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Associations between maternal methylenetetrahydrofolate reductase polymorphisms and adverse outcomes of pregnancy: the Hordaland Homocysteine Study.

https://arctichealth.org/en/permalink/ahliterature58260
Source
Am J Med. 2004 Jul 1;117(1):26-31
Publication Type
Article
Date
Jul-1-2004
Author
Eha Nurk
Grethe S Tell
Helga Refsum
Per M Ueland
Stein E Vollset
Author Affiliation
LOCUS for Homosysteine and Related Vitamins, Department of Public Health and Primary Health Care, University of Bergen, Norway.
Source
Am J Med. 2004 Jul 1;117(1):26-31
Date
Jul-1-2004
Language
English
Publication Type
Article
Keywords
Abnormalities - epidemiology - genetics
Abruptio Placentae - epidemiology - genetics
Adult
Alleles
Female
Fetal Growth Retardation - epidemiology - genetics
Genetic Predisposition to Disease
Genotype
Heterozygote
Homocysteine - blood
Humans
Logistic Models
Maternal Age
Methylenetetrahydrofolate Reductase (NADPH2) - genetics
Polymorphism, Genetic - genetics
Pregnancy
Pregnancy Complications - epidemiology
Pregnancy outcome
Pregnancy, High-Risk
Research Support, Non-U.S. Gov't
Risk factors
Abstract
PURPOSE: Methylenetetrahydrofolate reductase (MTHFR) is involved in the metabolism of folate and homocysteine; a polymorphism in the MTHFR gene (677C-->T) has been associated with adverse outcomes of pregnancy. We studied whether two polymorphisms in the MTHFR gene (677C-->T and 1298A-->C) are associated with pregnancy complications, adverse outcomes, and birth defects. METHODS: MTHFR polymorphisms were determined in blood collected in 1992 and 1993 from 5883 women aged 40 to 42 years, and linked with 14,492 pregnancies in the same women recorded in the Medical Birth Registry of Norway from 1967 to 1996. RESULTS: The 677TT genotype in mothers was associated with increased risk of placental abruption (odds ratio [OR] = 2.6; 95% confidence interval [CI]: 1.4 to 4.8) compared with the CC variant. The risk of intrauterine growth restriction increased with number of T alleles (P for trend = 0.04). Compared with the 1298AA variant, the CC variant was associated with a reduced risk of very low birth weight infants (OR = 0.4; 95% CI: 0.2 to 0.8). No significant associations were found between MTHFR polymorphisms and birth defects. CONCLUSION: The maternal MTHFR 677C-->T polymorphism was a risk factor for placental abruption. The unexpected protective effect of the 1298A-->C polymorphism on very low birth weight needs further study.
PubMed ID
15210385 View in PubMed
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Birth weight of relatives by maternal tendency to repeat small-for-gestational-age (SGA) births in successive pregnancies.

https://arctichealth.org/en/permalink/ahliterature34479
Source
Acta Obstet Gynecol Scand Suppl. 1997;165:35-8
Publication Type
Article
Date
1997
Author
P. Magnus
L S Bakketeig
H. Hoffman
Author Affiliation
Department of Epidemiology, National Institute of Public Health, Oslo, Norway.
Source
Acta Obstet Gynecol Scand Suppl. 1997;165:35-8
Date
1997
Language
English
Publication Type
Article
Keywords
Birth weight
Female
Fetal Growth Retardation - epidemiology - genetics
Humans
Infant, Newborn
Infant, Small for Gestational Age
Norway - epidemiology
Pregnancy
Recurrence
Registries
Research Support, U.S. Gov't, P.H.S.
Risk factors
Abstract
BACKGROUND AND METHOD: Small-for-gestational-age (SGA) infants represent a heterogeneous group of normal and growth-retarded children. To assess the familial aggregation of reduced fetal growth, birth weights in both maternal and paternal relatives of 1246 index children in the Scandinavian SGA Study were compared across groups defined by the SGA outcome of the index child as well as that of earlier siblings. RESULTS: Mean maternal birth weight +/- SEM was 3127 +/- 54 g for mothers who had experienced two SGA births as opposed to 3424 +/- 22 for mothers with no SGA births. Mean paternal birth weight was 3497 +/- 88 g and 3665 +/- 24 in the same two groups. The odds ratio (with 95% confidence interval) for having a mother with birth weight below the 10th percentile was 1.74 (0.85-3.58) for the group where two SGA births had occurred compared to no SGA births and it was 2.49 (1.22-5.07) for having a father with birth weight below the 10th percentile. There was no correlation between maternal and paternal birth weights. CONCLUSIONS: The association also to paternal birth weight suggests the presence of genetic or common environmental factors in explaining the tendency to have SGA children. Although taking parental birth weights into consideration will aid in diagnosing growth-retardation in a SGA child, SGA remains a heterogeneous group where familial and non-familial cases will be difficult to separate.
PubMed ID
9219454 View in PubMed
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History of fetal growth restriction is more strongly associated with severe rather than milder pregnancy-induced hypertension.

