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Preeclampsia(PEE1)

MedGen UID:
18608
Concept ID:
C0032914
Finding; Pathologic Function
Synonym: PEE1
SNOMED CT: Pre-eclampsia (398254007); EPH - Edema, proteinuria and hypertension of pregnancy (398254007); PET - Pre-eclamptic toxemia (398254007); Pre-eclamptic toxemia (398254007); PE - Pre-eclampsia (398254007); Proteinuric hypertension of pregnancy (398254007); Preeclampsia (398254007); Toxemia of pregnancy (398254007)
Modes of inheritance:
Autosomal dominant inheritance
MedGen UID:
141047
Concept ID:
C0443147
Intellectual Product
Sources: HPO, OMIM
A mode of inheritance that is observed for traits related to a gene encoded on one of the autosomes (i.e., the human chromosomes 1-22) in which a trait manifests in heterozygotes. In the context of medical genetics, an autosomal dominant disorder is caused when a single copy of the mutant allele is present. Males and females are affected equally, and can both transmit the disorder with a risk of 50% for each child of inheriting the mutant allele.
 
HPO: HP:0100602
Monarch Initiative: MONDO:0005081
OMIM®: 189800
OMIM® Phenotypic series: PS189800
Orphanet: ORPHA275555

Definition

Preeclampsia, which along with chronic hypertension and gestational hypertension comprise the hypertensive disorders of pregnancy, is characterized by new hypertension (blood pressure 140/90 or greater) presenting after 20 weeks' gestation with clinically relevant proteinuria. Preeclampsia is 1 of the top 4 causes of maternal mortality and morbidity worldwide (summary by Payne et al., 2011). Preeclampsia is otherwise known as gestational proteinuric hypertension (Davey and MacGillivray, 1988). A high proportion of patients with preeclampsia have glomerular endotheliosis, the unique histopathologic feature of the condition (Fisher et al., 1981). A distinct form of severe preeclampsia is characterized by hemolysis, elevated liver enzymes, and low platelets (HELLP syndrome) (Brown et al., 2000). Genetic Heterogeneity of Preeclampsia/Eclampsia Susceptibility loci for preeclampsia/eclampsia include PEE1 on chromosome 2p13, PEE2 (609402) on chromosome 2p25, and PEE3 (609403) on chromosome 9p13. PEE4 (609404) is caused by mutation in the STOX1 gene (609397) on chromosome 10q22. PEE5 (614595) is caused by mutation in the CORIN gene (605236) on chromosome 4p12. An association with PEE has been found with the EPHX1 gene (132810) on chromosome 1q. [from OMIM]

