Umbilical Cord Biometry and Fetal Abdominal Skinfold Assessment as Potential Biomarkers for Fetal Macrosomia in a Gestational Diabetes Romanian Cohort.

Backgroundand Objectives: Gestational diabetes mellitus (GDM) is a pregnancy-associated pathology commonly resulting in macrosomic fetuses, a known culprit of obstetric complications. We aimed to evaluate the potential of umbilical cord biometry and fetal abdominal skinfold assessment as screening tools for fetal macrosomia in gestational diabetes mellitus pregnant women. Materials and methods: This was a prospective case−control study conducted on pregnant patients presenting at 24−28 weeks of gestation in a tertiary-level maternity hospital in Northern Romania. Fetal biometry, fetal weight estimation, umbilical cord area and circumference, areas of the umbilical vein and arteries, Wharton jelly (WJ) area and abdominal fold thickness measurements were performed. Results: A total of 51 patients were enrolled in the study, 26 patients in the GDM group and 25 patients in the non-GDM group. There was no evidence in favor of umbilical cord area and WJ amount assessments as predictors of fetal macrosomia (p > 0.05). However, there was a statistically significant difference in the abdominal skinfold measurement during the second trimester between macrosomic and normal-weight newborns in the GDM patient group (p = 0.016). The second-trimester abdominal circumference was statistically significantly correlated with fetal macrosomia at term in the GDM patient group with a p value of 0.003, as well as when considering the global prevalence of macrosomia in the studied populations, 0.001, when considering both populations. Conclusions: The measurements of cord and WJ could not be established as predictors of fetal macrosomia in our study populations, nor differentiate between pregnancies with and without GDM. Abdominal skinfold measurement and abdominal circumference measured during the second trimester may be important markers of fetal metabolic status in pregnancies complicated by GDM.

Reduced glucose-stimulated insulin secretion following a 1-wk IGF-1 infusion in late gestation fetal sheep is due to an intrinsic islet defect.

Insulin and insulin-like growth factor-1 (IGF-1) are fetal hormones critical to establishing normal fetal growth. Experimentally elevated IGF-1 concentrations during late gestation increase fetal weight but lower fetal plasma insulin concentrations. We therefore hypothesized that infusion of an IGF-1 analog for 1 wk into late gestation fetal sheep would attenuate fetal glucose-stimulated insulin secretion (GSIS) and insulin secretion in islets isolated from these fetuses. Late gestation fetal sheep received infusions with IGF-1 LR3 (IGF-1, n = 8), an analog of IGF-1 with low affinity for the IGF binding proteins and high affinity for the IGF-1 receptor, or vehicle control (CON, n = 9). Fetal GSIS was measured with a hyperglycemic clamp (IGF-1, n = 8; CON, n = 7). Fetal islets were isolated, and insulin secretion was assayed in static incubations (IGF-1, n = 8; CON, n = 7). Plasma insulin and glucose concentrations in IGF-1 fetuses were lower compared with CON (P = 0.0135 and P = 0.0012, respectively). During the GSIS study, IGF-1 fetuses had lower insulin secretion compared with CON (P = 0.0453). In vitro, glucose-stimulated insulin secretion remained lower in islets isolated from IGF-1 fetuses (P = 0.0447). In summary, IGF-1 LR3 infusion for 1 wk into fetal sheep lowers insulin concentrations and reduces fetal GSIS. Impaired insulin secretion persists in isolated fetal islets indicating an intrinsic islet defect in insulin release when exposed to IGF-1 LR3 infusion for 1 wk. We speculate this alteration in the insulin/IGF-1 axis contributes to the long-term reduction in ß-cell function in neonates born with elevated IGF-1 concentrations following pregnancies complicated by diabetes or other conditions associated with fetal overgrowth.NEW & NOTEWORTHY After a 1-wk infusion of IGF-1 LR3, late gestation fetal sheep had lower plasma insulin and glucose concentrations, reduced fetal glucose-stimulated insulin secretion, and decreased fractional insulin secretion from isolated fetal islets without differences in pancreatic insulin content.

Heterozygous recurrent HNF4A variant p.Arg85Trp causes Fanconi renotubular syndrome 4 with maturity onset diabetes of the young, an autosomal dominant phenocopy of Fanconi Bickel syndrome with colobomas.

