European Journal of Obstetrics and Gynecology 283 (2023) 37–42

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European Journal of Obstetrics & Gynecology and

Reproductive Biology
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Full length article

Pravastatin for severe preeclampsia with growth restriction: Placental

findings and infant follow-up
Stefano Fruci a, Silvia Salvi a, *, Sascia Moresi a, Francesca Gallini b, c, Marco Dell’Aquila d,
Vincenzo Arena e, Enrico Di Stasio c, f, Sergio Ferrazzani a, c, Sara De Carolis a, c, 1,
Antonio Lanzone a, 1
a
UOC di Patologia Ostetrica, Dipartimento Scienze della Salute della Donna, del Bambino e di Sanità Pubblica, Fondazione Policlinico Universitario A. Gemelli IRCCS,
Largo Agostino Gemelli 8, 00168 Rome, Italy
b
UOC di Neonatologia, Dipartimento Scienze della Salute della Donna, del Bambino e di Sanità Pubblica, Fondazione Policlinico Universitario A. Gemelli IRCCS, Largo
Agostino Gemelli 8, 00168 Rome, Italy
c
Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 00168 Rome, Italy
d
Area of Pathology, Dipartimento Scienze della Salute della Donna, del Bambino e di Sanità Pubblica, Fondazione Policlinico Universitario ’A. Gemelli’ IRCCS, Largo
Agostino Gemelli 8, 00168 Rome, Italy
e
Area of Pathology and UOS Coordinamento attività di settorato, Dipartimento Scienze della Salute della Donna, del Bambino e di Sanità Pubblica, Fondazione
Policlinico Universitario A. Gemelli IRCCS, Largo Agostino Gemelli 8, 00168 Rome, Italy
f
Dipartimento di scienze laboratoristiche ed infettivologiche, UOC Chimica, Biochimica e Biologia Molecolare Clinica, Fondazione Policlinico Universitario A. Gemelli
IRCCS, Largo Agostino Gemelli 8, 00168 Rome, Italy

A R T I C L E I N F O A B S T R A C T

Keywords: Objective: Preeclampsia (PE) is the major cause of maternal morbidity and mortality and the leading cause of
Preeclampsia premature delivery worldwide. As well as intrauterine growth restriction (IUGR), PE is associated with patho­
Intrauterine growth restriction genic evidence of placental malperfusion and ischemia. Recent literature has highlighted the potential of pra­
Pravastatin
vastatin in the prevention and treatment of these conditions. Aim of this study is to describe perinatal outcomes
Placenta
and placental histopathological findings in a small series of pregnant women with severe PE and IUGR treated
Preterm delivery
with pravastatin on compassionate grounds. Two-year follow up of these babies is provided.
Study design: Between October 2017 and October 2019 in Fondazione Policlinico Universitario Agostino Gemelli,
IRCCS, Rome, Italy, women with singleton pregnancy between 19.6 and 27.6 gestational weeks, who presented
with severe PE and IUGR were counselled for a compassionate treatment with Pravastatin 40 mg a day. Treated
women were compared with controls identified with similar data in terms of gestational age at diagnosis, clinical
maternal data, Doppler severity findings. Neonates were followed up for two years.
Results: The median time from diagnosis to delivery was 39 days (IQR 20) for women in the pravastatin group
and 20 days (IQR 20.5) for controls. Looking to maternal blood exams, in the group of women treated with
pravastatin, maximum transaminase, creatinine levels were lower than in controls, where the minimum platelet
count was higher. Placenta examination did not reveal any significant differences in placental histopathological
findings. No significant differences were observed in the investigated perinatal data, as well as in infant follow-
up, although an increased prenatal weight gain was found in treated pregnancies in comparison to controls.
Conclusions: Our data did not allow us to find significant differences in pregnancy outcome and infant follow-up,
as well as in placental histological picture in preeclamptic patients when pravastatin is administered in the late
second trimester. However, we suggest its possible role in stabilizing the disease, increasing the prenatal weight
gain and prolonging the duration of pregnancy, thus preventing the progression to a more severe maternal
disease.