Additional descriptions

From MedlinePlus Genetics
Preeclampsia is a complication of pregnancy in which affected women develop high blood pressure (hypertension); they can also have abnormally high levels of protein in their urine (proteinuria). This condition usually occurs in the last few months of pregnancy and often requires early delivery of the infant. However, this condition can also appear shortly after giving birth (postpartum preeclampsia).\n\nMany women with mild preeclampsia do not feel ill, and the condition is often first detected through blood pressure and urine testing in their doctor's office. In addition to hypertension and proteinuria, signs and symptoms of preeclampsia can include excessive swelling (edema) of the face or hands and a weight gain of more than 3 to 5 pounds in a week due to fluid retention. Affected women may also experience headaches, dizziness, irritability, shortness of breath, a decrease in urination, upper abdominal pain, and nausea or vomiting. Vision changes may develop, including flashing lights or spots, increased sensitivity to light (photophobia), blurry vision, or temporary blindness.\n\nIn many cases, symptoms of preeclampsia go away within a few days after the baby is born. In severe cases, however, preeclampsia can damage the mother's organs, such as the heart, liver, and kidneys, and can lead to life-threatening complications. Extremely high blood pressure in the mother can cause bleeding in the brain (hemorrhagic stroke). The effects of high blood pressure on the brain (hypertensive encephalopathy) may also result in seizures. If seizures occur, the condition is considered to have worsened to eclampsia, which can result in coma. About 1 in 200 women with untreated preeclampsia develop eclampsia. Eclampsia can also develop without any obvious signs of preeclampsia.\n\nBetween 10 and 20 percent of women with severe preeclampsia develop another potentially life-threatening complication called HELLP syndrome. HELLP stands for hemolysis (premature red blood cell breakdown), elevated liver enzyme levels, and low platelets (cells involved in blood clotting), which are the key features of this condition.\n\nSevere preeclampsia can also affect the fetus, with impairment of blood and oxygen flow leading to growth problems or stillbirth. Infants delivered early due to preeclampsia may have complications associated with prematurity, such as breathing problems caused by underdeveloped lungs.\n\nWomen who have had preeclampsia have approximately twice the lifetime risk of heart disease and stroke than do women in the general population. Researchers suggest that preeclampsia, heart disease, and stroke may share common risk factors. Women who have health conditions such as obesity, hypertension, heart disease, diabetes, or kidney disease before they become pregnant have an increased risk of developing preeclampsia. Preeclampsia is most likely to occur in a woman's first pregnancy, although it can occur in subsequent pregnancies, particularly in women with other health conditions.  https://medlineplus.gov/genetics/condition/preeclampsia
From MedlinePlus Genetics
Preeclampsia is a complication of pregnancy in which affected women develop high blood pressure (hypertension); they can also have abnormally high levels of protein in their urine (proteinuria). This condition usually occurs in the last few months of pregnancy and often requires early delivery of the infant. However, this condition can also appear shortly after giving birth (postpartum preeclampsia).\n\nMany women with mild preeclampsia do not feel ill, and the condition is often first detected through blood pressure and urine testing in their doctor's office. In addition to hypertension and proteinuria, signs and symptoms of preeclampsia can include excessive swelling (edema) of the face or hands and a weight gain of more than 3 to 5 pounds in a week due to fluid retention. Affected women may also experience headaches, dizziness, irritability, shortness of breath, a decrease in urination, upper abdominal pain, and nausea or vomiting. Vision changes may develop, including flashing lights or spots, increased sensitivity to light (photophobia), blurry vision, or temporary blindness.\n\nIn many cases, symptoms of preeclampsia go away within a few days after the baby is born. In severe cases, however, preeclampsia can damage the mother's organs, such as the heart, liver, and kidneys, and can lead to life-threatening complications. Extremely high blood pressure in the mother can cause bleeding in the brain (hemorrhagic stroke). The effects of high blood pressure on the brain (hypertensive encephalopathy) may also result in seizures. If seizures occur, the condition is considered to have worsened to eclampsia, which can result in coma. About 1 in 200 women with untreated preeclampsia develop eclampsia. Eclampsia can also develop without any obvious signs of preeclampsia.\n\nWomen who have had preeclampsia have approximately twice the lifetime risk of heart disease and stroke than do women in the general population. Researchers suggest that preeclampsia, heart disease, and stroke may share common risk factors. Women who have health conditions such as obesity, hypertension, heart disease, diabetes, or kidney disease before they become pregnant have an increased risk of developing preeclampsia. Preeclampsia is most likely to occur in a woman's first pregnancy, although it can occur in subsequent pregnancies, particularly in women with other health conditions.\n\nBetween 10 and 20 percent of women with severe preeclampsia develop another potentially life-threatening complication called HELLP syndrome. HELLP stands for hemolysis (premature red blood cell breakdown), elevated liver enzyme levels, and low platelets (cells involved in blood clotting), which are the key features of this condition.\n\nSevere preeclampsia can also affect the fetus, with impairment of blood and oxygen flow leading to growth problems or stillbirth. Infants delivered early due to preeclampsia may have complications associated with prematurity, such as breathing problems caused by underdeveloped lungs.  https://medlineplus.gov/genetics/condition/preeclampsia

