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An estimated 50,000
women per year worldwide die from preeclampsia.
Preeclampsia is more likely to develop in women whose mothers
had preeclampsia than in women whose mothers did not.
According to data on approximately 1.7
million births in Norway, a woman who becomes pregnant by
a man who has already had a child with a different woman who
had preeclampsia during that pregnancy has a risk
of preeclampsia that is nearly twice
as high as that of a woman whose partner does not
have such a history.
In this issue of the Journal, investigators
report that men who were themselves born of pregnancies complicated
by preeclampsia are twice as likely to have a child who is
the product of a pregnancy complicated by preeclampsia as
are men who were born after a normal pregnancy.
There thus
seems to be both a maternally transmitted and a paternally
transmitted genetic predisposition to preeclampsia.
The ability to study this predisposition
is hampered by the obvious fact that preeclampsia is a disease
of pregnancy and no markers
for the disorder have yet been identified in nonpregnant
women, let alone men.
Women who have never born children has
been confirmed as a risk factor for preeclampsia, in both
large-scale epidemiologic studies and detailed clinical studies.
A change of partner for a second or subsequent pregnancy causes
a woman's risk to return to nearly the values associated with
women who have never born children, suggesting a poorly defined
immunologic contribution to the condition.
A curious but consistent finding is that
women who smoke cigarettes have a lower risk of preeclampsia
than women who do not smoke, even when confounders are carefully
excluded. The babies of cigarette smokers are smaller than
those of nonsmokers, presumably because of tobacco-related
interference with the transfer of placental nutrients, and
their average blood pressures are lower.
Environmental
factors may also contribute to the development of preeclampsia.
For example, the high incidence of preeclampsia
in many poor countries suggests that an inadequate diet
may be a risk factor. The dietary inadequacies
that have been proposed as relevant include deficiencies of
calcium, zinc, vitamins C and E, and n-3 essential fatty acids.
The New England
Journal of Medicine -- March 22, 2001 -- Vol. 344, No. 12
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