Diabetic Embryopathy Research Articles

Type 1 Diabetes and Pregnancy: Challenges in Glycemic Control and Maternal-Fetal Outcomes.

Managing type 1 diabetes during pregnancy presents significant challenges due to physiological and hormonal changes. These factors contribute to major changes in insulin sensitivity, complicating efforts to achieve and sustain optimal blood glucose levels. Poorly controlled glucose levels during pregnancy can result in diabetic embryopathy and elevate the risks of maternal complications such as hypertensive disorders and diabetic ketoacidosis. Fetal complications may include preterm birth, fetal demise, and admission to neonatal intensive care units. It is essential to recognize that there is no universal approach to managing glycemic control in pregnant women with T1DM and care should be individualized. Effective management requires a multidisciplinary approach involving regular monitoring, adjustments in insulin therapy, dietary modifications, and consistent prenatal care. Continuous glucose monitoring has emerged as a valuable tool for real-time glucose monitoring, facilitating tighter glycemic control. Education and support for self-management are important in addressing these challenges. Future developments in technology and personalized approaches to care show promising potential for advancing diabetes management during pregnancy. This provides a comprehensive overview of current literature on the challenges with the management of T1DM during pregnancy, focusing on its impact on maternal and neonatal outcomes and highlighting effective strategies for achieving optimal glycemic control.

Diabetes and Early Development: Epigenetics, Biological Stress, and Aging.

Pregestational diabetes, either type 1 or type 2 diabetes, induces structural birth defects including neural tube defects and congenital heart defects in human fetuses. Rodent models of type 1 and type 2 diabetic embryopathy have been established and faithfully mimic human conditions. Hyperglycemia of maternal diabetes triggers oxidative stress in the developing neuroepithelium and the embryonic heart leading to the activation of proapoptotic kinases and excessive cell death. Oxidative stress also activates the unfolded protein response and endoplasmic reticulum stress. Hyperglycemia alters epigenetic landscapes by suppressing histone deacetylation, perturbing microRNA (miRNA) expression, and increasing DNA methylation. At cellular levels, besides the induction of cell apoptosis, hyperglycemia suppresses cell proliferation and induces premature senescence. Stress signaling elicited by maternal diabetes disrupts cellular organelle homeostasis leading to mitochondrial dysfunction, mitochondrial dynamic alteration, and autophagy impairment. Blocking oxidative stress, kinase activation, and cellular senescence ameliorates diabetic embryopathy. Deleting the mir200c gene or restoring mir322 expression abolishes maternal diabetes hyperglycemia-induced senescence and cellular stress, respectively. Both the autophagy activator trehalose and the senomorphic rapamycin can alleviate diabetic embryopathy. Thus, targeting cellular stress, miRNAs, senescence, or restoring autophagy or mitochondrial fusion is a promising approach to prevent poorly controlled maternal diabetes-induced structural birth defects. In this review, we summarize the causal events in diabetic embryopathy and propose preventions for this pathological condition. KEY POINTS: · Maternal diabetes induces structural birth defects.. · Kinase signaling and cellular organelle stress are critically involved in neural tube defects.. · Maternal diabetes increases DNA methylation and suppresses developmental gene expression.. · Cellular apoptosis and senescence are induced by maternal diabetes in the neuroepithelium.. · microRNAs disrupt mitochondrial fusion leading to congenital heart diseases in diabetic pregnancy..

Central Nervous System Malformations Associated with Diabetic Embryopathy in Latin American Mothers without Glycemic Control: A Review

Objetivo: Describir las malformaciones del sistema nervioso asociadas a embriopatía diabética en madres sin adecuado control glicémico en Latinoamérica. Material y métodos: Se realizó una revisión minuciosa de publicaciones en reconocidas bases de datos en línea en español y en inglés. Los buscadores utilizados incluyeron MEDLINE, PubMed, Scielo, BVS, HINARI, EBSCO, Google Scholar. Se encontraron artículos de tipo descriptivo, observacional, retrospectivo, guías de práctica clínica, revisión sistemática, casos y controles, y metaanálisis. Resultados: Mediante la revisión sistematizada de artículos, se obtuvo que las malformaciones del sistema nervioso central secundarias a la embriopatía diabética guardan una relacion estrecha con diversos factores de riesgo de la mujer latinoamericana. Conclusiones: Se encontró asociación entre las características epidemiológicas multifactoriales de la mujer latinoamericana y el desarrollo de malformaciones del sistema nervioso central secundarias a embriopatia diabetica, resultantes de multiples procesos fisiopatológicos desencadenados por la hipeglicemia materna.