Clinical features

From HPO
Proteinuria
MedGen UID:
10976
Concept ID:
C0033687
Finding
Increased levels of protein in the urine.
Hypertensive disorder
MedGen UID:
6969
Concept ID:
C0020538
Disease or Syndrome
The presence of chronic increased pressure in the systemic arterial system.
Intrauterine growth retardation
MedGen UID:
473406
Concept ID:
C1386048
Pathologic Function
Seizures
MedGen UID:
20693
Concept ID:
C0036572
Sign or Symptom
A seizure is an intermittent abnormality of nervous system physiology characterised by a transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain.
Thrombocytopenia
MedGen UID:
52737
Concept ID:
C0040034
Disease or Syndrome
A reduction in the number of circulating thrombocytes.
Edema
MedGen UID:
4451
Concept ID:
C0013604
Pathologic Function
An abnormal accumulation of fluid beneath the skin, or in one or more cavities of the body.
Proteinuria
MedGen UID:
10976
Concept ID:
C0033687
Finding
Increased levels of protein in the urine.
Elevated hepatic transaminase
MedGen UID:
338525
Concept ID:
C1848701
Finding
Elevations of the levels of SGOT and SGPT in the serum. SGOT (serum glutamic oxaloacetic transaminase) and SGPT (serum glutamic pyruvic transaminase) are transaminases primarily found in the liver and heart and are released into the bloodstream as the result of liver or heart damage. SGOT and SGPT are used clinically mainly as markers of liver damage.
Eclampsia
MedGen UID:
4443
Concept ID:
C0013537
Disease or Syndrome
An acute and life-threatening complication of pregnancy, which is characterized by the appearance of tonic-clonic seizures, usually in a patient who had developed pre-eclampsia. Eclampsia includes seizures and coma that happen during pregnancy but are not due to preexisting or organic brain disorders.
Preeclampsia
MedGen UID:
18608
Concept ID:
C0032914
Pathologic Function
Preeclampsia, which along with chronic hypertension and gestational hypertension comprise the hypertensive disorders of pregnancy, is characterized by new hypertension (blood pressure 140/90 or greater) presenting after 20 weeks' gestation with clinically relevant proteinuria. Preeclampsia is 1 of the top 4 causes of maternal mortality and morbidity worldwide (summary by Payne et al., 2011). Preeclampsia is otherwise known as gestational proteinuric hypertension (Davey and MacGillivray, 1988). A high proportion of patients with preeclampsia have glomerular endotheliosis, the unique histopathologic feature of the condition (Fisher et al., 1981). A distinct form of severe preeclampsia is characterized by hemolysis, elevated liver enzymes, and low platelets (HELLP syndrome) (Brown et al., 2000). Genetic Heterogeneity of Preeclampsia/Eclampsia Susceptibility loci for preeclampsia/eclampsia include PEE1 on chromosome 2p13, PEE2 (609402) on chromosome 2p25, and PEE3 (609403) on chromosome 9p13. PEE4 (609404) is caused by mutation in the STOX1 gene (609397) on chromosome 10q22. PEE5 (614595) is caused by mutation in the CORIN gene (605236) on chromosome 4p12. An association with PEE has been found with the EPHX1 gene (132810) on chromosome 1q.
Maternal hypertension
MedGen UID:
107882
Concept ID:
C0565599
Disease or Syndrome
Increased blood pressure during a pregnancy.

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVPreeclampsia
Follow this link to review classifications for Preeclampsia in Orphanet.

