005 to Sep. 2014. The clinical data and the pregnancy outcomes were reviewed retrospectively to investigate the risk factors for the adverse perinatal outcomes. RESULTS: (1 ) Eighty-four patients were found pancytopenia before pregnancy while 22 were found for the first time during pregnancy. Sixty-four patients were diagnosed as aplastic anemia; 30 as myelodysplastic syndrome; 2 as paroxysmal nocturnal hemoglobinuria; 4 as hypersplenism, and 1 as anti-phospholipid syndrome. Diagnoses of the remaining 5 patients were uncertain. (2) Sixty-nine patients received at least one time blood transfusion before delivery. (3) As for the complications, nine women developed gestational diabetes; twenty-two suffered severe preeclampsia (SPE); two were diagnosed as anemic heart disease and three experienced respiratory tract infection. The postpartum blood loss ranged from 50 ml to 3 800 ml, with the median of 400 ml. And six women had the blood loss more than 1 000 ml. The gestational age at delivery ranged from 24 weeks to 40 weeks, with the median of 37.0 weeks. (4) Thirty-one patients suffered adverse perinatal outcomes, including 3 cases of intrauterine death, 4 therapeutic labor induction before 28 gestational weeks, 6 premature delivery before 34 weeks. There were 2 neonates complicated with intracranial hemorrhage, 2 with neonatal respiratory distress syndrome, 3 with hypoxic-ischemic encephalopathy, 2 with severe asphyxia and death, and 14 with small for gestational age. Among the patients with adverse perinatal outcomes, 26 women received blood transfusion during pregnancy and 17 developed SPE. The maximum and the minimum value of their white cell count (WBC), hemoglobin concentration (Hb) and blood platelet count (BPC) were (4.9±1.4)×10(9)/L, (2.9±0.8)×10(9)/L, (88.6±14.9) g/L, (57.9±14.5) g/L, (47.7±27.4)×10(9)/L and (11.9±12.3)×10(9)/L, respectively. For those patients without adverse perinatal outcomes, 43 received blood transfusion during pregnancy and 5 developed SPE. The maximum and the minimum value of their WBC, Hb and BPC were (5.2±1.5)×10(9)/L, (3.2±0.9)×10(9)/L, (101.4±16.2) g/L, (71.9 ± 14.5) g/L, (52.3 ± 24.0) × 10(9)/L and (19.0±12.1) × 10(9)/L, respectively. The multivariate regression analyses indicated that SPE, Hb less than 70 g/L and BPC less than 20×10(9)/L were the independent risk factors for the poor perinatal outcomes in pregnant women with pancytopenia (P<0.05). CONCLUSIONS: The incidence of adverse perinatal complications increased dramatically in pregnant women with pancytopenia. Concurrent SPE, minimum Hb less than 70 g/L and minimum BPC less than 20 × 10(9)/L may be the independent risk factors for the adverse perinatal outcomes.

Fetal thrombotic vasculopathy and perinatal thrombosis: should all placentas be examined?

OBJECTIVE: Numerous fetal placenta vascular lesions seem to be a predisposing condition for some types of perinatal disease. Placental disease and newborn thromboses might be both manifestations of the same underlying disorder. Objective of this study is to describe pathological lesions of the placenta in newborns with perinatal thrombosis. STUDY DESIGN: We present retrospective data review and analysis regarding neonates admitted at our neonatal intensive care unit and diagnosed with an episode of thromboembolic events (TE) in the period from 2009 to 2013; among them we report three cases of perinatal thrombosis in newborns whose placentas demonstrated fetal thrombotic vasculopathy (FTV). RESULTS: In all the three cases a prothrombotic maternal condition was found, and in one patient a maternal infection with chorioamnionitis; the histological examination of placenta, required soon after birth for maternal pathological conditions, was important in confirming and explaining the clinical diagnosis of neonatal thrombosis and for the management of future pregnancies. CONCLUSION: It is proposed that placenta of newborns with TE in first days of life should always be examined, for its association with FTV and thus the storage of placentas for a week after birth should be routinely implemented.

Morphometrical analysis of intervillous space and villous membrane thickness in maternal anaemia.