* Corresponding author.
E-mail addresses: [email protected], [email protected] (S. Salvi), [email protected] (S. De Carolis), [email protected]
(A. Lanzone).
1
Senior co-authors.

https://doi.org/10.1016/j.ejogrb.2023.01.036
Received 10 September 2021; Received in revised form 18 January 2023; Accepted 30 January 2023
Available online 1 February 2023
0301-2115/© 2023 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
S. Fruci et al. European Journal of Obstetrics & Gynecology and Reproductive Biology 283 (2023) 37–42

Introduction gestational age at diagnosis, maternal clinical data, fetal ultrasound, and
Doppler findings but they did not receive treatment with pravastatin.
Preeclampsia (PE) is the major cause of maternal and fetal death and Women who had clinical criteria for immediate delivery were not
the leading cause of premature delivery worldwide. Even today, the considered. According to the hospital protocols, women in both groups
definitive therapy remains the delivery with the removal of the placenta received antenatal steroids and magnesium sulfate for neuroprotection
and although delivery is always beneficial for the mother, it may not be before delivery. Maternal and feto-neonatal informations were extracted
optimal for the fetus, as it might be extremely premature. It occurs in 2 from the hospital electronic medical records. Maternal age, BMI (body
% to 8 % of pregnancies worldwide [1] and is defined as a syndrome mass index), parity, mode of conception, past medical and obstetric
since it is a multisystemic disorder. Preeclampsia is thought to be due to history were collected. Gestational age was established by ultrasound
placental malperfusion resulting from abnormal remodeling of maternal dating by crown rump length prior to 14 weeks of gestation. The esti­
spiral arteries that leads to placental dysfunction and endothelial injury mated fetal weight (EFW) was calculated using Hadlock IV Model [21],
that eventually manifest as maternal hypertension and end-organ injury while Arduini D. and Rizzo G. reference values were used for fetal
[2]. Not only preeclampsia (PE) but also intrauterine growth restriction Doppler evaluation [22]. The EFW percentile were calculated according
(IUGR), defined, as the failure of the fetus to reach its genetically to Intergrowth-21st [23]. The UA PI was examined using Color Doppler
determined growth potential, is associated with pathogenic evidence of in free loops of the umbilical cord and calculated according to a standard
placental malperfusion and ischemia. In both these cases, abnormal protocol, which is in keeping with current International Doppler
angiogenesis in the placenta determines impaired remodeling of the guidelines. The UA PI was considered abnormal when > 95th percentile.
maternal spiral arteries and placental malperfusion that may ultimately Uterine arteries were considered abnormal when the mean PI was >
lead to fetal growth restriction and maternal PE. 95th percentile. Cerebral redistribution was defined when the mean
There is a dearth of drugs to treat the pathophysiological progression cerebral artery pulsatility index < 5th percentile for gestational age
of PE. Only one drug, aspirin, clearly prevents this condition [3], and [24].
none has conclusively shown to improve the disease. Pravastatin is a Perinatal variables analyzed were birthweight, birthweight percen­
lipid-lowering drug widely taken to reduce the risk of cardiovascular tile, neonatal gender, Apgar score at 1st and at 5th minute <7, admission
events [4]. In the last years, in vitro and animal studies, case reports and to neonatal intensive care unit (NICU), deaths, developmental delay and
some clinical trials have highlighted the potential of pravastatin in the lost to follow up. Birthweight percentile was calculated according to a
prevention and treatment of PE [5–14]. Furthermore, some studies national standard curve [25]. Placental weight was measured, and
carried out on mouse models of PE have shown that pravastatin treat­ placental weight percentile calculated according to Almog et al. [26]
ment ameliorated the remodeling of maternal heart and improved Infants born to mothers of both groups were followed up for two years.
maternal cardiac output in the postpartum period [15,16]. It is note that
PE is a risk factor for future cardiovascular disease (CVD) and signifi­ Placental examination
cantly exceeds traditional risk factors when its onset is pre-term or when
it recurs in multiple pregnancies, conferring an eight to ninefold The placentas were sent to the Pathology laboratory for histopath­
increased risk of CVD [16–18]. Then PE induces irreversible structural ological examination. Specimens were fixed in 10 % buffered formalin.
changes of cardiac muscles and fibrosis, which can be moderated by The macroscopical examination and the resulting grossing of the pla­
pravastatin treatment [15,16]. This pathological cardiac remodeling centas was performed according to an internal protocol in adherence to
might be involved in increased cardiovascular risk later in life [16–18]. the Amsterdam placental workshop group consensus statement [27]. It
The aim of this study is to describe perinatal and infant outcomes and included an extensive sampling that comprised at least two sections of
placental histopathological findings in a series of pregnant women with the umbilical cord and of the membranes, and up to six full thickness
severe PE and IUGR treated with pravastatin on compassionate grounds; sections of the placental disk. Fetal and maternal surfaces of the
controls compared to treated women were identified according to placental disk were cut into slices of about one cm of thickness to better
gestational age at diagnosis, maternal clinical data at admission, fetal detect macroscopic lesions. Afterwards sections were formalin fixed,
ultrasound, and Doppler findings. Primary endpoint of this report is to paraffin embedded (FFPE), and subsequently stained with Hematoxylin
compare maternal and feto-neonatal outcomes in treated and untreated and Eosin (H&E). Histopathological findings were classified as fetal,
women; moreover, placental histopathologic findings and infant follow- maternal, or inflammatory, coherently with their origin [28–30]. Two
up in the two groups were described. expert pathologists made the histopathological examination of the pla­
centas in blind.
Materials and methods
Results
Study population, setting and data collection
Maternal clinical data
Between October 2017 and October 2019 in Fondazione Policlinico
Universitario Agostino Gemelli, IRCCS, Rome, Italy, women with Twelve women with severe PE and IUGR between October 2017 and
singleton gestation between 19.6 and 27.6 weeks of pregnancy who October 2019 were included. Clinical characteristics of both groups are
presented with severe preeclampsia and IUGR were counselled for a shown in Table 1. No woman had previous history of PE. Looking to
compassionate treatment with Pravastatin 40 mg a day. This treatment maternal blood exams, in the group of women treated with pravastatin,
was allowed as compassionate use on the ground of the favorable maximum transaminase, creatinine levels were lower than in controls,
opinion of the Ethics Committee of Università Cattolica del Sacro Cuore, where the minimum platelet count was higher. There were no maternal
Roma, Italy. Severe PE was defined according to the International So­ deaths.
ciety for the Study of Hypertension in Pregnancy (ISSHP) Guidelines
[19]. IUGR was defined as a fetus with estimated weight or abdominal Ultrasound findings
circumference < 3rd percentile for gestational age or with estimated
weight or abdominal circumference < 10th percentile with abnormal We found no differences between the two groups in the ultrasound
umbilical artery pulsatility index (UA PI) > 95th percentile [20]. Six evaluation performed at diagnosis (Table 1). In pravastatin group, at
patients received oral therapy with pravastatin 40 mg daily after diagnosis, AEDV (absent end diastolic velocity) was present in 66 % of
obtaining informed consent upon admission to hospital; six patients fetuses and cerebral redistribution was present in one. In non-treated
were identified as controls in the same period, since they showed similar group, AEDV was present in 40 % of fetuses whereas cerebral

