Maternal blood during pregnancy, cord blood, and placental villous tissues at the time of delivery were obtained from subjects to measure the HTLV-1 proviral load (PVL) using real-time PCR. As shown in Figure 1A, HTLV-1 provirus was detected in the maternal blood of 248 of 254 subjects (97.6%), in the placental villous tissues of 140 of 254 subjects (55.1%), and in the cord blood samples of 6 of 254 subjects (2.4%). Overall, 248 women had PVL in the maternal blood, of whom 140 also had PVL in the placenta. Of these 140 women, 6 had PVL in the cord blood. Significant differences in the PVL were observed between the maternal blood, cord blood, and placental villous tissues (Figure 1A). The 248 pregnant carriers with PVL in the maternal blood were divided into those with PVL (n = 140) and without PVL (n = 108) in the placental tissue, and their clinical backgrounds were compared. Women with PVL in the placental tissue had a significantly higher peripheral blood PVL, higher antibody titers, and more multiparas compared with women with no PVL in the placental tissue (Table 1 and Figure 1B). These 2 groups did not differ in terms of birth weight and pregnancy complications (Table 1). There was no significant difference in the clinical backgrounds of pregnant women with HTLV-1 in the placenta when divided into those who tested positive versus negative for HTLV-1 in the cord blood (Supplemental Table 1). This was at least in part due to the small number of pregnant women testing positive for HTLV-1 in the cord blood. In addition, there were insufficient numbers of follow-up surveys of cases of MTCT by intrauterine transmission to allow statistical analysis. These issues are subjects for future investigation. A weak positive correlation between the PVLs in the maternal blood and in the placental villous tissues was observed (Figure 1C), whereas PVL in HTLV-1-positive cord blood samples did not correlate with PVL in the maternal blood or placental villous tissues of the same subject (Figure 1, D and E). To test the possibility that HTLV-1 provirus detected in cord blood was derived from maternal blood contamination of cord blood, microsatellite analysis was performed using short tandem repeat (STR) markers (25). Differences in the patterns of representative STR markers were observed between maternal blood-derived DNA and fetal placental villous tissue-and cord blood-derived DNA (Figure 1F). Similar results were obtained for all 6 samples that tested positive for HTLV-1 provirus in the cord blood. Furthermore, STR analysis and HTLV-1 PVL assay were used to examine how much maternal blood in the cord blood was required to detect a positive signal. A mixing rate of 20% (maternal/fetal cell ratio = 20:80) was the detection limit in the STR analysis, and a mixing rate of 5% (maternal/fetal cell ratio = 5:95) was the detection limit in the HTLV-1 PVL assay (Supplemental Figure 1). A previous study reported that the median rates of maternal blood contamination in the cord blood were 0.27% and 0.

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Gestational diabetes mellitus (GDM) is known to be a significant risk factor for the future development of type 2 diabetes. Here, we investigated whether a precise evaluation of β-and α-cell functions helps to identify women at high risk of developing glucose intolerance after GDM. Fifty-six women with GDM underwent a 75-g oral glucose tolerance test (OGTT) at early (6-12 weeks) postpartum. We measured their concentrations of glucose, insulin, proinsulin and glucagon at fasting and 30, 60 and 120 min. At 1-year post-delivery, we classified the women into a normal glucose tolerance (NGT) group or an impaired glucose tolerance (IGT)/diabetes mellitus (DM) group. Forty-three of the 56 women completed the study. At 1-year post-delivery, 17 women had developed IGT/DM and 26 women showed NGT. In the early-postpartum OGTTs, the IGT/DM group showed a lower insulinogenic index, a less glucagon suppression evaluated by the change from fasting to 30 min (ΔGlucagon 30 min), and a higher glucagon-to-insulin ratio at 30 min compared to the NGT group. There were no significant between-group differences in proinsulin levels or proinsulin-to-insulin ratios. Insulinogenic index <0.6 and ΔGlucagon 30 min >0 pg/mL were identified as predictors for the development of IGT/DM after GDM, independent of age, body mass index, and lactation intensity. These results suggest that the bihormonal disorder of insulin and glucagon causes the postpartum development of glucose intolerance. The measurement of plasma insulin and glucagon during the initial OGTT at early postpartum period can help to make optimal decisions regarding the postpartum management of women with GDM.

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