https://arctichealth.org/en/permalink/ahliterature93657
Source
Hypertension. 2008 Apr;51(4):1231-8
Publication Type
Article
Date
Apr-2008
Author
Rasmussen Svein
Irgens Lorentz M
Author Affiliation
Medical Birth Registry of Norway, Locus of Registry Based Epidemiology, Institute of Community Medicine and Primary Health Care, University of Bergen and Norwegian Institute of Public Health, Bergen, Norway. Svein.Rasmussen@mfr.uib.no
Source
Hypertension. 2008 Apr;51(4):1231-8
Date
Apr-2008
Language
English
Publication Type
Article
Keywords
Birth weight
Fathers
Female
Fetal Growth Retardation - epidemiology - genetics
Genetic Predisposition to Disease - epidemiology
Humans
Hypertension, Pregnancy-Induced - epidemiology - genetics
Infant, Newborn
Infant, Small for Gestational Age
Logistic Models
Male
Mothers
Norway - epidemiology
Pre-Eclampsia - epidemiology - genetics
Pregnancy
Registries
Risk factors
Severity of Illness Index
Abstract
We assessed whether fetal growth restriction without pregnancy-induced hypertension (PIH) is associated with the different clinical subgroups of PIH in the subsequent pregnancy. We also assessed the maternal and paternal contributions to this effect. Pairs of first and second, second and third, third and fourth, and fourth and fifth births were identified among all of the births in Norway: 137 375 pairs with same mother and father, 18 376 pairs with same mother and different fathers, and 18 916 pairs with same father and different mothers. Second births in each pair were restricted to those that occurred in 1998-2005. Odds ratios to predict early onset, severe, and mild preeclampsia and transient hypertension in the second birth from birth weight
Notes
Comment In: Hypertension. 2008 Apr;51(4):989-9018259043
Erratum In: Hypertension. 2009 Jan;53(1):e11
PubMed ID
18259045 View in PubMed
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Intergenerational effects of preterm birth and reduced intrauterine growth: a population-based study of Swedish mother-offspring pairs.

https://arctichealth.org/en/permalink/ahliterature82599
Source
BJOG. 2006 Apr;113(4):430-40
Publication Type
Article
Date
Apr-2006
Author
Selling K E
Carstensen J.
Finnström O.
Sydsjö G.
Author Affiliation
Division of Obstetrics and Gynaecology, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden. katarina.ekholm.selling@lio.se
Source
BJOG. 2006 Apr;113(4):430-40
Date
Apr-2006
Language
English
Publication Type
Article
Keywords
Adult
Birth Weight - genetics
Body mass index
Educational Status
Female
Fetal Growth Retardation - epidemiology - genetics
Humans
Infant, Newborn
Infant, Small for Gestational Age - physiology
Marital status
Mothers - statistics & numerical data
Odds Ratio
Parity
Pedigree
Pregnancy
Premature Birth - epidemiology - genetics
Regression Analysis
Risk factors
Smoking - epidemiology
Socioeconomic Factors
Sweden - epidemiology
Abstract
OBJECTIVE: To estimate the intergenerational effects of preterm birth and reduced intrauterine growth. DESIGN: Population-based cohort study. SETTINGS: Mother-first-born offspring pairs recorded in the Swedish Medical Birth Registry. POPULATION: Children born before 2001 to 38 720 women born in 1973-75. METHODS: The relationships between the mother's and the child's birth characteristics were estimated using logistic regression analysis. Adjustments were made for smoking habits, body mass index (BMI), and current and childhood socio-economic conditions. Analyses were performed on all mother-offspring pairs and on the pairs for which information on neither of the included background variables was missing (n= 24 520). MAIN OUTCOME MEASURES: Preterm birth (
PubMed ID
16553655 View in PubMed
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Iron-overload disease in infants involving fetal growth retardation, lactic acidosis, liver haemosiderosis, and aminoaciduria.

