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1.
BMC Pediatr ; 21(1): 111, 2021 03 06.
Artículo en Inglés | MEDLINE | ID: mdl-33676430

RESUMEN

BACKGROUND: Offspring of mothers with gestational diabetes mellitus (GDM) have an increased risk of neonatal complications like birth trauma due to macrosomia or postnatal hypoglycemia, as well as long-term metabolic sequelae. Neonatal body composition may be a sensitive marker of metabolic effects on the fetus caused by suboptimal glycemic control during pregnancy. OBJECTIVE: To determine body composition in offspring of mothers with GDM compared to a reference cohort of healthy term neonates and to assess whether increased body fat would be associated with postnatal hypoglycemia. METHODS: This prospective, observational, cross-sectional study included 311 full-term, singleton infants born between June 2014 and July 2015. Body composition was measured within 96 h of birth using air displacement plethysmography. Results are indicated as median (1st Quartile - 3rd Quartile). RESULTS: Of 311 infants, 40 (12.9%) were born to mothers with GDM. Birth weight standard deviation scores (SDS) (0.24 vs. - 0.07, p = 0.04), fat mass (370 g vs. 333 g, p = 0.02) as well as fat mass/total body mass (BF%; 11.4% vs. 10.8%, p = 0.03) were significantly higher in infants following maternal GDM than in controls. In GDM offspring, anthropometric parameters, fat mass or BF% did not differ between infants with or without postnatal hypoglycemia. In this cohort, SDS for birth weight, fat mass, fat free mass, BF% or postnatal hypoglycemia were not associated with maternal blood glucose levels measured at an oral glucose tolerance test. CONCLUSIONS: SDS for birth weight, neonatal fat mass, and BF% were significantly higher in newborns following maternal GDM. In these infants born to mothers with GDM, body composition did not differ between those with or without postnatal hypoglycemia.


Asunto(s)
Diabetes Gestacional , Hipoglucemia , Peso al Nacer , Composición Corporal , Índice de Masa Corporal , Estudios Transversales , Femenino , Humanos , Hipoglucemia/diagnóstico , Hipoglucemia/etiología , Lactante , Recién Nacido , Embarazo , Estudios Prospectivos
2.
Front Immunol ; 13: 1078340, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-36685522

RESUMEN

Aim: To estimate the associations of cord meta-inflammatory markers with neurodevelopment, including the potential impact of cord blood vitamin D levels. Method: The prospective cohort study comprised 7198 participants based on the Maternal & Infants Health in Hefei study. Cord blood C-peptide, high-sensitive C-reactive protein (hsCRP), high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, total cholesterol, triglycerides and 25(OH)D levels were measured. The Gesell Developmental Schedules were used to assess neurodevelopmental outcomes in offspring. Results: After adjusting potential confounders, per quartile increase in cord blood 25(OH)D concentrations was associated with a decreased risk of neurodevelopmental delay [hazard ratios (HR) 0.65 (95% CI 0.57, 0.74)]. Conversely, significant positive associations with cord blood serum C-peptide levels above the 90th percentile [HR 2.38 (95% CI 1.81, 3.13)] and higher levels of cord hsCRP (per quartile increase) [HR 1.18 (95% CI 1.01, 1.37)] with neurodevelopmental delay were observed. These associations could vary by quartiles of cord blood 25(OH)D levels: the adjusted HRs in neurodevelopmental delay comparing children with vs without hyperinsulinemia were 1.28 (95% CI: 1.03, 1.59) for quartiles 1 (lowest), and 1.06 (95% CI: 0.78, 1.44) for quartile 4 (highest). Conclusions: Immune activation and metabolic abnormalities in fetal circulation were associated with neurodevelopmental delay in offspring, which could be attenuated by higher cord blood 25(OH)D levels in a dose-response manner.