Heterozygous pathogenic variants in HNF4A cause hyperinsulinism, maturity onset diabetes of the young type 1, and more rarely Fanconi renotubular syndrome. Specifically, the recurrent missense pathogenic variant c.253C>T (p.Arg85Trp) has been associated with a syndromic form of hyperinsulinism with additional features of macrosomia, renal tubular nephropathy, hypophosphatemic rickets, and liver involvement. We present an affected mother, who had been previously diagnosed clinically with the autosomal recessive Fanconi Bickel Syndrome, and her affected son. The son's presentation expands the clinical phenotype to include multiple congenital anomalies, including penile chordee with hypospadias and coloboma. This specific pathogenic variant should be considered in the differential diagnosis of Fanconi Bickel Syndrome when genetics are negative or the family history is suggestive of autosomal dominant inheritance. The inclusion of hyperinsulinism and maturity onset of the diabetes of the young changes the management of this syndrome and the recurrence risk is distinct. Additionally, this family also emphasizes the importance of genetic confirmation of clinical diagnoses, especially in adults who grew up in the premolecular era that are now coming to childbearing age. Finally, the expansion of the phenotype to include multiple congenital anomalies suggests that the full spectrum of HNF4A is likely unknown.

Epidemiology of Macrosomia in Korea: Growth and Development.

BACKGROUND: Macrosomia, as an infant with birth weight over 4 kg, can have several perinatal, and neonatal complications. This study aimed to estimate the incidence of macrosomia in Korea and to identify the growth and developmental outcomes and other neonatal complications. METHODS: In total, 397,203 infants who were born in 2013 with birth weight ≥ 2.5 kg and who underwent infant health check-up between their 1st and 7th visit were included from the National Health Insurance Service database. The information was obtained by the International Classification of Diseases-10 codes or self-reported questionnaires in the National Health Screening Program. RESULTS: The distribution of infants by birth weight was as follows: 384,181 (97%) infants in the 2.5-3.99 kg (reference) group, 12,016 (3%) infants in the 4.0-4.49 kg group, 772 (0.2%) infants in the 4.5-4.99 kg group, and 78 (0.02%) infants in the ≥ 5 kg group. Macrosomia showed significantly higher incidence of sepsis, male sex, and mothers with GDM and birth injury. There was a significant difference in weight, height, and head circumference according to age, birth weight group, and combination of age and birth weight, respectively (P < 0.001). The number of infants with the weight above the 90th percentile in macrosomia at each health check-up showed higher incidence than in reference group. The mean body mass index significantly differed among the groups, as 50.6 in infants with 2.5-3.99 kg of birth weight, 63.5 with 4.0-4.49 kg, 71.0 with 4.5-4.99 kg, and 73.1 with ≥ 5 kg. There was a significant difference in the incidence of poor developmental results between infants with macrosomia and the reference group at 24, 36 and 48 month of age. CONCLUSION: Macrosomia was significantly associated with the risk of sepsis, birth injury, obesity and developmental problem especially in a boy born from mothers with gestational diabetes mellitus. Careful monitoring and proper strategies for monitoring growth and development are needed.

Fetal overgrowth in pregnancies complicated by diabetes: validation of a predictive index in an external cohort.

PURPOSE: To assess validity of a fetal overgrowth index in an external cohort of women with diabetes in pregnancy METHODS: We performed a retrospective analysis of data derived from women with singleton gestations complicated by diabetes who delivered January 2015-June 2018. The following index variables were used to calculate risk of fetal overgrowth as defined by a customized birthweight ≥ 90th centile: age, history of fetal overgrowth in a prior pregnancy, gestational weight gain, fetal abdominal circumference measurement and fasting glucose between 24 and 30 weeks. RESULTS: In our validation cohort, 21% of 477 pregnancies were complicated by fetal overgrowth. The predictive index had a bias-corrected bootstrapped area under receiver operating characteristic curve of 0.90 (95% CI 0.86-0.93). 55% of the cohort had a low-risk index (≤ 3) which had a negative predictive value of 97% (95% CI 94-98%), while 18% had a high-risk index (≥ 8) that had a positive predictive value of 74% (95% CI 66-81%). CONCLUSION: The fetal overgrowth index incorporates five factors that are widely available in daily clinical practice prior to the period of maximum fetal growth velocity in the third trimester. Despite substantial differences between our cohort and the one studied for model development, we found the performance of the index was strong. This finding lends support for the general use of this tool that may aid counseling and allow for targeted allocation of healthcare resources among women with pregnancies complicated by diabetes.