Conditions with this feature

Preeclampsia
MedGen UID:
18608
Concept ID:
C0032914
Pathologic Function
Preeclampsia, which along with chronic hypertension and gestational hypertension comprise the hypertensive disorders of pregnancy, is characterized by new hypertension (blood pressure 140/90 or greater) presenting after 20 weeks' gestation with clinically relevant proteinuria. Preeclampsia is 1 of the top 4 causes of maternal mortality and morbidity worldwide (summary by Payne et al., 2011). Preeclampsia is otherwise known as gestational proteinuric hypertension (Davey and MacGillivray, 1988). A high proportion of patients with preeclampsia have glomerular endotheliosis, the unique histopathologic feature of the condition (Fisher et al., 1981). A distinct form of severe preeclampsia is characterized by hemolysis, elevated liver enzymes, and low platelets (HELLP syndrome) (Brown et al., 2000). Genetic Heterogeneity of Preeclampsia/Eclampsia Susceptibility loci for preeclampsia/eclampsia include PEE1 on chromosome 2p13, PEE2 (609402) on chromosome 2p25, and PEE3 (609403) on chromosome 9p13. PEE4 (609404) is caused by mutation in the STOX1 gene (609397) on chromosome 10q22. PEE5 (614595) is caused by mutation in the CORIN gene (605236) on chromosome 4p12. An association with PEE has been found with the EPHX1 gene (132810) on chromosome 1q.
Familial partial lipodystrophy 3
MedGen UID:
328393
Concept ID:
C1720861
Disease or Syndrome
Researchers have described at least six forms of familial partial lipodystrophy, which are distinguished by their genetic cause. The most common form of familial partial lipodystrophy is type 2, also called Dunnigan disease. In addition to the signs and symptoms described above, some people with this type of the disorder develop muscle weakness (myopathy), abnormalities of the heart muscle (cardiomyopathy), a form of heart disease called coronary artery disease, and problems with the electrical system that coordinates the heartbeat (the conduction system).\n\nMost people with familial partial lipodystrophy also have high levels of fats called triglycerides circulating in the bloodstream (hypertriglyceridemia), which can lead to inflammation of the pancreas (pancreatitis). Familial partial lipodystrophy can also cause an abnormal buildup of fats in the liver (hepatic steatosis), which can result in an enlarged liver (hepatomegaly) and abnormal liver function. After puberty, some affected females develop multiple cysts on the ovaries, an increased amount of body hair (hirsutism), and an inability to conceive (infertility), which are likely related to hormonal changes.\n\nAbnormal storage of fat in the body can lead to health problems in adulthood. Many people with familial partial lipodystrophy develop insulin resistance, a condition in which the body's tissues cannot adequately respond to insulin, which is a hormone that normally helps to regulate blood sugar levels. Insulin resistance may worsen to become a more serious disease called diabetes mellitus. Some people with familial partial lipodystrophy develop acanthosis nigricans, a skin condition related to high levels of insulin in the bloodstream. Acanthosis nigricans causes the skin in body folds and creases to become thick, dark, and velvety.\n\nFamilial partial lipodystrophy is a rare condition characterized by an abnormal distribution of fatty (adipose) tissue. Adipose tissue is normally found in many parts of the body, including beneath the skin and surrounding the internal organs. It stores fat as a source of energy and also provides cushioning. In people with familial partial lipodystrophy, adipose tissue is lost from the arms, legs, and hips, giving these parts of the body a very muscular appearance. The fat that cannot be stored in the limbs builds up around the face and neck, and inside the abdomen. Excess fat in these areas gives individuals an appearance described as "cushingoid," because it resembles the physical features associated with a hormonal disorder called Cushing disease. This abnormal fat distribution can begin anytime from childhood to adulthood.
Preeclampsia/eclampsia 4
MedGen UID:
322874
Concept ID:
C1836255
Disease or Syndrome
Any preeclampsia in which the cause of the disease is a mutation in the STOX1 gene.
Thrombophilia due to factor V Leiden
MedGen UID:
396074
Concept ID:
C1861171
Disease or Syndrome
Factor V Leiden thrombophilia is characterized by a poor anticoagulant response to activated protein C (APC) and an increased risk for venous thromboembolism (VTE). Deep vein thrombosis (DVT) is the most common VTE, with the legs being the most common site. Thrombosis in unusual locations is less common. Evidence suggests that heterozygosity for the Leiden variant has at most a modest effect on risk for recurrent thrombosis after initial treatment of a first VTE. It is unlikely that factor V Leiden thrombophilia (i.e., heterozygosity or homozygosity for the Leiden variant) is a major factor contributing to pregnancy loss and other adverse pregnancy outcomes (preeclampsia, fetal growth restriction, and placental abruption). The clinical expression of factor V Leiden thrombophilia is influenced by the following: The number of Leiden variants (heterozygotes have a slightly increased risk for venous thrombosis; homozygotes have a much greater thrombotic risk). Coexisting genetic thrombophilic disorders, which have a supra-additive effect on overall thrombotic risk. Acquired thrombophilic disorders: antiphospholipid antibody (APLA) syndrome, paroxysmal nocturnal hemoglobinuria, myeloproliferative disorders, and increased levels of clotting factors. Circumstantial risk factors including but not limited to pregnancy, central venous catheters, travel, combined oral contraceptive (COC) use and other combined contraceptives, oral hormone replacement therapy (HRT), selective estrogen receptor modulators (SERMs), obesity, leg injury, and advancing age.
Rubinstein-Taybi syndrome 2
MedGen UID:
462291
Concept ID:
C3150941
Disease or Syndrome
Rubinstein-Taybi syndrome (RSTS) is characterized by distinctive facial features, broad and often angulated thumbs and halluces, short stature, and moderate-to-severe intellectual disability. The characteristic craniofacial features are downslanted palpebral fissures, low-hanging columella, high palate, grimacing smile, and talon cusps. Prenatal growth is often normal, then height, weight, and head circumference percentiles rapidly drop in the first few months of life. Short stature is typical in adulthood. Obesity may develop in childhood or adolescence. Average IQ ranges between 35 and 50; however, developmental outcome varies considerably. Some individuals with EP300-RSTS have normal intellect. Additional features include ocular abnormalities, hearing loss, respiratory difficulties, congenital heart defects, renal abnormalities, cryptorchidism, feeding problems, recurrent infections, and severe constipation.
Preeclampsia/eclampsia 5
MedGen UID:
482918
Concept ID:
C3281288
Disease or Syndrome
Preeclampsia, which along with chronic hypertension and gestational hypertension comprise the hypertensive disorders of pregnancy, is characterized by new hypertension (blood pressure 140/90 or greater) presenting after 20 weeks' gestation with clinically relevant proteinuria. Preeclampsia is 1 of the top 4 causes of maternal mortality and morbidity worldwide (summary by Payne et al., 2011). For a general phenotypic description and a discussion of genetic heterogeneity of preeclampsia/eclampsia, see PEE1 (189800).
Lethal congenital contracture syndrome 9
MedGen UID:
903881
Concept ID:
C4225303
Disease or Syndrome
Any lethal congenital contracture syndrome in which the cause of the disease is a mutation in the ADGRG6 gene.
Neurodevelopmental disorder with seizures and speech and walking impairment
MedGen UID:
1672912
Concept ID:
C5193119
Disease or Syndrome
Neurodevelopmental disorder with seizures and speech and walking impairment (NEDSSWI) is an autosomal recessive disorder with onset in infancy. Patients show global developmental delay, particularly of speech acquisition, as well as walking difficulties due to hypotonia, hypertonia, spasticity, or poor coordination. Other features include seizures, mild dysmorphic features, and variable short stature. The pregnancies tend to be complicated by hyper- or hypotension (summary by Ganapathi et al., 2019).