Nerolidol Attenuates Diabetic Embryopathy in Streptozotocin-induced Diabetic Pregnant Rats by Reducing Embryonic and Maternal Oxidative Stress

Background Pregnancy complicated by diabetes leads to congenital disorders, spontaneous abortion, and neonatal morbidity and mortality, which are termed diabetic embryopathy or fetopathy. Objectives In this work, we planned to investigate the therapeutic potentials of nerolidol against streptozotocin (STZ)-induced diabetic embryopathy in rats through attenuating maternal and fetal oxidative stress. Materials and Methods The male and female Wistar rats were allowed to mate for a night at a 1:1 ratio. After the confirmation of pregnancy, the rats were administered 40 mg/kg of STZ (i.p.) to initiate diabetes and treated with 20 and 40 mg/kg of nerolidol. The changes in food intake, body weight, blood glucose, and urine output were regularly monitored. The levels of lipid profiles were estimated using assay kits. The oxidative stress and antioxidant biomarkers in the liver tissues and embryonic fractions were measured using assay kits. Results The nerolidol treatment considerably depleted the blood glucose and urine output and augmented the body weight and diet intake in diabetic rats. The nerolidol suppressed the cholesterol (Ch), triglycerides (TG), and very low density lipoprotein (VLDL) and elevated the high density lipoprotein (HDL) level in diabetic pregnant rats. The maternal and embryonic oxidative stress levels are effectively reduced by the nerolidol treatment by decreasing the malondialdehyde (MDA) and reactive oxygen species (ROS) levels. The levels of antioxidants were also increased by the nerolidol on both liver and embryonic fractions of diabetic pregnant rats. Conclusion Our results exhibited that the nerolidol treatment considerably reduced embryonic and maternal oxidative stress and embryonic deaths. Hence, it can be a hopeful therapeutic candidate to treat diabetic embryopathy.

Effects of dietary polyphenols on maternal and fetal outcomes in maternal diabetes.

The incidences of short-term or long-term adverse maternal and fetal outcomes caused by maternal diabetes are increasing. Due to toxicity or side effects, economic pressures, and other problems associated with injections or oral hypoglycemic drugs, many researchers have investigated natural treatment methods. Polyphenols can protect against chronic pathologies by regulating numerous physiological processes and provide many health benefits. Moreover, polyphenols have anti-diabetic properties and can be used to treat diabetic complications. Diets rich in polyphenols are beneficial to pregnant women with diabetes. Here, we review the epidemiological and experimental evidence on the impact of dietary polyphenols on maternal and fetal outcomes in pregnant women with diabetes, and the effects of polyphenols on biological changes and possible mechanisms. Previous data (mainly from in vitro and animal experiments) showed that polyphenols can alleviate gestational diabetes mellitus and diabetic embryopathy by reducing maternal hyperglycemia and insulin resistance, alleviating inflammation and oxidative stress, and regulating related signaling pathways. Although polyphenols have shown many health benefits, further research is needed to better understand the complex interactions between polyphenols and maternal diabetes.

Nigericin Abrogates Maternal and Embryonic Oxidative Stress in the Streptozotocin-Induced Diabetic Pregnant Rats.