BACKGROUND: Anaemia in pregnancy is linked with an increased risk of preterm delivery, low birth weight, perinatal and maternal mortality and it is related with variable histo-morphological changes in placenta which show a reflection for the poor foetal outcome. The objective of this study is to assess the micro-morphometery of intervillous space and villous membrane of placenta in anaemic mothers. METHODS: This case control study was carried out at Army Medical College, National University of Sciences and Technology Islamabad in collaboration with Department of Obstetrics and Gynaecology, Military Hospital, Rawalpindi, Pakistan, from December 2011 to November 2012. A total of 75 placentas were included, that were divided into study and control group. In control group (n = 15) placentas were taken from mothers having normal haemoglobin levels and study group (n = 60) included placentas from anaemic mothers having haemoglobin less than 11g/dl. Study group was subdivided into three groups, i.e., mildly (10.0-10.9 g/dl), moderately (7.0-9.9 g/dl) and severely (< 7 g/dl) anaemic group. Three representative sections were taken from placenta, i.e., one close to umbilical cord (A), one from periphery (C) and one midway between A and C (B).Ocular micro-meter was used to measure intervillous space and villous membrane thickness. RESULTS: Intervillous space was prominent in study groups (41.26 ± 16.33 ìm) as compared to control group (15.98 ± 3.81 ìm) (p < 0.05). Thickness of villous membrane was significantly less in study group as compared to control group (2.97 ± 0.70) (p < 0.05). CONCLUSION: The present study showed wide intervillous space and thin villous membrane in study group as compared to control group reflecting adaptive changes in response to hypoxiain maternal anaemia.

[Placental morphology in inherited thrombophilia].

OBJECTIVE: To study placental morphological changes in inherited thrombophilia. SUBJECT AND METHODS: A morphometric method was used to examine placentas from 37 patients divided into 3 groups: 1) 13 pregnant women with verified inherited thrombophilia; 2) 14 pregnant women with inherited thrombophilia and signs of placental inflammatory manifestations (basal deciduitis, intervillositis, placentitis); 3) 10 women with normal pregnancy (a control group). RESULTS: In inherited thrombophilia, the placentas exhibited morphological manifestations of chronic placental insufficiency as pathological immaturity with a predominance of intermediate differentiated villi and as dissociated maturity of cotyledones, with a substantial reduction in the specialized terminal villi, excessive intervillous fibrinoid formation and villous immuring, evolving pseudoinfarctions, fewer capillaries in the terminal villi, and their increased stromal proportion. At the same time, no significant differences were found in the morphological pattern in inherited thrombophilia concurrent with placental inflammatory changes. CONCLUSION: In inherited thrombophilia, there is chronic placental insufficiency caused by delayed development of the shaggy chorion.

[Ovarian vein thrombophlebitis during pregnancy--with a contribution of one clinical case].

Ovarian vein thrombosis (OVT) is a rare, but serious condition that affects mostly postpartum women but may also be associated with pelvic inflammatory disease, malignancies and pelvic surgical procedures. Concerning ovarian vein thrombosis in earlier stages of pregnancy there are only very few case reports. The authors consider this rare but potentially deadly disease and describe the clinical case study.

[The detection of thrombocyte-bound IgG in patients with throbocytopenia].

The article presents the mode of detection of anti-thrombocyte auto-antibodies using flow cytometry technique. The values of IgG conjugated with thrombocytes are established in healthy persons. The rate of frequency of auto-antibodies to thrombocytes is analyzed in patients with primarily diagnosed immune thrombocytopenia, with relapse of disease and after therapy of immune thrombocytopenia. The carried out studies demonstrate that flow cytometry technique has a high sensitivity to detect thrombocyte-related antibodies and can be applied under examination of patients with thrombocytopenia.

Proliferative glomerulonephritis with monoclonal IgG deposits in a patient with autoimmune hemolytic anemia.

A 25-year-old woman was admitted because of proteinuria. A renal biopsy showed mesangial/endocapillary proliferative glomerulonephritis with IgG2-κ deposits. Electron microscopy showed immune complex-type deposits. She also had Coombs-positive hemolytic anemia, anticardiolipin antibodies, and antinuclear antibodies. Middle-dose steroid therapy led to improvement of proteinuria and hemolytic anemia. Six years later, she developed crescentic glomerulonephritis with IgG2-κ deposits during pregnancy. Middle-dose steroid therapy improved renal dysfunction. This is an exceptional case of proliferative glomerulonephritis with monoclonal IgG deposits (PGNMID), a recently described rare dysproteinemia-related glomerulonephritis, associated with autoimmune disease. This case also suggests that crescentic glomerulonephritis can be superimposed on PGNMID.

Pathophysiological, immunogenetic, anatomopathological profile of thrombophilia in pregnancy.

Thrombophilic states have been associated with early and/or late pregnancy loss and possibly other severe obstetrical complications. Pregnancy-induced hypercoagulability, increased stasis, and the consequences of inherited and acquired thrombophilia are just a few of the factors that contribute to the development of thrombosis in pregnancy. In this review, we illustrate the impact that these factors have on the development of thrombophilia during pregnancy. We also explore how thrombophilia impact pregnancy outcomes. Next, we discuss how human leukocyte antigen G plays a part in thrombophilia during pregnancy by regulating cytokine release to prevent trophoblastic cell invasion and maintain local immunotolerance constant. Human leukocyte antigen class E is briefly explored with thrombophilia in pregnancy. Regarding the anatomopathologic aspect, we describe the different histopathological lesions of the placenta found in women with thrombophilia.

