The protective effect of oestrogens is probably caused also by the active inhibition of the inflammatory reaction of the acute phase and release of inflammatory cytokines type IL-1 beta or TNF-alpha by this hormone. We formulated this hypothesis because we recorded a drop of the protein of the acute stage, orosomucoid, in relation to the rising oestrogen level during pregnancy (r = -0.511, p < 0.0001). It ensues also from the finding of a lower level of cytoadhesive molecules of sE-selectins in a group of 66 pregnant women (sE-sel.: 32.95 +/- 12.5 ng/ml) with a higher level of 17-beta estradiol (17-beta E2: 9.34 +/- 7.8 nmol/l), as compared with the sE-selectin level in a group of 14 women after ovariectomy (sE-sel.: 43.97 +/- 8.174 ng/ml, p < 0.016) who lacked oestrogen (17-beta E2 0.14 +/- 0.13 nmol/l) and in a group of pregnant women (n 19) in the first trimester with level of 17-beta E2: 1.89 +/- 0.711 nmol/l where the sE-selectin concentrations at the onset pregnancy was higher (sE-sel.: 35.59 +/- 9.5 ng/ml) than in a group of pregnant women (n 38) during the second and third trimester (sE-sel.: 30.58 +/- 13.3 ng/ml, p < 0.05) with 17-beta E2 concentration 11.96 +/- 7.18 ng/ml. The finding of lower sE-selectin levels which is a sign that the endothelium is not exposed to the action of inflammatory cytokines IL-1 or TNF may thus be associated with the active "control" of thrombophilia in pregnancy. When during pregnancy in conjunction with oestrogen levels changes in the lipid concentration were investigated a compensating mechanism could be observed. Hypercholesterolaemia and hypertriglyceridaemia in pregnant women was associated with a rise of oestrogen levels as well as of "cardioprotective" HDL-cholesterol (the HDL level was during the first trimester 1.31 +/- 0.26 nmol/l, in the second and third trimester 1.69 +/- 0.48 nmol/l, p < 0.0167).

Oddĕlení klinické hematologie VFN Praha