The missing umbilical artery. II. Paediatric follow-up.

Bryan, Elizabeth; Köhler, Henrik

doi:10.1136/adc.50.9.714

Cited by 21 publications

(7 citation statements)

References 12 publications

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“…Examples of this are the variations in size and source of the samples; reports exist on series of consecutive births [10], of fetuses with prenatal diagnosis of SUA, rates of SUA in pregnancy terminations, and in fetuses or newborns with malformations [27]. In some studies, the data were obtained prospectively from autopsies and placentas [28]; in others, data were obtained retrospectively from records of LBs with and without malformations [18], as well as from the prospective follow-up of newborn infants [14,29]. Descriptions can be found of data obtained retrospectively from registers of placentas [28], autopsies [30], and from hospital records of newborns with SUA diagnosed at birth [19].…”

Section: Discussionmentioning

confidence: 99%

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Single Umbilical Artery and Associated Malformations in over 5500 Autopsies: Relevance for Perinatal Management

Rittler

Mazzitelli

Fuksman³

et al. 2010

Pediatr Dev Pathol

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With a birth prevalence rate of about 1%, single umbilical artery (SUA) is the most frequent of all congenital anomalies. It is recognizably associated with a variety of birth defects, but disagreement exists as to whether a SUA can predict an adverse perinatal outcome; disagreement also exists related to if, when present, other birth defects should be ruled out. The aims of the study were to estimate the association between SUA and other birth defects in a series of perinatal autopsies, to establish if preferential associations between SUA and certain birth defects exist, and to quantify the risks for other birth defects when a SUA is diagnosed. In a series of 5539 perinatal autopsies conducted at the Hospital Materno Infantil Ramón Sardá and the Private Laboratory of Perinatal Pathology, Buenos Aires, Argentina, the rate of each malformation (grouped by organ/system) associated with SUA and the risks of associated malformations were estimated. In this series of autopsies, the rate of SUA showed a 10-fold increase when other malformations were present. The risk for other malformations increased significantly, by a 3-fold to 9-fold measure, when a SUA was present. Urinary and gut anomalies showed a preferential association with SUA. The absence of other birth defects lowered the risk of chromosome anomalies associated with SUA in 56% (odds ratio = 0.44). These results, obtained from a series of perinatal autopsies, are in agreement with most observations found in the literature, namely, high association rates between SUA and urinary and cardiovascular anomalies as well as a low risk for chromosome anomalies in SUA cases without other malformations.

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Section: Discussionmentioning

confidence: 99%

“…It has also been associated with maternal diabetes, preeclampsia, and poli-and oligohydramnios [1,12], and its prevalence is about 4 times higher in autopsy reports [13] or when other BDs [12,[14][15][16] (unspecific [10,17,18] or giving rise to recognizable patterns, such as in Potter or caudal regression [19,20]) are present.…”

Section: Introductionmentioning

confidence: 99%

Single Umbilical Artery and Associated Malformations in over 5500 Autopsies: Relevance for Perinatal Management

Rittler

Mazzitelli

Fuksman³

et al. 2010

Pediatr Dev Pathol

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“…A single umbilical artery, which is found in fewer than 1% of deliveries (Bryan and Kohler 1975), has not been 90 Fig. 3 A, B Genetic analysis of the hGH/hPL cluster of the HPLdeficient placenta DNA.…”

Section: Discussionmentioning

confidence: 99%

Absence of human placental lactogen and placental growth hormone (HGH-V) during pregnancy: PCR analysis of the deletion

et al. 1998

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Human placental lactogen (HPL) is produced in large amounts in normal pregnancies. We report a pregnancy with complete lack of HPL and the placental variant of the human growth hormone HGH-V. The pregnancy resulted in a severely growth-retarded but otherwise normal male baby. PCR analysis of DNA extracted from the placenta showed that the HPL encoding genes hPL-4 and hPL-3 were deleted along with the human growth hormone variant gene (hGH-V), which is located between these two active hPL genes and also expressed in the normal placenta. Of the five members of this multigene family, hGH-N, which is expressed in the pituitary gland, and hPL-1, a presumed pseudogene, were left intact. The latter (hPL-1) was expressed as RNA transcripts only at very low levels as is usually reported in normal pregnancies. Analysis of the parents' DNA showed that both of them carried a different heterozygous deletion at the 3' end of the hGH/hPL locus.

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“…Velamentous umbilical cord insertion occurs in 0.24 -1.8% of all singleton pregnancies and is associated with circulating disturbances and IUGR [192,194]. Both hypo-and hypercoiled cords may cause reduced umbilical blood flow, decreased placental blood flow and concequently IUGR [195][196][197].…”

Section: Umbilical Cord Anomaliesmentioning

confidence: 98%

“…Pregnancies with one umbilical artery may be associated with chromosome defects, fetal anomalies, IUGR and increased fetal mortality [192,193]. Velamentous umbilical cord insertion occurs in 0.24 -1.8% of all singleton pregnancies and is associated with circulating disturbances and IUGR [192,194].…”

Section: Umbilical Cord Anomaliesmentioning

confidence: 99%

Growth Restriction: Etiology, Maternal and Neonatal Outcome. A Review

Haram¹,

Svendsen²,

Myking

2007

CWHR

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Intrauterine growth restriction (IUGR) is an important clinical problem associated with increased perinatal mortality and morbidity. The most preferred small for gestational age (SGA) definition is birth weight below the 10th percentile, adjusted for gestational age. The incidence of IUGR is about 4 to 7 %. A variety of hormones are involved. IUGR may be due to chromosomal defects, smoking, early-onset preeclampsia (< 34 weeks), connective tissue and inflammatory rheumatic diseases, maternal infections, several drugs, twin-to twin transfusion, anorexia nervosa, low maternal pre-pregnancy or small weight gain during pregnancy. High hemoglobin (Hb) levels during the first 10-20 weeks of pregnancy may also cause IUGR. Complications due to IUGR include fetal or neonatal death, dysmaturity, and physical as well as temporary or permanent mental defects. Low birth weight children may have behavioral problems, psychiatric disorders and lower intelligence test scores later in life. There is a relationship between IUGR, timing and progression of puberty, and polycystic ovary syndrome. Fetal changes of lipid metabolism and homeostasis in IUGR may place the grown adult at risk for hypertension, diabetes mellitus and coronary artery disease. Mothers of low weight offspring have an increased risk for cardiovascular and kidney disease later in life.

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The missing umbilical artery. II. Paediatric follow-up.

Cited by 21 publications

References 12 publications

Single Umbilical Artery and Associated Malformations in over 5500 Autopsies: Relevance for Perinatal Management

Single Umbilical Artery and Associated Malformations in over 5500 Autopsies: Relevance for Perinatal Management

Absence of human placental lactogen and placental growth hormone (HGH-V) during pregnancy: PCR analysis of the deletion

Growth Restriction: Etiology, Maternal and Neonatal Outcome. A Review

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