Maternal
malaria is associated with
placental insufficiency that leads to
intrauterine growth retardation and reduced
birth weight.
Malaria may impair the exchange of drugs across the placenta especially the transmission of
antimalarial drugs to the foetus. The distribution of
quinine and its 3-hydroxymetabolite in blood, tissues and foeto-placental unit was evaluated on day 18 of pregnancy of mice infected or not with Plasmodium berghei. During pregnancy,
quinine distribution volume increases gradually with the rise of free
quinine concentrations in plasma.
Quinine concentrations increase in erythrocytes and most tissues without change in systemic clearance. A maternal-to-foetal gradient of 8:1 limits the exposure of foetus to
quinine. During
malaria, the systemic clearance of
quinine and the
3-hydroxyquinine gradually decrease with the rising parasitaemia.
Quinine concentrations increase slightly in most of the tissues. The weight of placentas decreases in a parasitaemia-dependant manner and is strongly related to the low uptake of
quinine by placenta. Foetal weights and
quinine concentrations in foetus only decrease for the highest parasitaemia. In this experimental model, pregnancy facilitates
quinine uptake by erythrocytes and peripheral tissues.
Malaria induces a hypotrophy of both placenta and foetus. In placenta, the marked decrease of
quinine concentrations may impair the clearance of sequestered parasites.