38
S. Fruci et al. European Journal of Obstetrics & Gynecology and Reproductive Biology 283 (2023) 37–42

Table 1 No significant differences were found between the two groups. Two
Clinical features on admission with Pre-eclampsia. infants, one in each group, showed a language delay. All infants assessed
Maternal Clinical Data Pravastatin (n◦ No treatment at two years showed an adequate growth.
6) (n◦ 6)

Age, years (mean ± SD) 34.5 ± 6.9 40.7 ± 5.8 Discussion

Parity > 1 (n,%) 0/6 (0%) 3/6 (50%)
Pre-pregnancy BMI (kg/m2) (mean ± SD) 25.4 ± 4.3 24.7 ± 4.5 Clinical use of statins for the prevention and treatment of PE and/or
Spontaneous conception (n,%) 3/6 (50%) 4/6 (67%)
IUGR is justified by multiple preclinical studies. Studies conducted in
Pre-existing maternal disease (n,%):
Congenital heart disease 0/6 (0%) 1/6 (17%)
vitro have demonstrated the ability of this molecule to reduce sFlt1
Chronic hypertension 2/6 (33%) 0/6 (0%) secretion by human umbilical venous endothelial cells, trophoblast cells
Prepregnancy diabetes 0/6 (0%) 0/6 (0%) and placenta explants taken from women with PE; moreover, statins
Insulin resistance 1/6 (17%) 1/6 (17%) have been shown to reduce oxidative stress by activating the heme-
Thyroiditis 0/6 (0%) 2/6 (33%)
oxygenase 1 enzyme [31]. Furthermore, studies on mouse models of
Microcythemia 1/6 (17%) 2/6 (33%)
Congenital Thrombofilia (n,%) 0/6 (0%) 1/6 (17%) PE have shown that pravastatin is able not only to reduce the secretion
Acquired Thrombofilia (n,%) 2/6 (33%) 0/6 (0%) of sFlt1, but also to increase the secretion of Placental Growth Factor
Gestational Age on admission (weeks) 23.6 (3.3) 24.6 (1.1) (PlGF) improving the clinical phenotype of the disease [7,32]. Although
(median, IQR)
statins are contraindicated in pregnancy (category X according to the
Max Creatinine, mg/dl (mean ± SD) 0.8 ± 0.2 1.0 ± 0.5
Min Platelet count (mean ± SD) 171,000 ± 113,670 ±
Food and Drug Administration), epidemiological data collected to date
58,680 73,030 suggest that statins are not major teratogenic agents; among these, those
Max GPT, UI/L (mean ± SD) 27.3 ± 15.6 245.17 ± with the best pharmacokinetic and safety profile are hydrophilic statins
116.88 such as pravastatin [33–39].
Max LDH, mg/dl (mean ± SD) 256.3 ± 144.3 756.6 ± 714.9
In the crucial axis represented by the mother, the placenta, and the
Max Uric Acid, mg/dl (mean ± SD) 5.9 ± 2.1 7.8 ± 2.6
Abnormal 2nd Trimester Uterine arteries 4/6 (67%) 4/6 (67%) fetus of all these severe and extremely premature cases of PE and IUGR,
Doppler the compassionate treatment with Pravastatin seems to act on each
EFW, grams (median, IQR) 431.0 (238.0) 510.5 (298.5) component in a different way. From the maternal point of view, our
EFW percentile at admission (median, 0 (0.0–0.0) 0.75 (0.0–4.6)
clinical data confirm what was already been observed. In our study, we
minimum and maximum values)
UA PI at admission (median, IQR) 1.6 (0.3) 1.5 (0.4)
compared two groups similar for maternal clinical characteristics,
MCA PI at admission (median, IQR) 1.6 (0.2) 1.81 (0.4) severity of disease and gestational age at diagnosis. As shown in Table 1,
patients receiving pravastatin 40 mg daily showed less severe liver,
BMI: Body mass index; GPT: glutamic pyruvic transaminase; LDH: lactic dehy­
kidney and hematological compromise as established by lower trans­
drogenase; SD: standard deviation; EFW: estimated fetal weight; UA: Umbilical
Artery; MCA: Middle Cerebral Artery; PI: pulsatility index; IQR: interquartile aminase and creatinine values, but higher platelet count. The ability to
range. ameliorate the maternal profile is one of the reasons explaining the