https://arctichealth.org/en/permalink/ahliterature206481
Source
Lancet. 1998 Feb 14;351(9101):490-3
Publication Type
Article
Date
Feb-14-1998
Author
V. Fellman
J. Rapola
H. Pihko
T. Varilo
K O Raivio
Author Affiliation
Children's Hospital, University of Helsinki, Stenbäckinkatu II, Finland.
Source
Lancet. 1998 Feb 14;351(9101):490-3
Date
Feb-14-1998
Language
English
Publication Type
Article
Keywords
Acidosis, Lactic - epidemiology - genetics
Female
Ferritins - blood
Fetal Growth Retardation - epidemiology - genetics
Finland - epidemiology
Genes, Recessive
Hemosiderosis - epidemiology - genetics - pathology
Humans
Infant, Newborn
Iron Overload - epidemiology - genetics
Kidney - pathology
Liver - pathology
Male
Pedigree
Renal Aminoacidurias - epidemiology - genetics
Transferrin - metabolism
Abstract
Several cases of a distinctive lethal neonatal disorder have been found in the Children's Hospital, Helsinki, Finland. However, the combination of presenting features is not typical of any known metabolic disease. We have analysed all known cases of this disorder in the hospital since 1965 and in Finland since 1990 to define clinical features of the disease.
We studied 17 newborn infants with severe growth retardation from 12 Finnish families and traced their genealogy. In addition to routine clinical studies, diagnostic workup included analysis of respiratory-chain function in isolated muscle mitochondria and necropsy specimens, pyruvate dehydrogenase complex activities in fibroblasts, analysis of aminoacids and organic acids in urine, staining of tissue samples for iron, and assay of liver iron content.
The infants were born near term (mean 37.8 [SD 3] gestational weeks) but were severely growth retarded (birthweight 1690 [460] g--ie, -3.8 [SD 0.6] SD score for gestational age). By age 24 h, mean pH was 7.00 (0.12), lactate 12.2 (7.5) mmol/L, and pyruvate 121 (57) micromol/L. All had aminoaciduria and failed to thrive; nine died neonatally (age 2-12 days), and eight died in infancy (1-4 months). The liver of four infants showed microscopic haemosiderosis and increased iron content (2.8-5.5 mg iron/g dry weight). In those four infants serum ferritin concentration (1260-2700 microg/L) and transferrin saturation (61-100%) were high, transferrin concentration (0.54-0.76 g/L) was low.
We describe a previously unrecognised clinical picture of a genetic disease, which presents with fetal growth retardation and lactic acidosis after birth. Genealogical studies indicate an autosomal-recessive mode of inheritance for this disease, which is distinct from other lactic acidoses, neonatal haemochromatosis, and hepatitis. The diagnostic criteria are: fetal growth retardation; severe lactic acidosis; aminoaciduria; iron overload with haemosiderosis of the liver, increased serum ferritin concentration, hypotransferrinaemia, and increased transferrin iron saturation. Organ dysfunction may be partly due to the toxic effects of free iron.
Notes
Comment In: Lancet. 1998 Apr 25;351(9111):1286-79643773
PubMed ID
9482441 View in PubMed
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