Recent clinical studies

Etiology

Mai H, Liang Z, Chen Z, Liu Z, Xu Y, Chen X, Du X, Peng Y, Chen Y, Dong T
BMC Pregnancy Childbirth 2021 Oct 3;21(1):669. doi: 10.1186/s12884-021-04145-1. PMID: 34602066Free PMC Article
Holmquist E, Brantsæter AL, Meltzer HM, Jacobsson B, Barman M, Sengpiel V
Sci Total Environ 2021 Dec 1;798:149271. Epub 2021 Jul 27 doi: 10.1016/j.scitotenv.2021.149271. PMID: 34333435
Lisonkova S, Bone JN, Muraca GM, Razaz N, Wang LQ, Sabr Y, Boutin A, Mayer C, Joseph KS
Am J Obstet Gynecol 2021 Nov;225(5):538.e1-538.e19. Epub 2021 May 8 doi: 10.1016/j.ajog.2021.04.261. PMID: 33974902
Seely EW, Celi AC, Chausmer J, Graves C, Kilpatrick S, Nicklas JM, Rosser ML, Rexrode KM, Stuart JJ, Tsigas E, Voelker J, Zelop C, Rich-Edwards JW
J Womens Health (Larchmt) 2021 Mar;30(3):305-313. Epub 2020 Sep 28 doi: 10.1089/jwh.2020.8384. PMID: 32986503Free PMC Article
Abbasi R, Bakhshimoghaddam F, Alizadeh M
J Matern Fetal Neonatal Med 2021 Nov;34(21):3529-3536. Epub 2019 Nov 17 doi: 10.1080/14767058.2019.1686474. PMID: 31736380