The triad macrosomia, obesity, and hypertriglyceridemia in gestational diabetes.

AIMS: Offspring of women with gestational diabetes (GD) have more macrosomia than newborns of normal mothers. We studied macrosomia frequency, possible pathogenesis, and main predictors of its appearance at different gestational ages. MATERIALS AND METHODS: A total of 1870 pregnant women with GD were recruited in primary care centres and maternity hospitals in the Argentine provinces of Corrientes, Chaco, Buenos Aires, and in Buenos Aires City; 1088 completed gestation and delivered an infant. We collected clinical and metabolic data, personal and obstetric history, and gestational and delivery characteristics. Presence of macrosomia was analysed in the whole population, the entire pregnancy, and in each trimester of gestation. Data were statistically analysed and values were expressed as mean ± SD and percentages. The study protocol was approved by the Ethics Committee and all participants signed informed consent. RESULTS: Macrosomia was found in 12.9% of newborns and obesity in all mothers with no significant differences between mothers with/without macrosomic offspring. In early pregnancy, the main significant indicators of macrosomia were: history of dyslipidaemia (5.6% vs 1.2%, respectively) and macrosomia in previous pregnancies (27% vs 13%, respectively). However, the third trimester showed a significant combination of higher BMI, FBG, and triglycerides. CONCLUSIONS: Offspring of women with GD presented macrosomia in 12.9% of cases, maternal history of dyslipidaemia and macrosomia in previous pregnancies being early predictors. The combination of maternal obesity, FBG, and hypertriglyceridemia became significant during the last trimester of pregnancy.

The effect of vascular complications of diabetes mellitus on human umbilical cord tissue and the number of Wharton Jelly's mesenchymal stem cells.

The current study investigated the change in umbilical cord tissue and the number of markers of Wharton's jelly mesenchymal stem cells (WJ-MSC) in pregnant women with gestational diabetes (GDM), with chronic diabetes who developed nephropathy as vascular complication (VC-PGDM), and healthy pregnant women as the control. The umbilical cords (UC) were investigated by the histomorphological method and the number of WJ-MSC were detected by flow-cytometry using the CD90, CD44, CD105, and CD73 markers in Wharton's jelly (WJ) isolated from fresh umbilical cords. The number of positive cells for CD 90, CD44, CD105, and CD73 were found to be elevated in the GDM group, whereas it was significantly diminished in the VC-PGDM group (p = 0.001, p = 0.001, p = 0.001, and p = 0.001). The only histopathological sign in the GDM group were an increased number of pores in the Wharton jelly. Artery wall thickness/cord diamater ratio was increased, which indicates an increase of the artery wall thickness in the VC- PGDM group (p = 0.039 and p = 0.048). The increase in umbilical cord diameter and number of Wharton jelly mesenchymal stem cells in babies of gestational diabetic mothers was considered as an effect of macrosomia seen in babies of mothers with gestational diabetes. Vasculopathy, a long-term complication of diabetes, is known to affect all tissues by causing marked lower perfusion and hypoxia, as well as a decrease in the MSC number in our study.

Disadvantages of a weight estimation formula for macrosomic fetuses: the Hart formula from a clinical perspective.

