Search for: [Abstract = "ium. In women who poorly responded to ASA, urinary 11\-dTXB2 concentration increased during the 3rd trimester and during pregnancy. There were no signifficant differences with the median of 11\-dTXB2 in the control group but after puerperium 11\-dTXB2 concentrations were similar to those in women responsive to ASA. Women responsive and nonresponsive to ASA had a similar prevalence of APS and PlA2 allele. However, these groups differed in the prevalence of SLE \(37.5% vs 5.0%, p=0.04\), preeclampsia \(p=0.02\), exacerbations of SLE \(p=0.04\) and small for gestational age newborns delivery \(p=0.01\). In women with APS the highest quartile of urinary 11\-dTXB2 concentrations was associated in the 2nd trimester with higher concentrations of TAT \(p=0.03\), tHcy \(p=0.01\), aCL IgG \(p=0.01\) and aCL IgM \(p=0.05\) as well as with higher levels of aCL IgG in the 3rd trimester \(p=0.04\) and after puerperium \(p=0.01\) compared with the lowest quartile. Pregnancies in the highest quartile lasted shorter \(p=0.008\) and showed a tendency to small for gestational age newborns delivery \(p=0.07\). The method of RI in group with APS showed no statistically significant differences between responsive and nonresponsive to ASA women with respect to markers of inflammation. Nonresponsive to ASA women in the 2nd trimester had higher concentrations of tHcy \(p=0.01\), 11\-dTXB2 \(p=0.005\), in the 3rd trimester had higher le"]
