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Unexplained pregnancy loss: a marker of basal endothelial dysfunction?
Oleh:
Pasquier, Elisabeth
;
De Saint Martin, Luc
;
Bohec, Caroline
;
Collet, Michel
;
George, Francoise Dignat
Jenis:
Article from Journal - ilmiah internasional
Dalam koleksi:
Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 100 no. 04 (Oct. 2013)
,
page 1013-1017.
Topik:
Case-control study
;
endothelium
;
microparticles
;
pregnancy loss
;
thrombin generation test
Ketersediaan
Perpustakaan FK
Nomor Panggil:
F02.K.2013.02
Non-tandon:
1 (dapat dipinjam: 0)
Tandon:
tidak ada
Lihat Detail Induk
Isi artikel
Objective To compare the microparticle levels of women referred for unexplained pregnancy loss with those of parous controls. Design Incident case-control study. Setting University medical center. Patient(s) 124 women consecutively referred for unexplained pregnancy losses (two or more losses at or before 21 weeks of gestational age, or at least one later loss), and 273 parous women without pregnancy loss. Intervention(s) Numeration of circulating microparticles by flow cytometry after differentiation of subpopulations according to the expression of membrane-specific antigens (CD51, CD144, or CD146 for endothelial, CD41 for platelet, CD45 and CD66b for leukocyte and neutrophil microparticles). Main Outcome Measure(s) Plasma levels of microparticles. Results A relative hypercoagulable state assessed by thrombin generation test had been previously reported in such cases, so we hypothesized that this could be explained by an excess of procoagulant microparticles. The study women displayed statistically significantly lower platelet and higher endothelial microparticle levels than the controls. The parameters of the thrombin generation test were only correlated with the level of endothelial microparticles, with a low coefficient of Speerman’s correlation (r=0.15). Conclusion(s) The difference in microparticle levels between the patients and controls does not clearly explain the hypercoagulable state reported in the patients but could reflect chronic endothelium damage.
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