PURPOSE: Sonographic fetal weight (FW) estimation to detect macrosomic fetuses is an essential part of everyday routine work in obstetrics departments. Most of the commonly used weight estimation formulas underestimate FW when the actual birth weight (BW) exceeds 4000 g. One of the best-established weight estimation formulas is the Hadlock formula. In an effort to improve the detection rates of macrosomic infants, Hart et al. published a specially designed formula including maternal weight at booking. The usefulness of the Hart formula was tested. METHODS: Retrospective study of 3304 singleton pregnancies, birth weight ≥ 3500 g. The accuracy of the Hadlock and Hart formula were tested. A subgroup analysis examined the influence of the maternal weight. The Chi-squared test and one-way analysis of variation were carried out. For all analyses, p < 0.05 was considered statistically significant. RESULTS: The overall percentages of births falling within ± 5% and ± 10% of the BW using the Hadlock formula were 27% and 53%, respectively. Using the Hart formula, 24% and 54% were identified within these levels. With the Hart formula, 94% of all weight estimations fall within 4200 g ± 5% and nearly 100% fall within 4200 g ± 10%. CONCLUSIONS: Applying the Hart formula results in an overestimation of fetal weight in neonates with a birth weight < 4000 g and fails to identify high-risk fetuses. We, therefore, do not consider Hart's formula to be of clinical relevance.

Maternal pre-pregnancy obesity and the risk of macrosomia: a meta-analysis.

PURPOSE: The aim of our meta-analysis was to explore whether pre-pregnancy obesity is regarded as an important risk factor for predicting macrosomia or not. METHODS: Three databases were systematically reviewed and reference lists of relevant articles were checked. Meta-analysis of published cohort studies comparing whether pre-pregnancy obesity was associated with macrosomia and adjusting for potential confounding factors. Calculations of pooled estimates were conducted in random-effect model. Heterogeneity was tested by using Chi-square test and I 2 statistics. Publication bias was estimated from Egger's test (linear regression method) and Begg's test (rank correlation method). RESULTS: Sixteen cohort studies met the inclusion criteria. The meta-analysis showed that pre-pregnancy obesity was associated with macrosomia as an important risk factor. The adjusted odds ratio was 1.93, 95% CI (1.65, 2.27) in random-effect model, stratified analyses showed no differences regarding different quality grade, definition of macrosomia, location of study and number of confounding factors adjusted for. There was no indication of a publication bias either from the result of Egger's test or Begg's test. CONCLUSION: Our findings indicated that pre-pregnancy obesity should be considered as an important risk factor for macrosomia. The effect of pre-pregnancy obesity on macrosomia need to be carefully assessed and monitored.

Histological Features of Oral Cavity Mucous Membrane Epithelium in Six-Month-Old Experimental Animals Born with Macrosomia.

We examined the histological features of the mucobuccal fold of oral cavity mucous membrane from the area of the masticatory teeth roots' projection in 6-month-old Wistar Albino Glaxo rats with fetal macrosomia. The animals were divided into groups according to the body weight, the body length, and the Quetelet index at birth. A morphological study was performed using the Leica SP8 AOBS laser scanning confocal microscope and a conventional light (Axiostar, Zeiss) microscopy. Morphometric parameters were used to estimate the degree of acanthosis development in the epithelium of the oral mucosa, which indicates the intensity of its proliferation. Numerous narrow and deep acanthotic outgrowths and densely located 'juvenile' epitheliocytes in the basal layer on the apex of the acanthotic protrusions were found in animals with fetal macrosomia that was due to intrauterine obesity. In these animals, the morphometric index, which we used, was maximally different from that in the control group. In animals with fetal macrosomia that was due to intrauterine growth acceleration of the body, the hyperproliferation of the mucous membrane epithelium of the oral cavity was absent or little pronounced. It can be assumed that fetal macrocosmia with obesity causes instability in the epithelium of the oral cavity mucosa, its rapid death, and therefore, a more active stimulation of proliferation.

Long term survival of a patient with Perlman syndrome due to novel compound heterozygous missense mutations in RNB domain of DIS3L2.

Perlman syndrome is a rare overgrowth syndrome characterized by polyhydramnios, macrosomia, distinctive facial appearance, renal dysplasia, and a predisposition to Wilms' tumor. The syndrome is often associated with a high neonatal mortality rate and there are few reports of long-term survivors. We studied a 6-year-old Japanese female patient, who was diagnosed with Perlman syndrome, with novel compound heterozygous mutations in DIS3L2 (c.[367-2A > G];[1328T > A]), who has survived long term. Most reported DIS3L2 mutations have been the homozygous deletion of exon 6 or exon 9, and these mutations would certainly have caused the loss of both RNA binding and degradation activity. We have identified new compound heterozygous mutations in the DIS3L2 of this long-term survivor of Perlman syndrome. The reason our patient has survived long-term would be a missense mutation (c.1328 T > A, p.Met443Lys) having retained RNA binding in both the cold-shock domains and the S1 domain, and through partial RNA degradation. If partial exonuclease functions remain in at least one allele, long-term survival may be possible. Further studies of Perlman syndrome patients with proven DIS3L2 mutations are needed to clarify genotype-phenotype correlation.

