Avtor/Urednik     Žegura, Branka; Gužič-Salobir, Barbara; Keber, Irena; Šebeštjen, Miran; Koenig, Wolfgang
Naslov     Effects of norethisterone acetate on markers of inflammation in postmenopausal women receiving estradiol
Prevedeni naslov     Učinak noretisteron acetata na upalne biljege u postmenopauzalnih žena koje primeju estradiol
Tip     članek
Vir     Gynaecol Perinatol
Vol. in št.     Letnik 14, št. Suppl 1
Leto izdaje     2005
Obseg     str. 12-17
Jezik     eng
Abstrakt     Objective. The increase of C-reactive protein (CRP) after oral estrogen replacement therapy, could be one possible mechanism for the increased cardiovascular risk in the first year of hormonal replacement therapy (HRT). Androgenic progestins such as norethisterone acetate (NETA) may inhibit proinflammatory effects of estrogen. We compared the effects of oral estradiol and estradiol combined with NETA on markers of inflammation. Methods. 104 healthy women were randomized to receive 28 weeks of oral treatment with estradiol (E2), estradiol combined with NETA (E2+NETA), transdermal E2 or placebo. At baseline and after 28 weeks of HRT, levels of CRP, serum amyloide A, fibrinogen and cytokines interleukin-6 and tumor necrosis factor alpha were determined. Reults. E2 significantly increased CRP from 2.15 (0.71-4.05) to 3.41 (1.12-5.92) mg/l (p=0.04) and from 1.12 (0.81-2.06) to 1.95 (1.34-3.38) mg/l (p<0.01) after E2+NETA. Transdermal E2 showed no influence on CRP. The addition of NETA influenced the change in CRP levels, as the increase in CRP was more significant after E2 without NETA (p=0.005). Oral E2 significantly decreased fibrinogen levels from 3.58 (2.81-3.77) to 2.58 (2.47-2.80) g/l, (p=0.002) and from 3.62 (3.17-3.95) to 3.20 (2.65-3.61) g/l, (p=0.007) for transdermal E2, while E2+NETA showed no effect. The decrease of fibrinogen was larger after oral E2 (p=0.02). Conclusion. The addition of NETA to E2 decreased the proinflammatory effect of E2, but it also attenuated the favourable effect of E2 on fibrinogen, an independent predictor of cardiovascular disease. Transdermal E2 had lesser effect on markers of inflammation although it decreased fibrinogen.
Deskriptorji     ESTROGEN REPLACEMENT THERAPY
C-REACTIVE PROTEIN
NORETHINDRONE
INTERLEUKIN-6
TUMOR NECROSIS FACTOR
ESTRADIOL
AMYLOID PROTEIN AA
POSTMENOPAUSE
RANDOMIZED CONTROLLED TRIALS