Diagnosis

Mai H, Liang Z, Chen Z, Liu Z, Xu Y, Chen X, Du X, Peng Y, Chen Y, Dong T
BMC Pregnancy Childbirth 2021 Oct 3;21(1):669. doi: 10.1186/s12884-021-04145-1. PMID: 34602066Free PMC Article
Papageorghiou AT, Deruelle P, Gunier RB, Rauch S, García-May PK, Mhatre M, Usman MA, Abd-Elsalam S, Etuk S, Simmons LE, Napolitano R, Deantoni S, Liu B, Prefumo F, Savasi V, do Vale MS, Baafi E, Zainab G, Nieto R, Maiz N, Aminu MB, Cardona-Perez JA, Craik R, Winsey A, Tavchioska G, Bako B, Oros D, Rego A, Benski AC, Hassan-Hanga F, Savorani M, Giuliani F, Sentilhes L, Risso M, Takahashi K, Vecchiarelli C, Ikenoue S, Thiruvengadam R, Soto Conti CP, Ferrazzi E, Cetin I, Nachinab VB, Ernawati E, Duro EA, Kholin A, Firlit ML, Easter SR, Sichitiu J, Bowale A, Casale R, Cerbo RM, Cavoretto PI, Eskenazi B, Thornton JG, Bhutta ZA, Kennedy SH, Villar J
Am J Obstet Gynecol 2021 Sep;225(3):289.e1-289.e17. Epub 2021 Jun 26 doi: 10.1016/j.ajog.2021.05.014. PMID: 34187688Free PMC Article
Shinar S, Melamed N, Abdulaziz KE, Ray JG, Riddell C, Barrett J, Murray-Davis B, Mawjee K, McDonald SD, Geary M, Berger H; for DOH-NET (Diabetes, Obesity, Hypertension in Pregnancy Research Network), SOON (Southern Ontario Obstetrical Network) InvestigatorsTM.
Acta Obstet Gynecol Scand 2021 Sep;100(9):1627-1635. Epub 2021 Jul 9 doi: 10.1111/aogs.14199. PMID: 34043808
Tzur Y, Rimon E, Geva G, Herzlich J, Kupferminc MJ
Acta Obstet Gynecol Scand 2021 Sep;100(9):1620-1626. Epub 2021 Jun 19 doi: 10.1111/aogs.14198. PMID: 34043807
Wang M, Chen S, He Y, Zhao M, Yang H, Chen Q
J Nephrol 2021 Oct;34(5):1631-1639. Epub 2021 Apr 29 doi: 10.1007/s40620-021-01049-3. PMID: 33914255

Therapy

Walsh SW, Strauss JF 3rd
Int J Mol Sci 2021 Jun 29;22(13) doi: 10.3390/ijms22136985. PMID: 34209594Free PMC Article
Ji X, Li C, Lv Y, Miao Z, Wu L, Long W, Wang X, Ding H
Am J Hypertens 2021 Oct 27;34(10):1116-1124. doi: 10.1093/ajh/hpab086. PMID: 34037692
Wang M, Chen S, He Y, Zhao M, Yang H, Chen Q
J Nephrol 2021 Oct;34(5):1631-1639. Epub 2021 Apr 29 doi: 10.1007/s40620-021-01049-3. PMID: 33914255
Peguero A, Herraiz I, Perales A, Melchor JC, Melchor I, Marcos B, Villalain C, Martinez-Portilla R, Mazarico E, Meler E, Hernandez S, Matas I, Del Rio M, Galindo A, Figueras F
Am J Obstet Gynecol 2021 Sep;225(3):308.e1-308.e14. Epub 2021 Apr 3 doi: 10.1016/j.ajog.2021.03.044. PMID: 33823150
Chatzakis C, Liberis A, Zavlanos A, Petousis S, Tsakmaki E, Dinas K, Sotiriadis A
Acta Obstet Gynecol Scand 2021 Aug;100(8):1392-1400. Epub 2021 Apr 13 doi: 10.1111/aogs.14149. PMID: 33742472

Prognosis

Mai H, Liang Z, Chen Z, Liu Z, Xu Y, Chen X, Du X, Peng Y, Chen Y, Dong T
BMC Pregnancy Childbirth 2021 Oct 3;21(1):669. doi: 10.1186/s12884-021-04145-1. PMID: 34602066Free PMC Article
Lisonkova S, Bone JN, Muraca GM, Razaz N, Wang LQ, Sabr Y, Boutin A, Mayer C, Joseph KS
Am J Obstet Gynecol 2021 Nov;225(5):538.e1-538.e19. Epub 2021 May 8 doi: 10.1016/j.ajog.2021.04.261. PMID: 33974902
Simard JF, Rossides M, Wikström AK, Falasinnu T, Palmsten K, Arkema EV
Paediatr Perinat Epidemiol 2021 Sep;35(5):596-600. Epub 2021 May 6 doi: 10.1111/ppe.12759. PMID: 33956365
Peguero A, Herraiz I, Perales A, Melchor JC, Melchor I, Marcos B, Villalain C, Martinez-Portilla R, Mazarico E, Meler E, Hernandez S, Matas I, Del Rio M, Galindo A, Figueras F
Am J Obstet Gynecol 2021 Sep;225(3):308.e1-308.e14. Epub 2021 Apr 3 doi: 10.1016/j.ajog.2021.03.044. PMID: 33823150
Seely EW, Celi AC, Chausmer J, Graves C, Kilpatrick S, Nicklas JM, Rosser ML, Rexrode KM, Stuart JJ, Tsigas E, Voelker J, Zelop C, Rich-Edwards JW
J Womens Health (Larchmt) 2021 Mar;30(3):305-313. Epub 2020 Sep 28 doi: 10.1089/jwh.2020.8384. PMID: 32986503Free PMC Article

