No abstract

A lipotoxic placental environment is recognized in maternal obesity, with increased inflammation and oxidative stress. These changes might alter mitochondrial function, with excessive production of reactive oxygen species, in a vicious cycle leading to placental dysfunction and impaired pregnancy outcomes. Here, we hypothesize that maternal pregestational body mass index (BMI) and glycemic levels can alter placental mitochondria. We measured mitochondrial DNA (mtDNA, real-time PCR) and morphology (electron microscopy) in placentas of forty-seven singleton pregnancies at elective cesarean section. Thirty-seven women were normoglycemic: twenty-one normal-weight women, NW, and sixteen obese women, OB/GDM(−). Ten obese women had gestational diabetes mellitus, OB/GDM(+). OB/GDM(−) presented higher mtDNA levels versus NW, suggesting increased mitochondrial biogenesis in the normoglycemic obese group. These mitochondria showed similar morphology to NW. On the contrary, in OB/GDM(+), mtDNA was not significantly increased versus NW. Nevertheless, mitochondria showed morphological abnormalities, indicating impaired functionality. The metabolic response of the placenta to impairment in obese pregnancies can possibly vary depending on several parameters, resulting in opposite strains acting when insulin resistance of GDM occurs in the obese environment, characterized by inflammation and oxidative stress. Therefore, mitochondrial alterations represent a feature of obese pregnancies with changes in placental energetics that possibly can affect pregnancy outcomes.

Our results indicate a potential compensatory mechanism to increased obesity-related OxS and inflammation, indicated by the higher hepcidin levels found in obese mothers. Increased placental mitochondrial biogenesis, due to lipotoxic environment, may account for the greater mtDNA amount released in maternal circulation. This increase is namely related to F-carrying pregnancies, suggesting a gender-specific placental response.

Introduction: Spontaneous hemoperitoneum in pregnancy is defined as a sudden non-traumatic intraperitoneal bleeding in pregnancy and up to 42 days postpartum.In the present study we aim to estimate the incidence and investigate the risk factors, the management and the outcomes of spontaneous hemoperitoneum in pregnancy in order to improve its clinical identification and reduce avoidable maternal deaths. Material and methods: This is a prospective population-based cohort study, set in maternity units from nine Italian regions covering 75% of the national births. The study population comprises all women admitted for spontaneous intraperitoneal hemorrhage during pregnancy and up to 42 days postpartum between November 2017 and March 2020. Incident cases were reported by trained clinicians through electronic data collection forms. Descriptive statistics were performed. The main outcome measures included incidence rate of spontaneous hemoperitoneum in pregnancy, association with potential risk factors, clinical management and maternal and perinatal outcomes.Results: Twenty-nine cases met the adopted definition of spontaneous hemoperitoneum in pregnancy with an estimated incidence rate of 0.04 per 1000 births. An increased risk ratio (RR) of this condition was observed in pregnancies conceived by assisted reproductive technology (RR = 6.60, 95% CI 2.52-17.29), in the case of multiple pregnancies (RR = 6.57, 95% CI 1.99-21.69) and maternal age ≥35 years (RR 2.10, 95% CI 1.01-4.35). In 17/29 cases the bleeding site was intra-pelvic (23.5% in the posterior uterine wall and 35.2% in the left hemipelvis). Laparotomy represented the surgical treatment in 27 cases (93%), and most women underwent a cesarean delivery (92.6%). Median blood loss was 1900 mL, one hysterectomy was necessary, and two women died. Twenty-two preterm births were recorded.Conclusions: Spontaneous hemoperitoneum in pregnancy is a rare, life-threatening condition associated with high perinatal morbidity and mortality. Maternal age ≥35 years, multiple pregnancies and assisted reproductive technology were associated to a higher risk of the condition. Two women of 29 died and 70% of births occurred preterm.

Placental growth factor (PlGF) is an angiogenic molecule produced by the placenta and implicated in the pathogenesis of preeclampsia (PE) and intrauterine growth restriction (IUGR). We have evaluated utility and applicability of the PlGF test in a clinical setting of pregnancies at risk of PE or complicated by IUGR in order to assess its relationship with pregnancy outcomes. Seventy-three pregnancies were enrolled between 19 and 35 weeks: 57 pregnancies at risk of PE and 16 at diagnosis of IUGR. Maternal circulating PlGF levels were measured by the Triage PlGF test (Alere, San Diego, CA). Pregnancy outcomes were evaluated in relation to three categories of plasma PlGF levels: very low (<12 pg/ml), low (12-100 pg/ml) and normal (≥100 pg/ml). Uterine artery Doppler velocimetry (UADV) pulsatility index (PI) was measured in the same patients on the day of maternal sampling. Pregnancies at risk with very low plasma PlGF levels had significantly lower gestational age at delivery than patients with low or normal PlGF. The rate of emergency C-section was significantly higher in the group with PlGF<12 pg/ml. IUGR pregnancies with very low and low PlGF delivered earlier than patients with normal PlGF. All IUGR with very low and low PlGF had UADV PI > 95th percentile. Our data indicate that PlGF may provide useful information to identify fetuses requiring increased surveillance and possibly urgent delivery in pregnancies at risk of adverse outcomes. Furthermore, in IUGR, PlGF can predict adverse pregnancy outcomes that may be secondary to placental insufficiency.