increased median time from diagnosis to delivery, even if this difference
(two weeks) is not statistically significant. Lefkou et al. [40], in a study
redistribution was not found in any of these fetuses.
on 21 patients with obstetric APS refractory to antithrombotic therapy,
showed that in the 11 patients treated with pravastatin there was an
Placental histopathological findings evident improvement in both blood pressure and proteinuria. Moreover,
these patients all gave birth almost at term, with significant prolonga­
The placentas of both groups were evaluated according to the tion of pregnancy and no fetal loss or neonatal death.
Amsterdam criteria for the detection of FVM (fetal vascular malperfu­ Regarding fetal and neonatal outcomes, as mentioned above, the
sion) and MVM (maternal vascular malperfusion). No differences were severity of fetal compromise at diagnosis was similar in our two groups;
highlighted between the two groups, neither as regards the weight of the the prenatal weight gain was of 79.8 % in treated pregnancies and 15.1
placentas nor as regards the anatomopathological lesions investigated. % in controls. However, neonatal variables at birth, perinatal and two-
year follow-up outcome were similar. In the group of patients treated
Perinatal data and infant outcome with pravastatin there were two neonatal deaths as well as in the control
group. Therefore, if administered in the late second trimester, pravas­
The median interval time from diagnosis to delivery was 39 days tatin seems not able to interfere or reverse the fetal condition due to the
(IQR 20.0) for women in the pravastatin group and 20 days (IQR 20.5) already established placental dysfunction. Our data are in accordance
for the control group. The prenatal weight gain was of 79.8 % in treated with the recently published literature on this topic. Mendoza M et al
pregnancies and 15.1 % in controls. Perinatal data are shown in Table 2. [13] found that treatment with pravastatin 40 mg daily in women with
early-onset IUGR was associated with ameliorated maternal angiogenic
Table 2 profile; moreover, increased median pregnancy duration and reduced
Perinatal outcome and infant follow-up data. incidence of PE was also detected, although none of these differences
Perinatal Data Pravastatin (n◦ No treatment
were statistically significant. Furthermore, no significant differences
6) (n◦ 6) were observed in Doppler progression throughout pregnancy.
These observations are in accordance with our placental findings.
Gestational Age at delivery (weeks) (median, 28.1 (2.6) 26.6 (3.2)
IQR) Our study is the first one to evaluate the effects of pravastatin therapy on
Birthweight, grams (median, IQR) 775.0 (426.2) 587.5 (233.7) placental histology in women with severe PE and IUGR. Pravastatin does
Birthweight percentile (median, minimum and 0.7 (0.0–3.5) 0.4 (0.2–1.1) not appear to reduce placental lesions from maternal and fetal malper­
maximum values) fusion in women with preeclampsia and IUGR.
Apgar 1st < 7 (n,%) 4/6 (67 %) 3/6 (50 %)
Apgar 5th < 7 (n,%) 1/6 (17 %) 0/6 (0 %)
We can hypothesize that pravastatin was not able to reverse or
NICU admission (n,%) 6/6 (100 %) 6/6 (100 %) reduce the placental damage in our cases when administered at diag­
Neonatal deaths (n,%) 2/6 (33 %) 2/6 (33 %) nosis, since it is too late to improve or even reverse the pathological
Neurodevelopmental delay (n,%) 1/6 (17 %) 1/6 (17 %) mechanism involved in PE. In our opinion, only a preventive and early
Lost to follow up (n,%) 0/6 (0 %) 1/6 (17 %)
pharmacological strategy could invert the natural history of this
IQR: interquartile range; NICU: neonatal intensive care unit. syndrome.