Clinical prediction guides

Mai H, Liang Z, Chen Z, Liu Z, Xu Y, Chen X, Du X, Peng Y, Chen Y, Dong T
BMC Pregnancy Childbirth 2021 Oct 3;21(1):669. doi: 10.1186/s12884-021-04145-1. PMID: 34602066Free PMC Article
Papageorghiou AT, Deruelle P, Gunier RB, Rauch S, García-May PK, Mhatre M, Usman MA, Abd-Elsalam S, Etuk S, Simmons LE, Napolitano R, Deantoni S, Liu B, Prefumo F, Savasi V, do Vale MS, Baafi E, Zainab G, Nieto R, Maiz N, Aminu MB, Cardona-Perez JA, Craik R, Winsey A, Tavchioska G, Bako B, Oros D, Rego A, Benski AC, Hassan-Hanga F, Savorani M, Giuliani F, Sentilhes L, Risso M, Takahashi K, Vecchiarelli C, Ikenoue S, Thiruvengadam R, Soto Conti CP, Ferrazzi E, Cetin I, Nachinab VB, Ernawati E, Duro EA, Kholin A, Firlit ML, Easter SR, Sichitiu J, Bowale A, Casale R, Cerbo RM, Cavoretto PI, Eskenazi B, Thornton JG, Bhutta ZA, Kennedy SH, Villar J
Am J Obstet Gynecol 2021 Sep;225(3):289.e1-289.e17. Epub 2021 Jun 26 doi: 10.1016/j.ajog.2021.05.014. PMID: 34187688Free PMC Article
Wang M, Chen S, He Y, Zhao M, Yang H, Chen Q
J Nephrol 2021 Oct;34(5):1631-1639. Epub 2021 Apr 29 doi: 10.1007/s40620-021-01049-3. PMID: 33914255
Seely EW, Celi AC, Chausmer J, Graves C, Kilpatrick S, Nicklas JM, Rosser ML, Rexrode KM, Stuart JJ, Tsigas E, Voelker J, Zelop C, Rich-Edwards JW
J Womens Health (Larchmt) 2021 Mar;30(3):305-313. Epub 2020 Sep 28 doi: 10.1089/jwh.2020.8384. PMID: 32986503Free PMC Article
Abbasi R, Bakhshimoghaddam F, Alizadeh M
J Matern Fetal Neonatal Med 2021 Nov;34(21):3529-3536. Epub 2019 Nov 17 doi: 10.1080/14767058.2019.1686474. PMID: 31736380

Recent systematic reviews

Chatzakis C, Liberis A, Zavlanos A, Petousis S, Tsakmaki E, Dinas K, Sotiriadis A
Acta Obstet Gynecol Scand 2021 Aug;100(8):1392-1400. Epub 2021 Apr 13 doi: 10.1111/aogs.14149. PMID: 33742472
Margioula-Siarkou G, Margioula-Siarkou C, Petousis S, Margaritis K, Alexandratou M, Dinas K, Sotiriadis A, Mavromatidis G
Eur J Obstet Gynecol Reprod Biol 2021 Mar;258:366-381. Epub 2021 Jan 26 doi: 10.1016/j.ejogrb.2021.01.039. PMID: 33529972
Hounkpatin OI, Amidou SA, Houehanou YC, Lacroix P, Preux PM, Houinato DS, Bezanahary H
BMC Pregnancy Childbirth 2021 Jan 30;21(1):97. doi: 10.1186/s12884-021-03566-2. PMID: 33516185Free PMC Article
Vahedian-Azimi A, Karimi L, Reiner Ž, Makvandi S, Sahebkar A
Pregnancy Hypertens 2021 Mar;23:123-130. Epub 2020 Dec 11 doi: 10.1016/j.preghy.2020.11.014. PMID: 33333432
Kay VR, Wedel N, Smith GN
J Obstet Gynaecol Can 2021 Feb;43(2):227-236.e19. Epub 2020 Aug 25 doi: 10.1016/j.jogc.2020.08.010. PMID: 33268309

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