RESUMEN
BACKGROUND Placenta accreta spectrum (PAS) is a complex obstetric complication that poses a major risk for life-threatening hemorrhage. The pathogenesis of PAS is known to be related to placentogenesis, trophoblastic cells invasion, and previous obstetrical procedures that cause uterine wall defects. However, the precise mechanism of this disease has not been fully explained. This study aimed to evaluate the differences in maximum depth of invasion and distribution pattern of implantation site intermediate trophoblasts between PAS and non-accreta cases. MATERIAL AND METHODS This was an observational, analytic, cross-sectional study that utilized paraffin block specimen of peripartum hysterectomy performed in Hasan Sadikin General Hospital Bandung from 2018 to 2020. Sixty-four samples were obtained, then classified as PAS and non-accreta (normal placenta). Implantation site-intermediate trophoblasts were identified using CD-146 staining. Maximum invasion depth of intermediate trophoblasts was measured in micrometers, while the distribution pattern was assessed and classified into 2 groups: confluent and scattered. RESULTS We found that the maximum invasion depth of the intermediate trophoblasts was significantly higher in the PAS group compared to that of the non-accreta group (2453.52±1172.122 µm vs 1613.59±822.588 µm, P=0.009). The confluent distribution pattern was significantly more common in the PAS group compared to that of the non-accreta group (87.2% vs 17.6%, P=0.0001). CONCLUSIONS The findings of our study suggested that implantation site intermediate trophoblasts play a role in the pathophysiology of placenta accreta. Further studies are needed to determine factors that affect trophoblast invasion leading to placenta accreta spectrum.
Asunto(s)
Placenta Accreta , Embarazo , Femenino , Humanos , Trofoblastos/patología , Miometrio/patología , Estudios Transversales , Útero/patología , Placenta/patologíaRESUMEN
BACKGROUND: Placental soluble fms-like tyrosine kinase-1 (sFlt-1) which is an antagonist of vascular endothelial growth factor and placental growth factor (PIGF), is considered as one of etiology factors cause endothelial damage in preeclampsia due to increase of sFlt-1 level that change vascular endothelial integrity. This study aims to analyze the difference of sFlt-1 and PlGF concentration in severe preeclampsia and normal pregnancy, and the correlation between both in occurrence of severe preeclampsia. METHOD: This is case control study involving 18 subjects with severe preeclampsia and 19 subjects with normal pregnancy as controls who met inclusion and exclusion criteria. Concentration of sFlt-1 and PlGF are measured with ELISA. Statistical analysis is performed with Chi square test, Fisher's exact test, T test, Mann-Whitney test, and Spearman's rank correlation test. RESULTS: This study results in no significant difference in characteristics of gestational age, and parity in both study groups. Median concentration of sFlt-1 in severe preeclampsia is higher (20,524.75 pg/mL) compared with normal pregnancy (6820.4 pg/mL). Concentration of PlGF is lower in severe preeclampsia (47 pg/mL) compared with normal pregnancy (337 pg/mL). sFlt-1 concentration is higher in severe preeclampsia compared to normal pregnancy. PlGF concentration is lower in severe preeclampsia compared to normal pregnancy. Ratio of sFlt-1 and PlGF concentration is significantly correlated in both severe preeclampsia and normal pregnancy. CONCLUSIONS: There is a significant negative correlation between the concentration of sFLt-1 and PlGF in normal pregnancy.
Asunto(s)
Placenta/metabolismo , Preeclampsia/sangre , Proteínas Gestacionales/sangre , Receptor 1 de Factores de Crecimiento Endotelial Vascular/sangre , Femenino , Edad Gestacional , Humanos , Paridad , Factor de Crecimiento Placentario , Embarazo , SolubilidadRESUMEN
BACKGROUND: Preeclampsia is a major cause of morbidity and mortality, both maternal and perinatal. The etiology and pathophysiology of preeclampsia remain unknown. Research shows the implantation of the placenta in preeclampsia occurs due to incomplete angiogenic imbalance as one of the preeclampsia pathogenesis. PlGF is angiogenic protein which is synthesized in placenta by mRNA PlGF. When damage occurs, mRNA will be released from cell and form cell-free mRNA. This study aims to analyze the differences between the PlGF mRNA expression in severe preeclampsia and normal pregnancy as well as to measure the relationship between cell-free mRNA and levels of PlGF with the incidence of severe preeclampsia. METHODS: The method used in this study is an observational analytic study with cross-sectional design. Blood samples were obtained from patients with preeclampsia and normal pregnancies as the controlling factors in accordance with inclusion and exclusion criterias. Examination of the PlGF level was measured by ELISA method and mRNA PIGF expression was measured by RT-PCR. Physical and laboratory examinations of patients were recorded and collected as data. Calculations were done by statistical analysis. RESULTS: Mean of the cell-free mRNA PlGF expression level in severe preeclampsia is 2.2983 ng/mL within the scale of 1.96-2.83 ng/mL and deviation standard of 0.1897. Using Pearson Analysis Test, the result shows that there is a positive correlation between cell-free mRNA expression and PlGF protein level in severe preeclampsia, with r = 0.640 dan p < 0.004. CONCLUSION: There is no difference between expression of cell-free mRNA PlGF in severe preeclampsia serum and normal pregnancy. There is a significant correlation between expression of cell-free mRNA and PlGF protein level in severe preeclampsia.