Background: Breastfeeding women are at risk of developing mastitis during the lactation period. Staphylococcus aureus has emerged as the community-acquired pathogen responsible for virulence (methicillin resistance and Panton-Valentine leukocidin toxin producing). Research aim: The aim was to compare the microorganisms responsible for mastitis and breast abscesses during breastfeeding. Methods: This observational study was conducted with a sample of women ( N = 60) admitted to our hospital between 2016 and 2018. Participants affected by mastitis and breast abscess were studied and cared for by a multidisciplinary working group. A diagnostic breast ultrasound identified the pathology. Results: Twenty-six participants (43.3%) were affected by mastitis and 34 (56.7%) by breast abscess. The most common microorganism identified was Staphylococcus aureus ( S. aureus; mastitis, n = 13; abscesses, n = 24). Methicillin resistance was identified in 21 (44.7%) S. aureus strains: 17 (80.9%) cases of abscess and four (19.1%) cases of mastitis. The median number of months of breastfeeding was smaller in the methicillin-resistant S. aureus (MRSA) cases (median = 3, range = 1–20 months) than in the methicillin-sensitive S. aureus (MSSA) cases (median = 6.5, range = 3–21 months). The Panton-Valentine leukocidin toxin gene was detected in 12 (25.5%) cases (MRSA, n = 8, 66.7%; MSSA, n = 4, 33.3%). Hospitalization was required more frequently in MRSA ( n = 8, 38%; five Panton-Valentine leukocidin positive) than in MSSA cases ( n = 5, 19%; one Panton-Valentine leukocidin positive). Four women out of the eight MRSA cases (50%) that were Panton-Valentine leukocidin positive stopped breastfeeding during mammary pathologies, three (37.5%) participants continued breastfeeding until the follow-up recall, and one case was lost at follow-up. Conclusion: Clinical severity was probably complicated by the presence of the Panton-Valentine leukocidin toxin, which required hospitalization more frequently.

With this study we filled several gaps occurring in previous studies: we analyzed a very well-defined population of PE, PIH and IUGR pregnancies, considering both fetal and maternal HLA-G 14 bp polymorphism, individually and jointly. Our findings showed that fetal and maternal HLA-G 14 bp genotypes are not associated with increased risk for the development of obstetrical complications, suggesting that this polymorphism has no immuno-modulatory role in the development of PE, PIH or IUGR.

ObjectiveThe prevalence of coeliac disease (CD) in Vietnam is unknown. To fill this void, we assessed the prevalence of serological markers of CD autoimmunity in a population of children in Hanoi.SettingThe outpatient blood drawing laboratory of the largest paediatric hospital in North Vietnam was used for the study, which was part of an international project of collaboration between Italy and Vietnam.ParticipantsChildren having blood drawn for any reason were included. Exclusion criteria were age younger than 2 years, acquired or congenital immune deficiency and inadequate sample. A total of 1961 children (96%) were enrolled (838 females, 1123 males, median age 5.3 years).OutcomesPrimary outcome was the prevalence of positive autoimmunity to both IgA antitransglutaminase antibodies (anti-tTG) assessed with an ELISA test and antiendomysial antibodies (EMA). Secondary outcome was the prevalence of CD predisposing human leucocyte antigens (HLA) (HLA DQ2/8) in the positive children and in a random group of samples negative for IgA anti-tTG.ResultsThe IgA anti-tTG test was positive in 21/1961 (1%; 95% CI 0.61% to 1.53%); however, EMA antibodies were negative in all. HLA DQ2/8 was present in 7/21 (33%; 95% CI 14.5% to 56.9%) of the anti-tTG-positive children and in 72/275 (26%; 95% CI 21% to 32%) of those who were negative.ConclusionsCoeliac autoimmunity is rare in Vietnam, although prevalence of HLA DQ2/8 is similar to that of other countries. We hypothesise that the scarce exposure to gluten could be responsible for these findings.