629: Gestational age and long term pediatric urinary morbidity of the offspring

Small for gestational age (SGA) and fetal growth restriction (FGR) is difficult to define exactly. In this pregnancy condition, the fetus does not reach its biological growth potential as a consequence of impaired placental function, which may be because of a variety of factors. Fetuses with FGR are at risk for perinatal morbidity and mortality, and poor long-term health outcomes, such as impaired neurological and cognitive development, and cardiovascular and endocrine diseases in adulthood. At present no gold standard for the diagnosis of SGA/FGR exists. The first aim of this review is to: summarize areas of consensus and controversy between recently published national guidelines on small for gestational age or fetal growth restriction; highlight any recent evidence that should be incorporated into existing guidelines. Another aim to summary a number of interventions which are being developed or coming through to clinical trial in an attempt to improve fetal growth in placental insufficiency. Key words: fetal growth restriction (FGR), Small for gestational age (SGA)

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One-Year Data from a Long-Term Phase IV Study of Recombinant Human Growth Hormone in Short Children Born Small for Gestational Age

Biologics in Therapy ◽

10.1007/s13554-014-0014-4 ◽

2014 ◽

Vol 4 (1-2) ◽

pp. 1-13 ◽

Cited By ~ 9

Author(s):

Hans-Peter Schwarz ◽

Dorota Birkholz-Walerzak ◽

Mieczyslaw Szalecki ◽

Mieczyslaw Walczak ◽

Corina Galesanu ◽

...

Keyword(s):

Growth Hormone ◽

Human Growth Hormone ◽

Gestational Age ◽

Small For Gestational Age ◽

Recombinant Human Growth Hormone ◽

Human Growth ◽

Short Children ◽

One Year ◽

Phase Iv

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The Relative Kicking Frequency of Infants Born Full-term and Preterm During Learning and Short-term and Long-term Memory Periods of the Mobile Paradigm

Physical Therapy ◽

10.1093/ptj/85.1.8 ◽

2005 ◽

Vol 85 (1) ◽

pp. 8-18 ◽

Cited By ~ 29

Author(s):

Jill C Heathcock ◽

Anjana N Bhat ◽

Michele A Lobo ◽

James (Cole) Galloway

Keyword(s):

Gestational Age ◽

Short Term Memory ◽

Full Term ◽

Long Term Memory ◽

Early Assessment ◽

Short Term ◽

Term Memory ◽

Lack Of Control ◽

Specific Manner

Abstract Background and Purpose. Infants born preterm differ in their spontaneous kicking, as well as their learning and memory abilities in the mobile paradigm, compared with infants born full-term. In the mobile paradigm, a supine infant's ankle is tethered to a mobile so that leg kicks cause a proportional amount of mobile movement. The purpose of this study was to investigate the relative kicking frequency of the tethered (right) and nontethered (left) legs in these 2 groups of infants. Subjects. Ten infants born full-term and 10 infants born preterm (<33 weeks gestational age, <2,500 g) and 10 comparison infants participated in the study. Methods. The relative kicking frequencies of the tethered and nontethered legs were analyzed during learning and short-term and long-term memory periods of the mobile paradigm. Results. Infants born full-term showed an increase in the relative kicking frequency of the tethered leg during the learning period and the short-term memory period but not for the long-term memory period. Infants born preterm did not show a change in kicking pattern for learning or memory periods, and consistently kicked both legs in relatively equal amounts. Discussion and Conclusion. Infants born full-term adapted their baseline kicking frequencies in a task-specific manner to move the mobile and then retained this adaptation for the short-term memory period. In contrast, infants born preterm showed no adaptation, suggesting a lack of purposeful leg control. This lack of control may reflect a general decrease in the ability of infants born preterm to use their limb movements to interact with their environment. As such, the mobile paradigm may be clinically useful in the early assessment and intervention of infants born preterm and at risk for future impairment.

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Neonatal Mortality and Long-Term Outcome of Infants Born between 27 and 32 Weeks of Gestational Age in Breech Presentation: The EPIPAGE Cohort Study

PLoS ONE ◽

10.1371/journal.pone.0145768 ◽

2016 ◽

Vol 11 (1) ◽

pp. e0145768 ◽

Cited By ~ 12

Author(s):

Elie Azria ◽

Gilles Kayem ◽

Bruno Langer ◽

Laetitia Marchand-Martin ◽

Stephane Marret ◽

...

