Objectives The modified myocardial performance index (Mod‐MPI) can be used to assess myocardial function. Fetal growth restriction can affect fetal myocardial function, thereby altering the Mod‐MPI. The results of previous studies on the utility of the Mod‐MPI in growth‐restricted fetuses are conflicting. The aim of this study was to calculate the left modified‐MPI in growth‐restricted fetuses and to compare the results with those of healthy fetuses. Methods This was a prospective cross‐sectional case–control study. In total, 40 women with growth‐restricted fetuses and 40 women with fetuses of normal weight (controls) at 29–39 gestational weeks were enrolled in the study. An experienced obstetrician calculated the Mod‐MPI for each fetus. Women with systemic diseases or fetuses with chromosomal/structural abnormalities were excluded from the study. The results of Mod‐MPI measurements of the two groups were compared. Results The mean single deepest vertical pocket (SDVP) of amniotic fluid, estimated fetal weight (EFW), and isovolumetric relaxation time (IRT) was significantly lower in the fetal growth restriction (FGR) group as compared with these parameters in the control group (P < .05). The uterine artery (UtA) pulsatility index (PI) was significantly higher in the FGR group as compared with that in the control group (P < .05). There were six cases of absent end‐diastolic flow (AED) in the FGR group. There were no statistically significant between‐group differences in the Mod‐MPI, isovolumetric contraction time (ICT), and ejection time (ET) (P > .05). There was also no statistically significant correlation between the Mod‐MPI in the fetuses with AED and the control group for Mod‐MPI (P > .05). Conclusion The utility of the Mod‐MPI in FGR remains unclear. Future studies with larger populations are needed to determine the utility of the Mod‐MPI as a predictor of cardiac compromise in FGR.

Klinefelter syndrome (KS) is the most common sex chromosome disorder in men. It may be associated with an increased risk for venous thrombosis and thromboembolism, which is partially explained by hypofibrinolysis due to androgen deficiency. Additional genetic or acquired thrombophilic states have been shown in KS patients complicated with venous thrombosis as isolated case reports. Arterial thrombotic events had not been previously reported in KS. In this study, a young man with KS who developed acute arterial thrombosis during testosterone replacement therapy is presented. He was homozygous for the A1298C mutation of the methylenetetrahydrofolate reductase (MTHFR) gene.

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Selenoprotein P concentrations have been found to be associated with insulin resistance and elevated in patients with type 2 diabetes mellitus (DM). The aim of the present study was to investigate circulating selenoprotein P level and its possible relationship with metabolic parameters in gestational diabetes mellitus (GDM). Plasma selenoprotein P concentrations were measured in 30 pregnant women with GDM, 35 pregnant women without GDM and 22 healthy nonpregnant women. No difference in selenoprotein P levels was observed among the groups [6.2 (4.5-8.2), 7.9 (4.5-10.7) and 6.7 (5.3-9.1) ng/ml, respectively, p = 0.69]. In pregnant women with and without GDM, selenoprotein P did not correlate with age, gestational age, prepregnancy body mass index (BMI), HbA1c, glucose concentrations at oral glucose tolerance test (OGTT), area under curve (AUC) glucose, total cholesterol, LDL cholesterol and triglycerides levels (p > 0.05). But, there were statistically significant correlations between selenoprotein P and current BMI (r = -0.28, p = 0.04) and HDL cholesterol levels (r = 0.43, p = 0.01). We found that selenoprotein P concentrations are not elevated in women with GDM but associated with BMI and HDL cholesterol.

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