Hyperglycemic exposure in diabetic pregnancy can lead to many developmental changes, such as delayed development, fetal malformations, and fetal/embryo death. These detrimental complications are collectively known as diabetic embryopathy or teratogenesis. The current study focuses to discover the therapeutic properties of the nigericin against the STZ-stimulated diabetic embryopathy via alleviation of maternal and embryonic oxidative stress. The male and female rats at a 1:1 ratio were permitted to mate overnight to establish the course of pregnancy. The pregnant rats were distributed into four groups control, diabetic pregnant (via administering 40mg/kg of STZ), and diabetic + 10 and 20mg/kg of nigericin-administered (via oral gavage from days 5 to 12) groups, respectively. The glucose level, urine output, diet intake, and body weight were determined carefully. The embryo and placenta weight and implantation rates were examined, and data were tabulated. The total protein and lipid profiles were assessed using respective kits. The oxidative stress markers and antioxidant enzymes were examined using respective assay kits. The 10 and 20mg/kg of nigericin treatment decreased the glucose level and urine output and improved the diet intake and body weight gain in diabetic pregnant rats. The nigericin also decreased the total protein, cholesterol, triglycerides, and very-low-density lipoprotein (VLDL) and improved the high-density lipoprotein (HDL) in the serum of pregnant rats. The levels of malondialdehyde (MDA), reactive oxygen species (ROS), and protein carbonyls were decreased by the nigericin in both liver and embryos of the pregnant rats. The levels of glutathione (GSH), total thiols, and activities of catalase (CAT), glutathione reductase (GR), superoxide dismutase (SOD), glutathione peroxidase (GPX), and glutathione S-transferase (GST) were improved by the nigericin in the diabetic pregnant rats. Altogether, these results provide evidence that nigericin treatment remarkably attenuates the diabetes-stimulated embryopathy in rats. The nigericin effectively decreased embryo lethality, reduced glucose and dyslipidemia, and relieves oxidative stress via upregulating the antioxidant enzyme activities. Hence, it can be a talented therapeutic agent to treat diabetic pregnancy-associated complications.

Diabetic Embryopathies.

Diabetic embryopathy is defined as congenital anomalies that are linked to maternal diabetes. The association between diabetes and fetal, neonatal, and long-term complications is well-established. These complications include organ or structural maldevelopment, fetal growth abnormalities, and learning/psychiatric comorbidities. Recent studies have elucidated the pathophysiology behind these conditions and outlined new management approaches. Caudal regression syndrome, also known as sacral agenesis, is a well-known but less described complication of maternal diabetes. The purpose of this review is to summarize existing research on common neonatal morbidities in infants of mothers with diabetes with a focus on caudal regression syndrome and its long-term associations.

Neonate with Respiratory Distress, Bilateral Microtia, Hypocalcemia, and Lymphopenia.

Neonate with Respiratory Distress, Bilateral Microtia, Hypocalcemia, and Lymphopenia.

Congenital Abnormalities in the Infant of a Diabetic Mother.

Diabetes mellitus is among the most common chronic diseases worldwide. Infants of diabetic mothers are at increased risk of having congenital abnormalities. Tremendous progress has been achieved in the pregnancy care of diabetic women; however, the risk of birth defects associated with maternal diabetes still exists. These anomalies might arise in many organs and systems of the developing fetus. Many mechanisms have been implicated in the teratogenicity of maternal diabetes and it is critical to achieve good glycemic control before conception in women with diabetes. Neonatal clinicians must be able to identify patients at risk and recognize the signs of diabetic embryopathy. This article presents a review of congenital anomalies associated with maternal diabetes.

Ocimum basilicum alleviates blood glucose, lipid profile and iNOS in diabetes gestational rat model.

Gestational diabetes (GDM) complications affect maternal and fetus in utero. GDM's vascular dysfunction showed inducible nitric oxide synthase (iNOS) alteration and was linked to the higher production of nitrogen species, leading to diabetic embryopathy. Ocimum basilicum (O.basilicum) has been reported for its anti-inflammatory and anti-diabetic effects. Thus, the present study investigates the anti-diabetic effect, lipid-lowering effect, and iNOS expression in GDM animal models treated with O.basilicum extract. Four groups of pregnant rats consist of control and GDM groups. One GDM group was set for control positive. Two GDM groups were treated with O.basilicum extract in two doses (100 and 200mg/kg BW) for 14days. Blood glucose of all groups was observed at 72h after STZ injection and 14days after administration of O.basilicum extract. Lipid profile and iNOS expression using real-time PCR were measured afterward. O.basilicum extract lowered blood glucose levels in both doses, from 262.60mg/dL±6.89-136.80mg/dL ±15.6mg/dL and 113.20mg/dL±5.25mg/dL. Total cholesterol, LDL and triglyceride showed a reduction, especially in200mg/kg BW dose extract from 122.37mg/dL ±14.84mg/dL, 69.75mg/dL±3.78mg/dL and 137.51mg/dL ±8.12-74.64mg/dL±8.71mg/dL, 40.26mg/dL±3.31mg/dL and 87.57mg/dL±6.29mg/dL, respectively. iNOS expression downregulated in both doses, from 2.17±0.39 to 0.94±0.3 and 0.41±0.08. This study showed that O.basilicum extract has a potential therapeutic activity in lowering blood glucose, improved lipid profile, and downregulating iNOS in GDM.

