Safety and efficacy of inactivated COVID-19 vaccines in women vaccinated during the first trimester of pregnancy.

OBJECTIVES: This study aimed to investigate the safety of the inactivated COVID-19 vaccines in early pregnant women in view of their adverse-effect profile and associated maternal-fetal complications, as well as to evaluate their immunogenicity. METHODS: In this prospective observational cohort study, 232 women in their first trimester or those in the periconception period who inadvertently received two doses of inactivated COVID-19 vaccine between January 21, 2021, and January 14, 2022 were analyzed. Meanwhile, 735 unvaccinated early pregnancy women were also included in the study at a case-to-control ratio of 1:3. RESULTS: The vaccination group did not have an increased miscarriage rate compared with that of the control group (P = 0.918). Furthermore, the birth defect rates in the vaccine group and control group were 0.83% and 1.0%, respectively. Vaccination did not increase the risk of small for gestational age, gestational diabetes mellitus, preterm, or hypertensive disorders of pregnancy (P >0.01). Within 12 weeks after the second dose, the inactivated vaccine effectively produced neutralizing antibody (NAb) against SARS-CoV-2. The NAb levels in the paired umbilical cord serum and maternal serum samples during delivery were negative in both groups. The T-cell subset remained within the normal range in both groups. CONCLUSION: Therefore, our study proves that inactivated COVID-19 vaccines are safe for mothers and fetuses and also effective in producing NAb against SARS-CoV-2.

Enhanced PDGF signaling in gestational diabetes mellitus is involved in pancreatic ß-cell dysfunction.

Gestational diabetes mellitus (GDM) is often accompanied by the development of hyperinsulinemia as an adaptation to increased insulin demand, but this subsequently causes insulin resistance. Loss of function in pancreatic ß-cells further aggravates the development of GDM. The level of serum platelet-derived growth factor (PDGF) reportedly increases in GDM patients. The present study investigated whether enhanced PDGF signaling directly causes ß-cell dysfunction during gestation. Serum PDGF levels were negatively correlated with ß-cell function in GDM patients. Administration of PDGF-BB disrupted glucose tolerance and ß-cell function without inducing apoptosis in gestational mice but had no similar effect in non-gestational mice. The ß-cell-specific genes encoding insulin synthesis proteins were decreased in the islets of PDGF-BB-treated gestational mice. In vitro experiments using INS1 insulinoma cells showed that PDGF-BB promoted cell proliferation, whereas it downregulated ß-cell-specific genes. Taken together, these findings suggested that PDGF reduces ß-cell function during gestation possibly through ß-cell dedifferentiation.