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At least 19 recordsLinked to original sources
PubMed1977

IgG deficiency in association with placental oedema.

Deficiency of the immunoglobulin C (IgG) in the human newborn is rare in the absence of maternal hypogammaglobulinaemia. Low concentrations of IgG in cord blood were found in 3 conditions--the donor twin in the fetofetal transfusion syndrome, hydrops fetalis and congenital hepatic disease. These were all associated with placental oedema. It is suggested that the oedema may be responsible for a disturbance in maternofetal placental transfer.

Dysgammaglobulinemia↗
PubMed1976

Serum immunoglobulins in multiple pregnancy.

The concentrations of immunoglobulins (Ig) G.A.M. and E were determined in paired umbilical cord and maternal sera in 50 twin pregnancies. Mean IgG levels were higher in cord than maternal sera and in most cases the cord IgG level related more closely to that of the other twin than to either maternal level or birthweight, and was in the range for singletons of the same gestational age. The three cases of fetofetal transfusion syndrome were exceptional in the large difference between IgG concentrations in recipient and donor twins. The discrepancy was much greater than that found between the levels of proteins produced by the fetus, suggesting a disturbance in maternofetal placental transfer. IgM was detected in all cord sera, with one exception, and the level was not related to order of birth. IgA was detected in 16% of cord sera, 13% in sera from first borns. IgE was detected in only 8% of cord sera and there was no evidence of placental transfer.

Female↗
PubMed1978

Transfusion syndrome and the heritability of IQ.

The recent analysis of transfusion syndrome effects by Munsinger (1977) suggests that there is literally no effect of social environment on IQ variation in the population. The detailed analysis of Munsinger's report, however, indicates that his conclusions cannot be supported. Though Munsinger assigned birthweights to separated MZ twin pairs described in the literature, there do not in fact exist birthweight data for most pairs. Further, for some pairs, Munsinger also estimated their IQ's. There is no valid basis for Munsinger's claim that he has detected those separated MZ pairs within which transfusion syndrome occurred. When discussing six studies of birthweights of MZ pairs reared together, Munsinger in each case made transcription errors in selecting data from the original studies. Then he misapplied a statistical formula to the erroneous data, and concluded that inclusion of pairs with large birth-weight differences biased the IQ correlation of MZ's downwards. When Munsinger's own data base is correctly analysed, employing his own procedures, inclusion of pairs with large birthweight differences in fact increases the IQ correlation. There is thus no demonstrable basis for Munsinger's claims about transfusion syndrome and the heritability of IQ.

Birth Weight↗
PubMed1976

Peters' anomaly with the fetal transfusion syndrome.

Of identical twins with the fetal transfusion syndrome, the second twin who was anemic and hypoxemic from early gestation had Peters' anomaly by histologic examination of the host cornea excised during corneal transplantation at 7 months of age. The absence of a normally positioned lens with the incorporation of lens epithelium, capsule, and cortex within the posterior corneal stroma suggested a developmental disturbance in the separation of the lens from the cornea. The severe lenticular disturbance, microphthalmos, and fetal growth retardation in this case reflected early anemia and the resultant hypoxemia. To our knowledge, this is the first time that the fetal transfusion syndrome and Peters' anomaly have been associated.

Corneal Diseases↗
PubMed1978

Twins: causes of perinatal death in 12 United States cities and one African city.

The perinatal mortality rate in a large U. S. study was 139 per 1,000 births for twins and 33 per 1,000 for singletons. Sixteen per cent of the twin deaths were due to amniotic fluid infections, 11 per cent to premature rupture of the membranes, 8 per cent to the monovular twin transfusion syndrome, 8 per cent to large placental infarcts, 7 per cent to congenital anomalies, and the rest to over 20 other disorders. The perinatal mortality rate for monozygotic twins was 2.7 times that for dizygotic twins, mainly due to more amniotic fluid infections, congenital anomalies, and the twin transfusion syndrome in the monozygotic pairs. To study the role of poor maternal nutrition on twins, a similar study of perinatal mortality rates was undertaken in Addis Ababa, Ethiopia. Addis Ababa twins had 2.5 times the mortality rate of U. S. twins, mainly due to a higher frequency of amniotic fluid infections, abruptio placentae, cord accidents, obstructed labors, congenital syphillis, and the twin transfusion syndrome in the Ethiopians.