Hexokinase-2-Linked Glycolytic Overload and Unscheduled Glycolysis-Driver of Insulin Resistance and Development of Vascular Complications of Diabetes.

The recent discovery of the glucose-induced stabilization of hexokinase-2 (HK2) to proteolysis in cell dysfunction in model hyperglycemia has revealed a likely key initiating factor contributing to the development of insulin resistance and vascular complications in diabetes. Consequently, the increased flux of glucose metabolism without a change in the expression and activity of glycolytic enzymes produces a wave of increased glycolytic intermediates driving mitochondrial dysfunction and increased reactive oxygen species (ROS) formation, the activation of hexosamine and protein kinase C pathways, the increased formation of methylglyoxal-producing dicarbonyl stress, and the activation of the unfolded protein response. This is called HK2-linked glycolytic overload and unscheduled glycolysis. The conditions required to sustain this are GLUT1 and/or GLUT3 glucose uptake and the expression of HK2. A metabolic biomarker of its occurrence is the abnormally increased deposition of glycogen, which is produced by metabolic channeling when HK2 becomes detached from mitochondria. These conditions and metabolic consequences are found in the vasculature, kidneys, retina, peripheral nerves, and early-stage embryo development in diabetes and likely sustain the development of diabetic vascular complications and embryopathy. In insulin resistance, HK2-linked unscheduled glycolysis may also be established in skeletal muscle and adipose tissue. This may explain the increased glucose disposal by skeletal uptake in the fasting phase in patients with type 2 diabetes mellitus, compared to healthy controls, and the presence of insulin resistance in patients with type 1 diabetes mellitus. Importantly, glyoxalase 1 inducer—trans-resveratrol and hesperetin in combination (tRES-HESP)—corrected HK2-linked glycolytic overload and unscheduled glycolysis and reversed insulin resistance and improved vascular inflammation in overweight and obese subjects in clinical trial. Further studies are now required to evaluate tRES-HESP for the prevention and reversal of early-stage type 2 diabetes and for the treatment of the vascular complications of diabetes.

Preterm Infant of Diabetic Mother with a Retrorectal Mass: A Troubling Tail Tale.

Preterm Infant of Diabetic Mother with a Retrorectal Mass: A Troubling Tail Tale.

Embryonic hyperglycemia perturbs the development of specific retinal cell types, including photoreceptors.

Diabetes is linked to various long-term complications in adults, such as neuropathy, nephropathy and diabetic retinopathy. Diabetes poses additional risks for pregnant women, because glucose passes across the placenta, and excess maternal glucose can result in diabetic embryopathy. While many studies have examined the teratogenic effects of maternal diabetes on fetal heart development, little is known about the consequences of maternal hyperglycemia on the development of the embryonic retina. To address this question, we investigated retinal development in two models of embryonic hyperglycemia in zebrafish. Strikingly, we found that hyperglycemic larvae displayed a significant reduction in photoreceptors and horizontal cells, whereas other retinal neurons were not affected. We also observed reactive gliosis and abnormal optokinetic responses in hyperglycemic larvae. Further analysis revealed delayed retinal cell differentiation in hyperglycemic embryos that coincided with increased reactive oxygen species (ROS). Our results suggest that embryonic hyperglycemia causes abnormal retinal development via altered timing of cell differentiation and ROS production, which is accompanied by visual defects. Further studies using zebrafish models of hyperglycemia will allow us to understand the molecular mechanisms underlying these effects.