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S. Fruci et al. European Journal of Obstetrics & Gynecology and Reproductive Biology 283 (2023) 37–42

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[40] Lefkou E, Mamopoulos A, Dagklis T, Vosnakis C, Rousso D, Girardi G. Pravastatin Marco dell’Aquila Graduated from Sapienza University of
improves pregnancy outcomes in obstetric antiphospholipid syndrome refractory Rome in 2016, specializing in Pathology at the University of the
to antithrombotic therapy. J Clin Invest 2016;126:2933–40. Sacred Heart. His scientific and professional interests are
[41] Otten LA, van der Ven K, Kühr M, Gembruch U, Merz WM. Pravastatin for mainly directed to the histopathology of tumors and to feto­
prevention of HELLP syndrome: a case report. Medicine (Baltimore) 2017;96(42): placental pathology, perinatal autopsy and clinical autopsy. He
e8229. is currently a PhD student at Catholic University of the Sacred
[42] S. Tong, Tu’uhevaha J. Kaitu’u-Lino, R. Hastie, F. Brownfoot, C. Cluver, N. Heart.
Hannan. Pravastatin, proton-pump inhibitors, metformin, micronutrients, and
biologics: new horizons for the prevention or treatment of preeclampsia. Am J
Obstet Gynecol , 2020 Sep 16;S0002-9378(20)31071-1.

Stefano Fruci Stefano Fruci is a doctor specialized in Gyne­

cology and Obstetrics. His clinical activity is mainly aimed at
the study of maternal-fetal medicine with particular attention
to some maternal problems, in particular hypertensive disor­ Vincenzo Arena Dr. Vincenzo Arena is a pathologist at the
ders such as chronic hypertension, gestational hypertension IRCCS Fondazione Policlinico Universitario A.Gemelli (Italy). A
and preeclampsia (PE) and to some fetal problems such as fetal well known cardiovascular pathology expert, his major areas of
growth restriction (FGR). Together with his team colleagues, he clinical practice include autopsy pathology, feto-placental pa­
has focused on some specific topics including: use of pravastatin thology, breast and colon pathology. His research contributions
in the treatment of early onset PE and FGR, maternal hemo­ include the expression of ancillary prognosticators in human
dynamics using USCOM (Ultrasonic Cardiac Output Monitor), malignancies. He has authored>200 peer reviewed manu­
analysis of proangiogenic and antiangiogenic biomarkers on scripts. Degrees: MD, Catholic University of Rome – School of
maternal blood. Medicine (2001). Residencies: Catholic University of Rome –
School of Medicine (2006).