Severity of Anemia During Pregnancy and Adverse Maternal and Fetal Outcomes.

Importance: Anemia is the most widespread nutritional deficiency among pregnant females in the world. Despite numerous studies on anemia, evidence is limited about the association of severity of anemia with maternal and fetal health. Objective: To investigate the association between severity of anemia during pregnancy and risk of maternal and fetal adverse outcomes. Design, Setting, and Participants: This retrospective cohort study used data from China's Hospital Quality Monitoring System from January 1, 2016, to December 31, 2019, for pregnant females aged 15 to 49 years with birth outcomes reported at 1508 hospitals with maternity services in mainland China. Exposures: Anemia of varying severity during pregnancy was identified from daily standardized electronic inpatient discharge records using corresponding codes of the International Statistical Classification of Diseases and Related Health Problems, Tenth Revision. Mild anemia was defined as a hemoglobin concentration of 100 to 109 g/L (to convert g/L to g/dL, divide by 10.0); moderate anemia, as 70 to 99 g/L; and severe anemia, as less than 70 g/L. Main Outcomes and Measures: The main outcomes included 6 maternal outcomes (placental abruption, preterm birth, severe postpartum hemorrhage, shock, admission to the intensive care unit [ICU], and maternal mortality) and 3 neonatal outcomes (fetal growth restriction, malformation, and stillbirth). Multivariable logistic regression models were used to estimate the odds ratios (ORs) and 95% CIs of these outcomes among pregnant females with varying severity of anemia. Results: Among 18 948 443 pregnant females aged 15 to 49 years (mean [SD] age, 29.42 [4.87] years), 17.78% were diagnosed with anemia during pregnancy, including 9.04% with mild anemia, 2.62% with moderate anemia, 0.21% with severe anemia, and 5.90% with anemia of unknown severity. Compared with no anemia, anemia severity during pregnancy was associated with increased risks of placental abruption (mild: adjusted OR [aOR], 1.36 [95% CI, 1.34-1.38]; moderate: aOR, 1.98 [95% CI, 1.93-2.02]; severe: aOR, 3.35 [95% CI, 3.17-3.54]), preterm birth (mild: aOR, 1.08 [95% CI, 1.07-1.08]; moderate: aOR, 1.18 [95% CI, 1.17-1.19]; severe: aOR, 1.36 [95% CI, 1.32-1.41]), severe postpartum hemorrhage (mild: aOR, 1.45 [95% CI, 1.43-1.47]; moderate: aOR, 3.53 [95% CI, 3.47-3.60]; severe: 15.65 [95% CI, 15.10-16.22]), and fetal malformation (mild: aOR, 1.15 [95% CI, 1.14-1.17]; moderate: aOR, 1.19 [95% CI, 1.16-1.21]; severe: aOR, 1.62 [95% CI, 1.52-1.73]). Compared with no anemia, moderate or severe anemia were associated with increased risks of maternal shock (moderate: aOR, 1.50 [95% CI, 1.41-1.60]; severe: aOR, 14.98 [95% CI, 13.91-16.13]), ICU admission (moderate: aOR, 1.08 [95% CI, 1.01-1.16]; severe: aOR, 2.88 [95% CI, 2.55-3.25]), maternal death (moderate: aOR, 0.45 [95% CI, 0.30-0.65]; severe: aOR, 1.56 [95% CI, 0.97-2.48], fetal growth restriction (moderate: aOR, 0.80 [95% CI, 0.78-0.82]; severe: aOR, 1.08 [95% CI, 1.00-1.17]), and stillbirth (moderate: aOR,0.79 [95% CI, 0.76-0.81]; severe: aOR, 1.86 [95% CI, 1.75-1.98]), and mild anemia was associated with decreased risks (maternal shock: aOR, 0.67 [95% CI, 0.63-0.71]; ICU admission: aOR, 0.80 [95% CI, 0.76-0.84]; maternal death: aOR, 0.37 [95% CI, 0.29-0.49]; fetal growth restriction: aOR, 0.79 [95% CI, 0.77-0.80]; stillbirth: aOR, 0.59 [95% CI, 0.58-0.61]) after adjusting for sociodemographic characteristics and other complications during pregnancy. Conclusions and Relevance: The findings suggest that anemia during pregnancy is associated with maternal and fetal health outcomes and that mild anemia is associated with improved maternal and fetal survival and fetal growth. Further work is needed to validate the concentration of hemoglobin at which optimal maternal and fetal health are achieved.