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Neonatal alloimmune thrombocytopenia caused by maternal past lymphocytes immunotherapy: a case report
Abstracts for the 29th Annual Congress of Japanese Society / Journal of Reproductive Immunology 106 (2014) 1–20
Neonatal alloimmune thrombocytopenia caused by maternal past lymphocytes immunotherapy: a case report M. Ito ∗ , S. Soeda, S. Yoneda, Y. Ono, N. Yoneda, A. Shiozaki, S. Saito Department of Obstetrics & Gynecology, University of Toyama, Japan Background: Neonatal alloimmune thrombocytopenia (NAIT) occurs as a result of maternal alloimmunization against paternally inherited antigens on fetal platelets. Platelets express platelet specific antigens (HPA) along with human leucocyte antigens (HLA) class I. Especially anti-HLA class I antibodies are often produced by pregnancy and blood transfusion. Here we report a rare case of neonatal thrombocytopenia observed in a female infant delivered by woman with history of lymphocytes immunotherapy for habitual abortion. Case: A 34-year-old woman, had a history of 7 abortions. She was immunized with her husband’s leukocytes once after 3rd abortion. After that she suffered from infertility, she underwent in vitro fertilization. Since screening test for recurrent miscarriage found that her lupus anticoagulant was slightly high (1.15), she was prescribed low dose aspirin therapy. She was impregnated by in vitro fertilization. At 16 weeks she was tested for chromosome analysis of her fetus due to nuchal translucency. Because subchorionic hematomas were detected at 19 weeks, heparin therapy was added. Unfortunately her fetal growth was impaired gradually, cesarean section was performed at the 33rd week 6 day of gestation because of fetal growth arrest. A female baby weighing 1,476 g (−1.9 SD) was delivered with Apgar scores of 1 and 7 at 1 and 5 min, respectively. Her baby’s platelet count at birth was 16,000/L with no symptoms. Both she and her baby were anti-HLA A and B antibody positive. Conclusion: Special attention should be paid to the possibility of NAIT as a side effect of allogenic leukocyte immunization. http://dx.doi.org/10.1016/j.jri.2014.09.046 Contribution of the NKG2D receptor to murine placental development Y. Aoki ∗ , N. Otsuka, N. Yamamoto, T. Miyazaki, Y. Miyatake, M. Kasahara Department of Pathology, Hokkaido University Graduate School of Medicine, Japan Peripheral blood natural killer (NK) cells control viral infections and cancer by their cytotoxic ability. In contrast, uterine NK (uNK) cells, which comprise 70% of leukocytes at the murine fetomaternal interface, have enhanced cytokine-producing ability and play an important role in the maintenance of pregnancy. NKG2D is a major activating receptor of NK cells. Stimulation of uNK cells in vitro by NKG2D ligands expressed on decidual
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stromal cells and trophoblasts leads to production of various cytokines by uNK cells; however, in vivo contribution of NKG2D ligand–receptor interactions to placental development is poorly understood. To examine the influence of the NKG2D system on mouse placental development in vivo, we blocked NKG2D ligand–receptor interactions by injecting anti-NKG2D antibody intraperitoneally. As we reported previously, NKG2D blockade reduced placental size until embryonic day (E) 12.5. However, the weight of the placenta and embryos was restored by E18.5. The size of the placenta did not differ at the end of gestation, but histological analysis of the placenta revealed that the boundary between the labyrinth and junctional zones was irregular in mice treated with anti-NKG2D antibody (p < 0.02). These results suggest that the NKG2D system contributes to placental development at mid-gestation, consistent with the observation that the accumulation of uNK cells at the fetomaternal interface reaches a maximum at E10.5. Mice treated with anti-NKG2D antibody displayed attenuated labyrinth zone formation, suggesting altered vasculogenic cytokine expression. http://dx.doi.org/10.1016/j.jri.2014.09.047 Genotyping analysis for the 46C/T polymorphism of coagulation factor XII and the involvement of factor XII activity in patients with recurrent pregnancy loss E. Hashimoto 1,∗ , T. Ebara 2 , C. Yamada-Namikawa 3 , T. Kitaori 1 , N. Suzumori 1 , K. Katano 1 , Y. Ozaki 1 , M. Sugiura-Ogasawara 1 1
Department of Obstetrics and Gynecology, Japan Occupational and Environmental Health, Japan 3 Department of Biochemistry II, Nagoya City University, Graduate School of Medical Sciences, Japan 2
Objective: We previously found that low FXII activity, but not an associated common genetic polymorphism, 46C/T, was linked to PRL. There is no reported study indicating the influence of the FXII SNP on further pregnancy outcome. Thus, we conducted this cross-sectional and cohort study. Methods: The frequency of the C/T genotype and the FXII activity were compared between the 279 patients with PRL and 100 control women. Subsequent miscarriage rates were compared among the C/T genotype and according to the FXII activity. The association between lupus anticoagulant (LA) and FXII activity was also examined. Results: The FXII activity in patients with LA was significantly lower than in patients without LA (60.7 ± 17.9% vs. 83.4 ± 29.3%; p = 0.02). The CT genotype was confirmed to be a risk factor for PRL after excluding patients with LA in the cross-sectional study (OR, 2.21; 95% CI, 1.08–4.17; p = 0.02). Neither low FXII activity nor the CT genotype