Asunto(s)
Deficiencia de Vitamina D , Vitamina D , Lactante , Niño , Humanos , Estudios de Cohortes , Estudios Prospectivos , Sangre Fetal , Deficiencia de Vitamina D/complicaciones , Proteína C-Reactiva , Péptido C , Vitaminas , Inflamación/complicaciones , Colesterol
3.
Cureus ; 14(12): e32623, 2022 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-36654578

RESUMEN

Introduction According to the thrifty (Barker's) phenotype hypothesis, poor nutrition in fetal and early infancy plays a role in the development and function of the beta cells of the islets of Langerhans, which leads to the development of type 2 diabetes mellitus. Insulin resistance is due to decreased suppressive effect of insulin on hepatic glucose production. Thus, elevated insulin levels during perinatal life may predispose the infant to the development of diabetes mellitus in future life. Intrauterine undernutrition plays an important role in causing adult insulin resistance and diabetes but the exact cause is still unknown. Preterm infants born small for gestational age (SGA) show lower adrenocortical response to stimulation due to an immature hypothalamic-pituitary axis. Methods The cross-sectional study conducted at Rajendra Institute of Medical Sciences, Ranchi from June 2020 to November 2021 included 216 newborns enrolled as per the inclusion and exclusion criteria. Maternal and neonatal details were collected at birth and recorded. Cord blood samples for measurement of serum insulin, glucose, and cortisol were collected from 84 preterm and 132 term neonates. Using this information, homeostasis model assessment-insulin resistance (HOMA-IR) was calculated using a mathematical formula. Insulin resistance was defined as HOMA-IR > 2.5. Based on birth weight and gestational age, they were further categorized into SGA, appropriate for gestational age (AGA), and large for gestational age (LGA). The parametric data were presented as means ± standard deviation (SD), and nonparametric data as medians (first quartile and third quartile). The Student's (independent samples) t-test and Mann-Whitney U test were used to compare mean differences between the two groups for parametric and nonparametric data, respectively. The Spearman correlation coefficient was used to determine the significant association between variables. Results Umbilical cord plasma glucose and serum insulin were high in preterm in comparison to term newborns. Serum cortisol levels were high in term than in preterm newborns. HOMA-IR showed a very strong positive correlation with serum insulin and a moderate positive correlation with serum glucose. HOMA-IR showed a strong negative correlation with gestational age and a moderate negative correlation with birth weight. Insulin resistance was seen in 34 preterm newborns and two term newborns. Insulin resistance was seen in 29.8% (n = 25) of SGA preterm babies, 7.1% (n = 6) of AGA preterm babies, and 1.5% (n = 2) of AGA term newborns. A total of 55.6% of newborns were below normal weight (48.1% had low birth weight, 4.6% had very low birth weight, and 2.8% had extremely low birth weight). Conclusion Our study suggests that preterm newborns are more insulin resistant at birth than term newborns. SGA preterm babies are having a higher incidence of insulin resistance compared to AGA preterm babies. It is clear that high insulin level is needed to overcome high insulin resistance in the very early gestational period. Serum cortisol increases as gestational age and birth weight increase. Thus, serum cortisol helps in the maturation of the fetus and neonatal adaptation at birth.

4.
Cureus ; 14(11): e31532, 2022 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-36540507

RESUMEN

Diabetes mellitus in recent years has become a relentlessly evolving pandemic. Measures for the screening and early detection of diabetes are practiced all around the world. However, considering the ever-increasing magnitude of the problem, the present efforts should especially focus on the primordial prevention of diabetes. A ray of hope for preventing the development of diabetes in an individual arises from the concept that many adult-onset diseases have already been programmed while the individual was still in-utero. In women with hyperglycemia-in-pregnancy, maternal hyperglycemia results in fetal hyperinsulinemia, which leads to increased adiposity in the fetus, and insulin resistance and diabetes in adulthood. We have ventured to point out that the fetal beta-cells start secreting insulin at 10-11 weeks of pregnancy and fetal hyperinsulinemia persists with maternal hyperglycemia, in a pregnant woman who would develop gestational diabetes. Considering the fetal glucose-steal phenomenon and the fetal renal threshold for glucose, we have suggested a two-hour post-prandial blood-glucose (PPBG) value of >110 mg/dL as the cut-off for the prediction of gestational diabetes in the early weeks of pregnancy. Furthermore, we have emphasized the use of metformin in addition to medical nutrition therapy in the early weeks to maintain PPBG around 110 mg/dL to prevent gestational diabetes. In this paper, we recommend early, universal screening of all pregnant women during the early weeks of the first trimester and put forward that a two-hour PPBG of >110 mg/dl during the 8th-10th week of pregnancy would predict the risk of gestational diabetes in the pregnant woman. We suggest early testing and intervention to prevent the development of fetal hyperinsulinemia as a primordial prevention approach for diabetes.

