title: [Changes in levels of cell adhesion molecules, acute phase proteins, lipids and hemostasis in relation to levels of endogenous estrogens during pregnancy and after ovariectomy].
abstract: 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).
authors.affiliation: Oddĕlení klinické hematologie VFN, Praha.
authors.forename: J
authors.initials: J
authors.lastname: Kvasnicka
authors.forename: J
authors.initials: J
authors.lastname: Marek
authors.forename: J
authors.initials: J
authors.lastname: Zivný
authors.forename: P
authors.initials: P
authors.lastname: Calda
authors.forename: A
authors.initials: A
authors.lastname: Umlaufová
authors.forename: M
authors.initials: M
authors.lastname: Marková
authors.forename: L
authors.initials: L
authors.lastname: Pecen
mesh_terms: D000328:Adult; D015815:Cell Adhesion Molecules / Q000097:blood*; D004958:Estradiol / Q000097:blood*; D005260:Female; D006801:Humans; D007375:Interleukin-1 / Q000097:blood; D008055:Lipids / Q000097:blood*; D009961:Orosomucoid / Q000032:analysis*; D010052:Ovariectomy; D011247:Pregnancy / Q000097:blood*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D015815:Cell Adhesion Molecules; D007375:Interleukin-1; D008055:Lipids; D009961:Orosomucoid; D014409:Tumor Necrosis Factor-alpha; D004958:Estradiol
vernacular_title: Zmĕny v koncentracích cytoadhezivních molekul, proteinů akutní fáze, lipidů a hemostázy v závislosti na hladinĕ endogenního estrogenu v tĕhotenství a po ovarektomii.