Silvia Salvi Education: Degree in Medicine and Surgery at

Catholic University of Sacred Heart in Rome; Speciality Degree
in Obstetrics and Gynecology; PhD in Cellular and Molecular
Clinical Research at the Catholic University of the Sacred Heart, Enrico Di Stasio Prof. Enrico Di Stasio, MD is Adjunct Professor
Rome. Career: Research Fellow in Obstetrics and Gynecology at in Biochemistry, Catholic University of Rome, IRCSS-
the Policlinico A. Gemelli in Rome. Publications: Several In­ Fondazione Gemelli. His research was focused on biophysics
ternational publications. She has an H-index of 14, and 821 and biochemistry of ligand binding theory, mechanical statis­
citations (Scopus, 2023). Her main topic of interest is the feto- tics and thermodynamics of protein aggregation and chaos
maternal medicine, moving from maternal disease (in partic­ theory in biological systems. He principally worked on coagu­
ular hypertensive disorders, autoimmune diseases, cardiac lation processes and cryoglobulins aggregation. Moreover he
problems in pregnancy) to related fetal problems (fetal growth serves as statistician for many projects in medical field. Author
disorders), from bench (placental in vitro studies) to bedside of over 200 peer-reviewed publications, he has an H-index of
(maternal haemodynamic assessment). 38.

Sascia Moresi Sascia Moresi is a doctor specialized in Gyne­

cology and Obstetrics and he works at the Policlinico Agostino
Gemelli in Rome. His clinical activity develops in the field of
maternal-fetal medicine and involves the study of some Sergio Ferrazzani Sergio Ferrazzani was born on June 6, 1952
maternal pathologies, in particular hypertensive disorders of in Viterbo. Italy. On November 4, 1977: he graduated in Med­
pregnancy and preeclampsia (PE) and the clinical management icine and Surgery at the Catholic University of Rome. On 6
of some fetal complications including fetal growth restriction November 1981: he obtained the specialization diploma in
(FGR). Together with the team colleagues we are carrying out Obstetrics and Gynecology. From November 1, 1988: he was
various research protocols that make use of USCOM (ultrasonic winner of the competition for University Researcher at the
cardiac output monitor), drugs such as pravastatin for the Institute of Obstetrics and Gynecology. Since 1 January 1998 he
compassionate treatment of PE, markers for endothelial has been 1st level Medical Director at the Division of Obstetrics
dysfunction and placental histology. and Gynecology. Since 1 November 2001 he has been Associate
Professor in Gynecology and Obstetrics at the same University.
He has been retired since 1 November 2022.

Francesca Gallini Prof. Francesca Gallini, MD is Assistant

Professor in Pediatrics, Neonatology, Catholic University of
Rome, IRCSS-Fondazione Gemelli. Education: degree in Medi­
cine and Surgery in 1989; advanced Professional Degree in Sara De Carolis Prof. Sara De Carolis, MD is Adjunct Professor
Pediatrics in 1993. From 2001 she is Researcher in Pediatrics- in Obstetrics and Medical Manager (UOS) at High-Risk Preg­
Neonatology and now Assistant Professor. From 2004 she is the nancy Unit, Catholic University of Rome, IRCSS-Fondazione
Director of the Neonatal Follow-up Program. She has an H- Gemelli. She has received several research awards. Her
index of 20, and 1235 citations (Scopus). research tracks are investigation on the role of antiphospholipid
antibodies in pregnancy (treatment, obstetrical management
and outcome, risk factors), autoimmune disease in pregnancy,
pregnancy management of blood disorders (inherited throm­
bophilia, immune thrombocytopenia, coagulopathies), cancer
in pregnancy, preeclampsia, twin pregnancy, fetal growth,
preterm delivery, coeliac disease and pregnancy, and recurrent
abortion. Author of almost 130 peer-reviewed publications, she
has an H-index of 34, and 3.593citations (Scopus).

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S. Fruci et al. European Journal of Obstetrics & Gynecology and Reproductive Biology 283 (2023) 37–42

Antonio Lanzone Degree in Medicine; Speciality Degree in

Obstetrics and Gynecology; from 2012 to present Head of the
High Risk Pregnancy Department at Fondazione Policlinico
Univ. A. Gemelli in Rome. From November 2010 he was
appointed President of the Degree Course in Medicine and
Surgery at the Catholic University of the Sacred Heart in Rome.
From 2018: Director of Woman’s Health – Department of
Woman and Child Health Sciences and Public Health. Author
of>500 publications. H index: 46 (Scopus) 2023.

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