5.
Ital J Pediatr ; 47(1): 197, 2021 Sep 30.
Artículo en Inglés | MEDLINE | ID: mdl-34593008

RESUMEN

BACKGROUND: Hypertrophic cardiomyopathy (HCM) in neonates is a rare and heterogeneous disorder. HCM accounts for 25 to 40% of all pediatric cardiomyopathy cases and the highest incidence in pediatric population is reported in children < 1 year. CASE PRESENTATION: we report two clinical cases of neonates, born to mothers respectively with a pre-pregnancy insulin-dependent diabetic mellitus type 2 and a suspected diabetes, with inadequate prenatal glycemic control for the first and underestimated glycemic control for the second case, with a different evolution. In the first case, a slow evidence of improvement of the HCM was observed, persuading us to the diagnosis of a diabetes-related HCM; In the second case the progressive worsening of the HCM during follow-up in association with further investigations, resulted in the diagnosis of Pompe disease. CONCLUSIONS: Hypertrophic cardiomyopathy in newborns can be the clinical expression of different underlying disorders. We aim to show the importance both to reassess maternal and family history and critically evaluate the physical examination in order to address the correct differential diagnosis. Furthermore it is important to continue a regular cardiologic follow-up for this pathology with neonatal onset to prevent a poor prognosis.


Asunto(s)
Cardiomiopatía Hipertrófica/diagnóstico , Enfermedad del Almacenamiento de Glucógeno Tipo II/diagnóstico , Embarazo en Diabéticas , Cardiomiopatía Hipertrófica/etiología , Diabetes Mellitus Tipo 2 , Femenino , Humanos , Recién Nacido , Embarazo
6.
J Clin Endocrinol Metab ; 106(8): 2279-2290, 2021 07 13.
Artículo en Inglés | MEDLINE | ID: mdl-33982055

RESUMEN

CONTEXT: The association of maternal gestational diabetes mellitus (GDM) with neurodevelopmental outcomes remains controversial and evidence that maternal increasing levels of glucose during pregnancy associated with the risk for impaired neurodevelopment were limited. OBJECTIVE: To identify the continuous association of increasing maternal glucose levels with neurodevelopmental disorders in offspring and explore the potential contribution of cord metabolites to this association. METHODS: The prospective birth cohort study included 1036 mother-child pairs. Primary predictors were maternal exposure GDM and maternal glucose values at a 75-g oral-glucose-tolerance test at 24 to 28 weeks during pregnancy. Primary neurodevelopmental outcomes at 12 months in offspring were assessed by the Ages and Stages Questionnaires, Third Edition (ASQ-3). RESULTS: Maternal GDM was associated with failing the communication domain in offspring in the adjusted models [relative risk (RR) with 95% CI: 1.97 (1.11, 3.52)]. Increasing levels of fasting plasma glucose (FPG), 1-h plasma glucose (1-h PG) and 2-h plasma glucose (2-h PG) with 1 SD change were at higher risks in failing the personal social domain of ASQ-3 [RRs with 95% CI for FPG: 1.49 (1.09, 2.04); for 1-h PG: 1.70 (1.27, 2.29); for 2-h PG: 1.36 (1.01, 1.84)]. The linear association was also demonstrated. Compared with girls, boys exposed to higher maternal glucose levels were inclined to the failure of the personal social domain. Mediation analysis showed the contribution of maternal GDM to failure of communication domain mediated by C-peptide. CONCLUSIONS: Maternal glucose levels below those diagnostic of diabetes are continuously associated with impaired neurodevelopment in offspring at 12 months.


Asunto(s)
Glucemia/metabolismo , Diabetes Gestacional/sangre , Efectos Tardíos de la Exposición Prenatal/sangre , Adulto , Femenino , Prueba de Tolerancia a la Glucosa , Humanos , Lactante , Masculino , Embarazo , Estudios Prospectivos
7.
J Prenat Med ; 5(3): 63-4, 2011 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-22439078

RESUMEN

Our report aims to verify whether perinatal maternal glycemic control in gestational diabetes can only be achieved with insulin or with oral hypoglycaemic agents. Then we want to evaluate the efficacy and safety of oral hypoglycemic agents in the treatment of gestational diabetes and then to compare these results with those associated with the use of insulin.

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