Keyword(s):

Cohort Study ◽

Neonatal Mortality ◽

Gestational Age ◽

Breech Presentation ◽

Term Outcome ◽

Long Term Outcome

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Predictors of long-term outcome in very preterm infants: Gestational age versus neonatal cranial ultrasound.

Journal of Developmental & Behavioral Pediatrics ◽

10.1097/00004703-200402000-00029 ◽

2004 ◽

Vol 25 (1) ◽

pp. 74

Author(s):

M. M. M.

Keyword(s):

Preterm Infants ◽

Gestational Age ◽

Cranial Ultrasound ◽

Term Outcome ◽

Long Term Outcome ◽

Very Preterm Infants ◽

Very Preterm

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969: Long-term cardiovascular outcome of small for gestational age infants born to women with and without gestational diabetes mellitus

American Journal of Obstetrics and Gynecology ◽

10.1016/j.ajog.2017.11.456 ◽

2018 ◽

Vol 218 (1) ◽

pp. S573

Author(s):

Gali Pariente ◽

Tamar Wainstock ◽

Daniella Landao ◽

Eyal Sheiner

Keyword(s):

Diabetes Mellitus ◽

Gestational Diabetes ◽

Gestational Diabetes Mellitus ◽

Gestational Age ◽

Small For Gestational Age ◽

Cardiovascular Outcome

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SUN-690 HNF4A Mutation in Siblings with Diazoxide Responsive Congenital Hyperinsulinism

Journal of the Endocrine Society ◽

10.1210/jendso/bvaa046.1205 ◽

2020 ◽

Vol 4 (Supplement_1) ◽

Author(s):

Ayca Erkin-Cakmak ◽

Hannah Chesser ◽

Joseph Shieh ◽

Christine Ferrara ◽

Stephen Eric Gitelman ◽

...

Keyword(s):

Gestational Age ◽

Extended Family ◽

Late Onset ◽

Genetic Evaluation ◽

Congenital Hyperinsulinism ◽

Onset Diabetes ◽

Long Term Follow Up ◽

Appropriate For Gestational Age ◽

Loss Variant

Abstract Background: Congenital hyperinsulinism (HI) is the leading cause of severe, persistent hypoglycemia in infants. Transient HI seen at risk neonates due to prenatal stress and some of the congenital HI cases due to mutations in K-ATPase channel are responsive to diazoxide. It is not a common practice to obtain genetic evaluation for diazoxide responsive HI. However, children with dominant inactivating variants in HNF4A gene may present with diazoxide-responsive HI and mimic transient HI in infancy. Objective: To describe two siblings with diazoxide responsive HI with HNF4A mutation associated with maturity onset diabetes of youth type 1 (MODY1). Clinical Case: Case 1, term female with macrosomia and Case 2, preterm male appropriate for gestational age were born to same mother without gestational diabetes and with no perinatal stress. Siblings were non-dysmorphic and both presented with hypoglycemia during first week of life. Diagnosis of HI is confirmed based on inappropriately suppressed β-hydroxybutyrate at the time of hypoglycemia and inappropriate glycemic response to glucagon consistent with increased insulin action. Both siblings responded to diazoxide therapy. Family history was significant for late-onset diabetes in paternal extended family. Case 1 required very low dose diazoxide (2 mg/kg/day) during first year of life to sustain normoglycemia. She came off of diazoxide at 19 months of age. Case 2 is normoglycemic on 5mg/kg/day diazoxide at 4 months of age. Genetic evaluation through whole exome sequencing pursued upon diagnosis of Case 2 revealed paternally inherited heterozygous pathogenic start loss variant in HNF4A gene (c.3G>T) in both siblings. Father was completely asymptomatic without any history of hypo- or hyperglycemia. Conclusion: HNF4A gene encodes hepatocyte nuclear factor-4-alpha that regulates hepatic gluconeogenesis and lipid metabolism. Dominant inactivating variants in HNF4A gene associated with familial HI, are typically associated with increased size for gestational age, mild diazoxide-responsive hypoglycemia (which may be transient) and monogenic diabetes during adolescence. HNF4A mutations were described as one of the most common genetic cause of diazoxide-responsive congenital hyperinsulinism and are associated with MODY1. It is important to consider genetic evaluation in diazoxide responsive HI cases. Identifying children with HNF4A variant early on will impact their long-term follow-up leading to earlier diagnosis and treatment of MODY-1 and potentially improve long-term outcomes.

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