Pre-eclampsia/eclampsia in twin pregnancies - Journal of Medical ...

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cause of the greatly increased incidence of preeclampsia
in twins, they must be the result of the DZ
twins which comprise about two-thirds of the total
in Caucasian populations (Stevenson et al, 1971).
Even if our data are ignored, it would be surprising
if a threefold total increase could be the result of
increased antigenic differences between mother and
fetuses in two-thirds of the twins. If in a singleton
pregnancy the conceptus antigens not expressed in
the mother are F, it follows that the number of
antigens in a DZ pregnancy not expressed in the
mother would be < 2F, and this maximum increase
could only produce a rise in the pre-eclampsia/
eclampsia incidence of < 2/3 x 2 = < 1.3 while the
observed factor is 3.
Conclusion
While this study fails to show any consistent difference
in the incidence of pre-eclampsia/eclampsia
between DZ and MZ twin pregnancies, it does confirm
the very greatly increased incidence of preeclampsia
in association with twins-a threefold
order compared with singletons. On a quantitative
basis, considering numbers of antigen differences as
a possible factor in causing pre-eclampsia, one
would expect twin pregnancies to show an increase
of < 1-3. If total antigen 'dose' were involved
it would be < 2. The observed increase is
greater than this particularly in the severe form of
the disease. Furthermore, as indicated, the figures
probably give an underestimate of the difference.
Apparently the factor(s) responsible for the in-
Pre-eclampsia/eclampsia in twin pregnancies
211
creased incidence of pre-eclampsia in twins do not
represent a mere summation of those operative in
two singleton pregnancies.
REFERENCES
Adams, E. M. and MacGillivray, I. (1961). Long term effect of
pre-eclampsia in blood pressure. Lancet, 2, 1373-1375.
Benirschke, K. and Driscoll, S. G. (1967). The placenta of multiple
pregnancy. In The Pathology of the Human Placenta, p. 165.
Springer-Verlag, Berlin, Heidelberg New York.
Cameron, A. H. (1968). The Birmingham twin survey. Proceedings
of the Royal Society of Medicine, 61, 229-234.
Enders, T. and Stern, C. (1948). The frequencies of twins, relative
to age of mothers, in American populations. Genetics, 33, 263.
James, W. H. (1971). Excess of like-sexed pairs of dizygotic twins.
Nature (London), 232, 277-278.
Kalmus, H. (1946). Genetical antigenic incompatibility as a possible
cause of the toxaemias occurring late in pregnancy. Annals
of Eugenics, 13, 146-149.
McCartney, C. P. (1964). Pathological anatomy of acute hypertension
of pregnancy. Circulation, 29 and 30, Suppl. 11, 37-42.
Naeye, R. L. (1964). Fetal and neonatal development of twins.
Pediatrics, 33, 546-553.
Nylander, P. P. S. (1970). The determination of zygosity-a study
of 608 pairs born in Aberdeen. Journal of Obstetrics and Gynaecology
of the British Commonwealth, 77, 506-510.
Papiernik, E., Gerard, L., Hult, A. M., and Schneider, L. (1974).
Hypothesis of an ovular regulation of pregnancy weight-gain.
Acta Geneticae Medicae et Gemellologiae, 23, 56.
Penrose, L. S. (1946). On the familial appearances of maternal and
fetal incompatibility. Annals of Eugenics, 13, 141-145.
Platt, R., Stewart, A. E., and Emery, E. W. (1958). The aetiology,
incidence and heredity of pre-eclamptic toxaemia of pregnancy.
Lancet, 1, 552-556.
Salzmann, K. D. (1955). Do transplacental hormones cause
eclampsia ? Lancet, 2, 953-956.
Selvin, S. (1971). The number of pregnancies prior to the birth of
twins. Annals of Human Genetics, 34, 427-429.
Stevenson, A. C., Davison, B. C. C., Say, B., Ustuoplu, S., Lya, D.,
and Toppozoda, H. K. (1971). Contribution of fetal,/maternal
incompatibility to aetiology of pre-eclamptic toxaemia. Lancet,
2, 1286-1289.
Toivanen, P. and Hirvonen, T. (1970). Sex ratio of newborns: preponderance
of males in toxaemia of pregnancy. Science, 170, 187-
188.