A new case of holoprosencephaly-polydactyly syndrome with alobar holoprosencephaly, preaxial polydactyly and congenital glaucoma.

We report a case of a female baby born at 34 weeks of gestation. Birth weight was 1760 g (10th-25th centile), length 41cm (10th-25th centile) and head circumference 27cm (< 10th centile). Clinical examination revealed microcephaly, hypotelorism, micrognathia, a flat rudimentary nose, high palate, thick dysplastic low-set ears, a short neck, preaxial polydactyly of the right hand, and overriding toes. Investigations showed bilateral congenital glaucoma, alobar holoprosencephaly, severe ventriculomegaly and absence midline structures of the brain, a large atrial septal defect. The karyotype was 46,XX. The case was also diagnosed as having holoprosencephaly-polydactyly syndrome (pseudotrisomy 13) because she had alobar holoprosencephaly, preaxial polydactyly, facial dysmorfism (hypotelorism, micrognathia, a flat rudimentary nose, high palate, thick dysplastic low-set ears) and normal karyotype.

Perinatal nutrition programs the hypothalamic melanocortin system in offspring.

Epidemiological studies initially suggested that maternal undernutrition leading to low birth weight may predispose for long-lasting energy balance disorders. High birth weight due to maternal obesity or diabetes, inappropriate early postnatal nutrition, and rapid catch-up growth, may also sensitize to increased risk of obesity. As stated by the Developmental Origin of Health and Disease concept, the perinatal perturbation of fetus/neonate nutrient supply might be a crucial determinant of individual programming of body weight set-point. The hypothalamic melanocortin system composed of the melanocortin receptor 4, its agonist α-melanin-stimulating hormone (α-MSH), and its antagonist agouti-related protein (AgRP) is considered as the main central anorexigenic pathway controlling energy homeostasis. Studies in numerous animal models demonstrated that this system is a prime target of developmental programming by maternal nutritional manipulation. In rodents, the perinatal period of life corresponds largely to the period of brain maturation (i. e., melanocortin neuronal differentiation and development of their neural projections). In contrast, these phenomena essentially take place before birth in bigger mammals. Despite these different developmental time windows, altricial and precocial species share several common offspring programming mechanisms. Offspring from malnourished dams present a hypothalamic melanocortin system with a series of alterations: impaired neurogenesis and neuronal functionality, disorganization of feeding pathways, modified glucose sensing, and leptin/insulin resistance. Overall, these alterations may account for the long-lasting dysregulation of energy balance and obesity. Following maternal malnutrition, hormonal and epigenetic mechanisms might be responsible for melanocortin system programming in offspring.

Maternal weight gain in women with gestational diabetes mellitus.

OBJECTIVE: The aim of the study was to examine the perinatal outcomes in gestational diabetes in women with body mass index (BMI)-adjusted gestational weight gain (GWG) according to the Institute of Medicine (IOM) 2009 recommendations. MATERIAL AND METHODS: The clinic's database was used to analyze 675 singleton GDM pregnancy outcomes. GWG for the entire pregnancy was compared to IOM recommendations and adjusted for prepregnancy BMI categories: underweight <18.5; normal 18.5-24.9; overweight 25-29.9; and obese >30. The study group was divided into three categories: below IOM limits, within IOM limits and above IOM limits. RESULTS: Only 37% of women achieved the proper weight gain (n=256). Almost 30% of women with GDM (n=196) had an excessive weight gain. GWG above limits was associated with a significantly higher neonatal measurements and a higher rate of large-for-gestational-age neonates. In underweight and normal-prepregnancy-weight women, no relation between GWG and birth-weight percentile was noted. For the overweight and obese women, a positive significant correlation between GWG until GDM diagnosis and birth-weight percentile was noted (P=0.002), which was not present when GWG until delivery was considered. CONCLUSIONS: Limited weight gain in overweight and obese women with gestational diabetes mellitus results in favourable pregnancy outcomes.