Neonatal alloimmune thrombocytopenia caused by maternal past lymphocytes immunotherapy: a case report M. Ito ∗ , S. Soeda, S. Yoneda, Y. Ono, N. Yoneda, A. Shiozaki, S. Saito Department of Obstetrics & Gynecology, University of Toyama, Japan Background: Neonatal alloimmune thrombocytopenia (NAIT) occurs as a result of maternal alloimmunization against paternally inherited antigens on fetal platelets. Platelets express platelet specific antigens (HPA) along with human leucocyte antigens (HLA) class I. Especially anti-HLA class I antibodies are often produced by pregnancy and blood transfusion. Here we report a rare case of neonatal thrombocytopenia observed in a female infant delivered by woman with history of lymphocytes immunotherapy for habitual abortion. Case: A 34-year-old woman, had a history of 7 abortions. She was immunized with her husband’s leukocytes once after 3rd abortion. After that she suffered from infertility, she underwent in vitro fertilization. Since screening test for recurrent miscarriage found that her lupus anticoagulant was slightly high (1.15), she was prescribed low dose aspirin therapy. She was impregnated by in vitro fertilization. At 16 weeks she was tested for chromosome analysis of her fetus due to nuchal translucency. Because subchorionic hematomas were detected at 19 weeks, heparin therapy was added. Unfortunately her fetal growth was impaired gradually, cesarean section was performed at the 33rd week 6 day of gestation because of fetal growth arrest. A female baby weighing 1,476 g (−1.9 SD) was delivered with Apgar scores of 1 and 7 at 1 and 5 min, respectively. Her baby’s platelet count at birth was 16,000/L with no symptoms. Both she and her baby were anti-HLA A and B antibody positive. Conclusion: Special attention should be paid to the possibility of NAIT as a side effect of allogenic leukocyte immunization. http://dx.doi.org/10.1016/j.jri.2014.09.046 Contribution of the NKG2D receptor to murine placental development Y. Aoki ∗ , N. Otsuka, N. Yamamoto, T. Miyazaki, Y. Miyatake, M. Kasahara Department of Pathology, Hokkaido University Graduate School of Medicine, Japan Peripheral blood natural killer (NK) cells control viral infections and cancer by their cytotoxic ability. In contrast, uterine NK (uNK) cells, which comprise 70% of leukocytes at the murine fetomaternal interface, have enhanced cytokine-producing ability and play an important role in the maintenance of pregnancy. NKG2D is a major activating receptor of NK cells. Stimulation of uNK cells in vitro by NKG2D ligands expressed on decidual
19
stromal cells and trophoblasts leads to production of various cytokines by uNK cells; however, in vivo contribution of NKG2D ligand–receptor interactions to placental development is poorly understood. To examine the influence of the NKG2D system on mouse placental development in vivo, we blocked NKG2D ligand–receptor interactions by injecting anti-NKG2D antibody intraperitoneally. As we reported previously, NKG2D blockade reduced placental size until embryonic day (E) 12.5. However, the weight of the placenta and embryos was restored by E18.5. The size of the placenta did not differ at the end of gestation, but histological analysis of the placenta revealed that the boundary between the labyrinth and junctional zones was irregular in mice treated with anti-NKG2D antibody (p < 0.02). These results suggest that the NKG2D system contributes to placental development at mid-gestation, consistent with the observation that the accumulation of uNK cells at the fetomaternal interface reaches a maximum at E10.5. Mice treated with anti-NKG2D antibody displayed attenuated labyrinth zone formation, suggesting altered vasculogenic cytokine expression. http://dx.doi.org/10.1016/j.jri.2014.09.047 Genotyping analysis for the 46C/T polymorphism of coagulation factor XII and the involvement of factor XII activity in patients with recurrent pregnancy loss E. Hashimoto 1,∗ , T. Ebara 2 , C. Yamada-Namikawa 3 , T. Kitaori 1 , N. Suzumori 1 , K. Katano 1 , Y. Ozaki 1 , M. Sugiura-Ogasawara 1 1
Department of Obstetrics and Gynecology, Japan Occupational and Environmental Health, Japan 3 Department of Biochemistry II, Nagoya City University, Graduate School of Medical Sciences, Japan 2
Objective: We previously found that low FXII activity, but not an associated common genetic polymorphism, 46C/T, was linked to PRL. There is no reported study indicating the influence of the FXII SNP on further pregnancy outcome. Thus, we conducted this cross-sectional and cohort study. Methods: The frequency of the C/T genotype and the FXII activity were compared between the 279 patients with PRL and 100 control women. Subsequent miscarriage rates were compared among the C/T genotype and according to the FXII activity. The association between lupus anticoagulant (LA) and FXII activity was also examined. Results: The FXII activity in patients with LA was significantly lower than in patients without LA (60.7 ± 17.9% vs. 83.4 ± 29.3%; p = 0.02). The CT genotype was confirmed to be a risk factor for PRL after excluding patients with LA in the cross-sectional study (OR, 2.21; 95% CI, 1.08–4.17; p = 0.02). Neither low FXII activity nor the CT genotype