Effect of adenomyosis on adverse obstetrical outcomes in twin pregnancies achieved with assisted reproductive technology.

The incidence of twin pregnancy with adenomyosis (AD) is increasing due to advanced maternal age and infertility treatment. We retrospectively analysed the data of 45 dichorionic twin pregnancies complicated with AD in contrast to a control group of dichorionic twin pregnancies without AD (n = 130). Compared with those in the control group, the AD group had a higher overall foetal loss rate (8.9% vs. 0.8%; adjusted p = .031; odds ratio (OR), 13.6; 95% confidence interval (CI), 1.27-146.3), higher early preterm delivery rate (20% vs. 6.9%; adjusted p = .007; OR, 4.22; 95% CI, 1.47-12.13) and higher rate of hypertensive disorders of pregnancy (26.7% vs. 7.7%; adjusted p = .005; OR, 3.94; 95% CI, 1.5-10.2). Patients in the AD group were significantly more likely to require transfusion during or after delivery (17.8% vs. 5.4%; p = .026) and have smaller babies (2168 g vs. 2399 g; p = .004) compared with those in the control group. This is the first study to report that twin pregnancies with AD may be treated as high-risk for placental dysfunction and may need closer monitoring during pregnancy.Impact StatementWhat is already known on this subject? The incidence of twin pregnancy with adenomyosis (AD) is increasing due to advanced maternal age and infertility treatment. However, there are very few studies on the effect of AD on pregnancy outcomes.What the results of this study add? This is the first study to report that twin pregnancies with AD have higher rates of early preterm delivery, hypertensive disorders of pregnancy, and transfusion compared to controls.What the implications are of these findings for clinical practice and/or further research? The results of this study can be used in counselling twin pregnancies with AD. Further research is needed to confirm the current findings.

Cisplatin induces primary necrosis through poly(ADP-ribose) polymerase 1 activation in kidney proximal tubular cells.

Treatment with cisplatin for cancer therapy has a major side effect such as nephrotoxicity; however, the role of poly (ADP-ribose) polymerase 1 (PARP1) in necrosis in response to cisplatin nephrotoxicity remains to be defined. Here we report that cisplatin induces primary necrosis through PARP1 activation in kidney proximal tubular cells derived from human, pig and mouse. Treatment with high dose of cisplatin for 4 and 8 hours induced primary necrosis, as represented by the percentage of propidium iodide-positive cells and lactate dehydrogenase release. The primary necrosis was correlated with PARP1 activation during cisplatin injury. Treatment with PJ34, a potent PARP1 inhibitor, at 2 hours after injury attenuated primary necrosis after 8 hours of cisplatin injury as well as PARP1 activation. PARP1 inhibition also reduced the release of lactate dehydrogenase and high mobility group box protein 1 from kidney proximal tubular cells at 8 hours after cisplatin injury. Oxidative stress was increased by treatment with cisplatin for 8 hours as shown by 8-hydroxy-2'-deoxyguanosine and lipid hydroperoxide assays, but PARP1 inhibition at 2 hours after injury reduced the oxidative damage. These data demonstrate that cisplatin-induced PARP1 activation contributes to primary necrosis through oxidative stress in kidney proximal tubular cells, resulting in the induction of cisplatin nephrotoxicity and inflammation.