Fig 1.
pGSN levels during pregnancy and prediction of delivery within 28 days.
(A) Plasma gelsolin (pGSN) levels in samples from pregnant women during the first, second, and third trimesters, as well as non-pregnant (Non-Preg) women. The mean ± SD pGSN concentrations were 53.54 ± 14.84 μg/mL in non-pregnant controls (n = 8), 39.49 ± 15.22 μg/mL in normal pregnancies during the first trimester (n = 14), 30.00 ± 8.11 μg/mL in the second trimester (n = 18), and 21.57 ± 4.77 μg/mL in the third trimester (n = 18). The mean ± SD pGSN concentrations significantly decreased across gestational stages (one-way ANOVA, p < 0.0001). Post hoc comparisons revealed significant differences between non-pregnant controls and the second trimester (p = 0.013), non-pregnant controls and the third trimester (p < 0.0001), and between the first and third trimesters (p = 0.0002). Bars represent median values. * p < 0.05; *** p < 0.005; **** p < 0.0001. (B) Receiver operating characteristic (ROC) curve for the prediction of delivery within 28 days using pGSN levels. The area under the ROC curve (AUC) was 0.67.
Table 1.
Clinical characteristics of patients with preterm premature rupture of membranes.
Table 2.
Peripartum inflammatory markers and pGSN levels.
Fig 2.
Temporal changes in WBC, CRP, and pGSN levels in a patients with pPROM.
(A) Plasma gelsolin (pGSN) levels at the time of membrane rupture (day −2 to day 0) in cases of preterm premature rupture of membranes (pPROM), compared with levels in pregnant women without membrane rupture (Non-ROM) during the second trimester (25–33 weeks of gestation). No statistically significant difference in pGSN levels was observed between the two groups (p = 0.16). (B) Comparison of WBC, CRP, and pGSN levels at the time of membrane rupture (ROM; day −2 to day 0) and at delivery (0–7 days before delivery) in patients with pPROM. pGSN levels were significantly lower at delivery compared to the time of membrane rupture. (C) Correlation between the rate of pGSN decline and the interval from ROM to delivery (Spearman’s ρ = 0.84, p = 0.009). WBC, white blood cell; CRP, C-reactive protein; ROM, rupture of membrane.
Fig 3.
Temporal changes and correlation between pGSN and WBC in pPROM cases.
(A) Longitudinal changes in pGSN levels and white blood cell (WBC) counts in individual pPROM cases. The x-axis represents the number of days since membrane rupture. (B) Correlation between pGSN levels and WBC counts. Spearman’s rank correlation coefficient was ρ = −0.1874 (95% CI: −0.4689 to 0.2817, p = 0.2289), indicating no significant correlation. pGSN, plasma gelsolin; pPROM, preterm premature rupture of membranes.
Fig 4.
Temporal changes and correlation between pGSN and CRP in pPROM cases.
(A) Longitudinal changes in pGSN levels and C-reactive protein (CRP) in individual pPROM cases. The x-axis represents the number of days since membrane rupture. (B) Correlation between pGSN levels and CRP. Spearman’s rank correlation coefficient was ρ = −0.5138 (95% CI: −0.7119 to −0.2400, p = 0.0005), indicating a significant negative correlation. pGSN, plasma gelsolin; pPROM, preterm premature rupture of membranes.
Fig 5.
Representative immunohistochemical images of amniotic membranes.
(A) In one stage-Ⅲ CAM case, localized expression of GSN was observed in the chorionic membrane layer (arrows). In contrast, no GSN expression was detected in another stage-Ⅲ CAM case or a CAM-negative control. (B) Quantification of GSN-positive cells showed a significantly higher count in the CAM group compared to the non-CAM groups. Scale bar = 50 μm; pGSN, plasma gelsolin; CAM, chorioamnionitis.