Imaging Review of Obstetric Sequelae of Maternal Diabetes Mellitus

Diabetes mellitus, whether preexisting or gestational, poses significant risk to both the mother and the developing fetus. A myriad of potential fetal complications in the setting of diabetic pregnancies include, among others, congenital anomalies, delayed fetal lung maturity, macrosomia, and increased perinatal morbidity and mortality. Congenital anomalies most commonly involve the nervous, cardiovascular, genitourinary, and musculoskeletal systems. Delayed fetal lung maturity, probably secondary to hyperglycemia suppressing surfactant secretion, is a major determinant of perinatal morbidity and mortality. Besides the potential complications encountered during cesarean delivery in macrosomic fetuses, vaginal delivery is also associated with increased risks of shoulder dystocia, clavicular and humeral fractures, and brachial plexus palsy. Maternal complications are related to the increased risk of hypertensive diseases of pregnancy and associated preeclampsia and hemolysis, elevated liver function, and low platelets (HELLP) syndrome, as well as complications encountered at the time of delivery secondary to fetal macrosomia and cesarean delivery. Additional conditions encountered in the setting of maternal diabetes include polyhydramnios, placental thickening, and two-vessel umbilical cord, each of which is associated with adverse fetal and maternal outcomes including fetal growth restriction, preterm labor, placental abruption, and premature rupture of membranes. Imaging plays a vital role in the evaluation of the mother and the fetus and can provide invaluable information that can be used by maternal fetal medicine to manage this patient population effectively. The authors review the pathophysiologic alterations induced by diabetes in pregnancy, discuss the imaging spectrum of diabetic embryopathy, and provide a detailed review of potential associated maternal complications. Online supplemental material is available for this article.©RSNA, 2021.

Experience with cultured thymus tissue in 105 children

Currently, there are no approved therapies to treat congenital athymia, a condition of immune deficiency resulting in high early mortality due to infection and immune dysregulation. Multiple syndromic conditions, such as complete DiGeorge syndrome, 22q11.2 deletion syndrome, CHARGE (coloboma, heart defects, choanal atresia, growth or mental retardation, genital hypoplasia, and ear anomalies and/or deafness) syndrome, diabetic embryopathy, other genetic variants, and FOXN1 deficiency, are associated with congenital athymia. Our aims were to study 105 patients treated with cultured thymus tissue (CTT), and in this report, to focus on the outcomes of 95 patients with treatment-naive congenital athymia. A total of 10 prospective, single-arm open-label studies with patient enrollment from 1993 to 2020 form the basis of this data set. Patients were tested after administration of CTT for T-cell development; all adverse events and infections were recorded. A total of 105 patients were enrolled and received CTT (the full analysis set). Of those patients, 10 had diagnoses other than congenital athymia and/or received prior treatments. Of those 105 patients, 95 patients with treatment-naive congenital athymia were included in the efficacy analysis set (EAS). The Kaplan-Meier estimated survival rates at year 1 and year 2 after administration of CTT in the EAS were 77% (95% CI=0.670-0.844) and 76% (95% CI= 0.657-0.834), respectively. In all, 21 patients died in the first year before developing naive T cells and 1 died in the second year after receipt of CTT; 3 subsequent deaths were not related to immunodeficiency. Afew patients developed alopecia, autoimmune hepatitis, psoriasis, and psoriatic arthritis after year 1. The rates of infections, autologous graft-versus-host-disease manifestations, and autoimmune cytopenias all decreased approximately 1 year after administration of CTT. Treatment with CTT led to development of naive T cells with a 1-year survival rate of 77% and a median follow-up time of 7.6 years. Immune reconstitution sufficient to prevent infections and support survival typically develops 6 to12 months after administration of CTT.

Diabetic Embryopathy Susceptibility in Mice Is Associated with Differential Dependence on Glucosamine and Modulation of High Glucose-Induced Oxidative Stress.

The high KM glucose transporter, GLUT2 (SLC2A2), is expressed by embryos and causes high rates of glucose transport during maternal hyperglycemic episodes in diabetic pregnancies and causes congenital malformations (diabetic embryopathy). GLUT2 is also a low KM transporter of the amino sugar, glucosamine (GlcN), which enters the hexosamine biosynthetic pathway (HBP) and provides substrate for glycosylation reactions. Exogenous GlcN also increases activity of the pentose phosphate pathway (PPP), which increases production of NADPH reducing equivalents. GLUT2-transported GlcN is inhibited by high glucose concentrations. Not all mouse strains are susceptible to diabetic embryopathy. The aim of this study was to test the hypothesis that susceptibility to diabetic embryopathy is related to differential dependence on exogenous GlcN for glycosylation or stimulation of the PPP. We tested this using murine embryonic stem cell (ESC) lines that were derived from embryopathy-susceptible FVB/NJ (FVB), and embryopathy-resistant C57Bl/6J (B6), embryos in the presence of low or high glucose, and in the presence or absence of GlcN. There were no significant differences in Glut2 expression, or of glucose or GlcN transport, between FVB and B6 ESC. GlcN effects on growth and incorporation into glycoproteins indicated that FVB ESC are more dependent on exogenous GlcN than are B6 ESC. GlcN stimulated PPP activity in FVB but not in B6 ESC. High glucose induced oxidative stress in FVB ESC but not in B6 ESC. These results indicate that FVB embryos are more dependent on exogenous GlcN for glycosylation, but also for stimulation of the PPP and NADPH production, than are B6 embryos, thereby rendering FVB embryos more susceptible to high glucose to induce oxidative stress.

