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The underlying correlative mechanisms between Insulin resistance (IR) and recurrent pregnancy loss (RPL) in patients without polycystic ovarian syndrome (PCOS) remain inconclusive. To investigate the association between triglyceride (TG) levels, lymphocyte subsets, and IR in RPL patients without PCOS and obesity. Eighty-nine subjects with an unexplained RPL, independent of PCOS/obesity were enrolled in this study. A 75-g oral glucose tolerance test was performed on each subject with plasma tested for glucose and insulin. The fasting venous blood of all subjects was collected for routine clinical chemistry analysis. Lymphocyte subsets were analyzed by four-color flow cytometry. As a result, TG levels were significantly elevated in RPL patients with IR compared to those without IR. Pearson linear correlation model and receiver operating characteristic (ROC) curve analyses revealed a significant positive association between TG and HOMA-IR index value. In multiple logistic regression analysis, TG was significantly associated with the risk of hyperinsulinemia and increased CD3+CD4+/CD3+CD8+ ratio which was significantly negatively correlated with disposition index (DI30) and DI120, indicators for insulin sensitivity. In addition, DI30 and DI120 were significantly decreased in the higher CD3+CD4+/CD3+CD8+ group. Our findings showed that the elevated TG and altered immune responses in RPL patients with IR are independent of PCOS and obesity, and could be used as an indicator of IR in RPL patients. These results contribute to the understanding of the pathophysiology of IR in RPL for potential prevention and therapeutic targets.

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Background: The anti-PP1Pk antibody is a rare antibody associated with recurrent spontaneous abortion (RSA) in the first trimester. As it is a rare entity, few reports have been published, especially in China. Currently, there is no specific treatment for RSA associated with anti-PP1Pk antibody because it is a naturally occurring antibody. This study aims to report three cases of RSA associated with the anti-PP1Pk antibody to share our experiences with its management. Methods: The three patients' medical information was obtained from the medical records. Intravenous immunoglobulin and/or plasmapheresis was offered to the patients. We also made an extension research of the related literature about RSA associated with anti-PP1Pk antibody. Results: Although patients received intervention, the maternal anti-PP1Pk antibody titer remained stable and did not decrease. There were no live births. We summarized publications about pregnancy in women with anti-PP1Pk antibodies. Conclusions: Early initiation of plasmapheresis in high-risk patients with anti-PP1Pk antibodies should be strongly considered.