Relationship between sonographically estimated fetal subcutaneous adipose tissue measurements and neonatal skinfold measurements.

OBJECTIVE: Increased subcutaneous adipose tissue is a well known characteristic of diabetic fetopathy. Prenatal estimation of adipose tissue can be performed by ultrasound, while postnatally skinfold measurements are performed using a Holtain caliper. The aim of this study was to compare these methods in the same patients. METHODS: This was a prospective study of 172 pregnant patients (142 controls and 30 with gestational diabetes) at ≥ 37 gestational weeks. In addition to fetal weight estimation, fetal subcutaneous tissue was measured at the anterior abdomen lateral to the umbilicus (SonoSfAbd) and at the middle of the femur (SonoSfFem). Within 72 h after delivery, a Holtain caliper was used to measure neonatal skinfold thickness at the left anterior iliac spine (SfAbd), at the lower angle of the left scapula (SfSca), at the middle of the femur, above the left quadriceps femoris (SfFem) and at the middle of the left triceps (SfHum). Ultrasound and mechanical measurements were correlated. RESULTS: The sonographic and mechanical methods showed good correlation with each other. Linear regression analysis gave the following equations: SfAbd (mm) = SonoSfAbd (mm) × 0.489 + 1.988 (r(2) = 0.34, P < 0.001); SfSca (mm) = SonoSfAbd (mm) 0.457 + 2.043 (r(2) = 0.40, P < 0.001); SfFem (mm) = SonoSfFem (mm) × 0.714 + 1.763 (r(2) = 0.41, P < 0.001); SfHum (mm) = SonoSfFem (mm) 0.564 + 2.09 (r(2) = 0.39, P < 0.001). CONCLUSIONS: Ultrasound examination is a reliable method for non-invasive intrauterine measurement of fetal subcutaneous tissue and can be used to predict mechanical neonatal skinfold thickness measurements.

Independent effect of gestational weight gain and prepregnancy obesity on pregnancy outcomes among Saudi women: A sub-cohort analysis from Riyadh mother and baby cohort study (RAHMA).

BACKGROUND: Gestational weight gain (GWG) and prepregnancy obesity are garnering more attention as determining factors of pregnancy outcomes when it comes to the wellbeing of both the mother and her baby. This study was conducted to describe the pattern of GWG among participants of Riyadh Mother and Baby Multicenter Cohort Study (RAHMA) and to investigate the detrimental effects of excessive GWG and prepregnancy obesity on pregnancy outcomes. METHODS: RAHMA is a multicentre cohort study conducted in three hospitals in Riyadh, Saudi Arabia. Participants were categorized according to the Institute of Medicine into inadequate, adequate, and excessive GWG, and stratified by body mass index (BMI) into under/normal weight, overweight, and obese. To examine the independent effect of maternal prepregnancy obesity and GWG, a multivariate regression model was used and adjusted odds ratio (AOR) and 95% Confidence Interval (CI) for each outcome were calculated. RESULTS: A total of 7029 participants were included in this study; 31.8% had adequate GWG, 25.9% had excessive GWG and 42.3% had inadequate GWG, while 29.7% had normal BMI, 33.3% were overweight, 34.8% were obese, and 2.2% were underweight. Excessive GWG was independently associated with increased risk of hypertensive events, (AOR = 1.77, 95% CI 1.20-2.63). Obesity was associated with higher risk of gestational diabetes (AOR 2.11, 95% CI 1.76-2.53), hypertensive events (AOR 2.06, 95% CI 1.48-3.01), and delivery by emergency caesarean section (AOR = 1.63, 95% CI 1.35-1.97). Infants of obese women had increased odds of macrosomia (AOR 3.11, 95% CI 1.94-4.99) and lower odds of low birth weight (AOR = 0.68, 95% CI 0.53-0.88). CONCLUSION: In comparison to excessive GWG, which increases the risk of hypertensive events during pregnancy, prepregnancy obesity is associated with more adverse outcomes including GDM, hypertensive events in pregnancy and emergency CS.