Intracellular Metabolism in Diabetic Embryopathy

Diabetes mellitus in early pregnancy can cause congenital birth defects in infants, a complication known as diabetic embryopathy. Formation of structural abnormalities, commonly seen in the central nervous and cardiovascular systems, is associated with increased programmed cell death (apoptosis) and decreased cell proliferation in the developing organs. Under maternal hyperglycemic conditions, influx of glucose into cells of the embryos disturbs intracellular metabolic homeostasis. Disturbed glycolysis generates factors through side pathways to perturb cell signaling and organelle functions. Perturbed phospholipid metabolism produces signaling metabolites and peroxidation products to suppress cell survival and induce apoptosis. Targeting the key processes and factors in the metabolism of glucose and phospholipids is a potential intervention strategy to prevent birth defects in diabetic pregnancies.

Verbascoside-enriched fraction from Buddleja cordata Kunth ameliorates the effects of diabetic embryopathy in an animal model.

The deleterious effects of diabetes mellitus (DM) over development are apparently due to an increase in oxidative stress. Some antioxidants could prevent developmental alterations produced by diabetic state. Extracts of plants of the genus Buddleja are used traditionally for Mexican indigens to ameliorate some diseases. The purpose of this work was to evaluate the effect of the extract of Buddleja cordata over diabetic embryopathy. Two experimental approaches were used: an in vivo study and an in vitro model. In the first, rats were treated with streptozotocin, streptozotocin plus methanolic extract of B. cordata, or none. Females were sacrificed at gestational day (GD) 19, and biochemical clinical parameters were measured; also, the fetuses were obtained and morphologically analyzed. In the in vitro model, a verbascoside-enriched fraction (VEF) of the extract was used in whole embryo culture in order to search for the mechanisms for embryoprotection effect over hyperglycemia-induced malformations. In the in vivo experiments, B. cordata extract reduces the frequency and severity of fetal malformations produced by chemically induced diabetes, and additionally partially ameliorates the diabetic condition; in the in vitro model, both severity and frequency of embryo dysmorphogenesis were reduced by the VEF; also, this fraction reduces lipoperoxidation without affecting the activity of the antioxidant enzymes. The results suggest that verbascoside of methanolic extract and enriched fraction can directly affect the redox state, and thus, prevents the embryotoxicity mediated by oxidative stress, in embryos of diabetic pregnancy.

Maternal diabetes-related malformations in Utah: A population study of birth prevalence 2001-2016.

Maternal pregestational diabetes mellitus is associated with an increased risk for congenital malformations of about 2-4 times the background risk. Notably, the types and patterns of congenital malformations associated with maternal diabetes are nonrandom, with a well-established increased risk for specific classes of malformations, especially of the heart, central nervous system, and skeleton. While the increased risk in clinical and epidemiological studies is well documented in the literature, a precise estimate of overall birth prevalence of these specific congenital malformations among women with maternal pregestational diabetes, is lacking. The purpose of this study was to determine total prevalence of structural malformations associated with maternal pregestational diabetes mellitus in a population-based study. We identified infants with specific birth defects whose mother had pregestational diabetes mellitus in the Utah Birth Defect Network (UBDN), an active birth defects surveillance program that registers the occurrence of selected structural defects in the state of Utah. We defined specific maternal diabetes-related malformations based on epidemiologic and clinical studies in the literature. Of the 825,138 recorded Utah births between 2001 and 2016, a total of 91 cases were identified as likely having diabetic embryopathy within UBDN data. The prevalence of diabetes-related congenital malformation cases was calculated per year; the overall prevalence of diabetes-related malformations 2001-2016 was 1.1 per 10,000 births in Utah (95% CI, 0.9-1.3). Knowledge of the overall prevalence of diabetes-related malformations is important in predicting the number of cases that are potentially prevented with the implementation of programs to foster preconceptional management of maternal pregestational diabetes.

DiGeorge anomaly associated with diabetic embryopathy in an infant without a deletion on chromosome 22q11

DiGeorge anomaly associated with diabetic embryopathy in an infant without a deletion on chromosome 22q11