Abruptio Placentae↗
PubMed1977

The identical-twin transfusion syndrome: a source of error in estimating IQ resemblance and heritability.

Published studies show that among identical twins, lower birthweight is associated with lower adult intelligence. However, no such relation between birthweight and adult IQ exists among fraternal twins. A likely explanation for the association between birthweight and intelligence among identical twins is the identical twin transfusion syndrome which occurs only between some monochorionic identical twin pairs. The IQ scores from separated identical twins were reanalysed to explore the consequences of identical twin transfusion syndrome for IQ resemblance and heritability. Among 129 published cases of identical twin pairs reared apart, 76 pairs contained some birthweight information. The 76 pairs were separated into three classes: 23 pairs in which there was clear evidence of a substantial birthweight differences (indicating the probable existence of the identical twin transfusion syndrome), 27 pairs in which the information on birthweight was ambiguous (?), and 26 pairs in which there was clear evidence that the twins were similar in birthweight. The reanalyses showed: (1) birthweight differences are positively associated with IQ differences in the total sample of separated identical twins; (2) within the group of 23 twin pairs who showed large birthweight differences, there was a positive relation between birthweight differences and IQ differences; (3) when heritability of IQ is estimated for those twins who do not suffer large birthweight differences, the resemblance (and thus, h2/b) of the separated identical twins' IG is 0-95. Given that the average reliability of the individual IQ test is around 0-95, these data suggest that genetic factors and errors of measurement cause the individual differences in IQ among human beings. Because of the identical twin transfusion syndrome, previous studies of MZ twins have underestimated the effect of genetic factors on IQ. An analysis of the IQs for heavier and lighter birthweight twins suggests that the main effect of the identical twin transfusion syndrome is to lower the IQ of the lighter birthweight twin, rather than to raise the IQ of the more fortunate partner or to influence the IQ of both members. This reanalysis suggests that postnatal cultural and social environment produce little of the total phenotypic variation in IQ found in the normal population. In the future, investigators who use twin studies to estimated heritability must ascertain whether their identical twin pairs suffered from the identical twin transfusion syndrome. Accurate estimates of heritability can only be obtained using identical twins who do not suffer from placental circulation problems. Most likely, the identical twin transfusion syndrome produces anoxia and brain damage during early prenatal development in the smaller identical twin. The anoxia is caused by a lowering of the haemoglobin content of the smaller twin by 35% or more.

Adolescent↗
PubMed1977

Physiomorphology of twin transfusion syndrome. A study of 86 twin gestations.

The placentas of 86 pairs of twins were examined and correlated with the clinical characteristics of the neonate. The incidence of twin pregnancy in this group was 1 : 108 deliveries. Fetal prematurity and associated complications in twin pregnancy were the cause of increased perinatal and neonatal mortality.

Adult↗
PubMed1979

[Fetal death in utero 15 weeks following amniocentesis -- a legal case (author's transl)].

This is a report about fetal death in utero in a case of monozygote, monochrionic, monoamnionic twin pregnancy (46,xy) 15 weeks after amniocentesis. The public prosecutor was occupied with the case by the patient. The accusation run as follows: Stab wound with following death in utero of one twin and thereby damage of the second twin also with following death in utero. Directly after delivery the first diagnosis by aspect of the fetuses was: transfusion syndrome. The following endoradiography of the blood vessels of the umbilical chords and placenta confirmed the first diagnosis (anastomosis). Additionally both chords were entangled and knotted variously. It was concluded that the extremely smaller fetus died from malnutrition (transfusion syndrome) whereas the taller fetus died from acute asphyxia (knotted chords in monoamnionic twin pregnancy). The forensic investigation was, as aspected, without any pathological findings concerning sequelae of stab wounds but revealed the lack of one chordvessel of the smaller fetus and the typical histological findings of an aspiration lung of the taller fetus.

Amniocentesis↗