Alteration of antioxidant defense status precedes humoral immune response abnormalities in macrosomia.

BACKGROUND: This study aimed to investigate whether the anomalies affecting the antioxidant and humoral immune defenses could start at birth and to check whether the decrease in antioxidant defenses may precede the immune abnormalities in macrosomic newborns. MATERIAL/METHODS: Thirty macrosomic and 30 sex-matched control newborns were recruited for a retrospective case-control study at the Maghnia Maternity Hospital of Tlemcen Department (Algeria). RESULTS: The serum IgG levels were similar in both groups. However, plasma ORAC, albumin, vitamin E, SOD, CAT and GSH-Px levels were significantly decreased in macrosomic as compared to control newborns, yet no difference was observed after adjustment for weight. Additionally, serum concentrations of complement C3, MDA and XO were significantly higher in macrosomic as compared to controls before adjustment for weight. Moreover, macrosomia was significantly associated with high levels of complement C3 (OR=8, p=0.002); whereas no association with those of IgG was observed (OR<1, p>0.05). Furthermore, macrosomia was significantly associated with low levels of ORAC (OR=4.96, p=0.027), vitamin E (OR=4.5, p=0.018), SOD (OR=6.88, p=0.020) and CAT (OR=5.67, p=0.017), and with high levels of MDA (OR=10.29, p=0.005). CONCLUSIONS: Abnormalities of the humoral defense system in excessive weight could be preceded by alterations of the anti-oxidative defense and by inflammatory response and activation of innate immunity at birth. Additionally, excessive weight could be a potential factor contributing to decreased anti-oxidative capacity and increased oxidative stress.

Role of fetal abdominal circumference as a prognostic parameter of perinatal complications.

OBJECTIVE: To evaluate the potential of fetal abdominal circumference (AC) measurement as predictor of perinatal complications in term newborns. MATERIALS AND METHODS: This prospective study included 324 consecutive term pregnancies within a 6-month period between February and August 2009. Inclusion criteria were a singleton pregnancy with at least 37 weeks of gestation, vertex presentation, absence of structural or chromosomal disorders and complete ultrasound examination within 3 days of delivery. Patients with elective caesarean sections were excluded. Vaginal deliveries were assessed with regard to the impact of fetal AC on the mode of delivery, the neonatal outcome (pH, base excess, APGAR score at 5 min) and the incidence of perineal injuries. When appropriate, U tests and χ (2) tests were performed for group comparisons. RESULTS: Complete data were obtained for 258 patients. Sixty-six patients were excluded because they underwent elective caesarean section. Only 12 of the 30 fetuses with an AC ≥ 36.0 cm weighed more than 4,000 g. There was no significant difference in relation to incidence of surgical delivery (instrumental delivery, P = 0.754 and caesarean section, P = 0.405), the neonatal outcome (pH, P = 0.527; base excess, P = 0.146; APGAR score at 5 min, P = 0.552), and the occurrence of perineal injuries (2nd and 3rd degree, P = 0.951). CONCLUSION: The results of the study could not demonstrate a significant relationship between AC ≥ 36.0 cm and perinatal complications. For this, measuring the fetal AC is of no help in finding the correct clinical management.

Perinatal outcomes associated with the diagnosis of gestational diabetes: Systematic review and meta-analysis.

OBJECTIVE: To compare perinatal outcomes in pregnant women diagnosed with gestational diabetes using the one-step and the two-step test. METHODS: Meta-analysis of observational studies pregnancies women with gestational diabetes from January 2014 to February 2019. The outcomes studied were induction of labor and delivery, preterm delivery, fetal macrosomia, neonatal hypoglycemia, hyperbilirubinemia, low birth weight, and admission to the neonatal intensive care unit. RESULTS: Eight studies were included with a population of 108,609 pregnancies. Statistical differences were obtained for fetal macrosomia RR0.9 (95%CI0.85-0.97; I20%) and neonatal hypoglycemia RR1.1 (95%CI1.01-1.40; I248.5%). CONCLUSION: Neonatal macrosomia appears to be less present when the one-step diagnostic test is used and neonatal hypoglycemia was lower with the two-step test. Register PROSPERO CRD42020215062.