La pré-éclampsie du post-partum : hypothèses physiopathologiques

Background: Pre-eclampsia (PE) is an ischemic placental disease that is clinically expressed by a maternal-fetal syndrome. Only delivery can stop the progression of the disease. PE can occur after delivery and this atypical from of PE is not explained by our current understanding of the physiopathology. The objective of this work was to formulate physiopathological hypotheses for post-partum PE, to explore them by identifying the risk factors, potential triggers and to correlate them to a histological study of the placenta of women who would later present with post-partum pre-eclampsia. Methods: This is a case-control study, comparing the demographic and obstetrical characteristics of cases of post-partum PE (n=50) with cases of early-onset PE (n=100), late-onset PE (n=100) and normotensive pregnancies (n=100). For the pathological study, 30 placentas per group were included. Patients were identified on a registry of hypertensive disorders of pregnancy and through the codification of the International Classification of Diseases (ICD).  Results: There was no difference in term of age, body mass index, primiparity, use of reproductive technology and neonatal death between groups. Post-partum PE was associated with Afro-Caribbean ethnicity (OR 3.0, CI 95% 1.3-6.7; p <0.01), pre-gestationnal hypertension (OR 46.3, CI 95% 7.4-∞; p <0.01), twin pregnancies (OR 7.7, CI 95% 1.4-78.7); p<0.01), peri-partum infectious diseases (OR 6.5, IC 95% 1.8-29.7; p<0.01), induction of labor (OR 6.0, IC 95% 1.8-21.4; p <0.01), and normal-high blood pressure value before discharge of the maternity ward, for the systolic value (OR 10.2, IC 95% 4.3-25.4; p<0.01) as well as for the diastolic value (OR 30.2, IC 95% 8.3-168.3 ; p<0.01). Forty percent of placenta of post-partum PE had acute deciduitis (early PE: 5.7% (2), p<0.01; late PE: 16.7% (5), p=0.046; normal: 3.2% (1), p<0.01), 39.4% (13) had abnormal maturation of the villi (early PE: 77.2%(27), p<0.01; late PE: 26.7%(8), p=0.3; normal: 3.2 %(1), p<0.01), 18.2% (6) had decidual arteriolopathy (early PE: 34.3% (12), p=0.13; late PE: 10% (3), p=0.35; normal: 9.7% (3), p=0.33) and 9.1% (3) had villous ischemia and infarction (early PE: 51.4%  (18), p<0.01; late PE: 13.3% (4), p=0.6; normal: 16.1% (5), p=0.4). Conclusions: Our work suggests that patients presenting with post-partum PE have similar risk profile than the typical antepartum PE, in particular with late-onset PE (after 34 weeks of gestation). Modification of the delivery date by medical intervention and induction of labor, might act as a trigger, as well as an acute infection. First signs of post-partum PE can be detected through measurement of blood pressure before discharge of the maternity.  There were no significant differences in the placentas in terms of decidual arteriolopathy and villi ischemic changes between post-partum PE, late onset PE and the controls. There was a higher level of acute deciduitis in the placenta of post-partum PE. Altogether, our results suggests that post-partum preeclampsia is more of a maternal disease, characterized by an increased inflammatory state, potentially triggered by infection, and in which placental ischemic disease has little or no role to play.

Keyphrases: Post-partum, Hypertension, Placenta, Pre-eclampsia, Histopathology, Women health