Adenomyosis was associated not only with an increased incidence of preterm delivery, as previously reported, but also with an increased risk of second trimester miscarriage, preeclampsia, and placental malposition, which could lead to poor perinatal outcomes.

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Constitutive expression of elafin and SLPI in cervical cells during pregnancy suggests their essential roles in local tissue homeostasis and immune defense. The elevations in cervical elafin and SLPI expression in the women with preterm delivery might reflect the local response to the pathogen invasion into the cervix preceding preterm labor.

MFS patients after prophylactic ARR are still at high risk of type B aortic dissection during the peripartum period.

Recent evidence indicates that elevated placental adenosine signaling contributes to preeclampsia (PE). However, the molecular basis for the chronically enhanced placental adenosine signaling in PE remains unclear. Here, we report that hypoxia‐inducible factor‐1α (HIF‐1α) is crucial for the enhancement of placental adenosine signaling. Utilizing a pharmacologic approach to reduce placental adenosine levels, we found that enhanced adenosine underlies increased placental HIF‐1α in an angiotensin receptor type 1 receptor agonistic autoantibody (AT1‐AA)‐induced mouse model of PE. Knockdown of placental HIF‐1α in vivo suppressed the accumulation of adenosine and increased ecto‐5’‐nucleotidase (CD73) and adenosine A2B receptor (ADORA2B) in the placentas of PE mouse models induced by AT1‐AA or LIGHT, a TNF superfamily cytokine (TNFSF14). Human in vitro studies using placental villous explants demonstrated that increased HIF‐1α resulting from ADORA2B activation facilitates the induction of CD73, ADORA2B, and FLT‐1 expression. Overall, we demonstrated that (a) elevated placental HIF‐1α by AT1‐AA or LIGHT upregulates CD73 and ADORA2B expression and (b) enhanced adenosine signaling through upregulated ADORA2B induces placental HIF‐1α expression, which creates a positive feedback loop that promotes FLT‐1 expression leading to disease development. Our results suggest that adenosine‐based therapy targeting the malicious cycle of placental adenosine signaling may elicit therapeutic effects on PE.

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Uterine fibroids are known to degenerate during pregnancy, but it is unknown if similar pathologic condition occurs in adenomyosis. A 38‐year‐old para 1 woman exhibited uterine tenderness and a markedly elevated inflammatory response at 22 weeks of gestation. Based on magnetic resonance imaging (MRI) findings indicative of hemorrhagic components in an adenomyosis lesion, we judged these features resulted from degeneration of adenomyosis after excluding the possibility of underlying infection by amniocentesis. Although these symptoms improved with conservative management, nonreassuring fetal status prompted an emergency cesarean section at 27 weeks of gestation. MRI performed 4 months postpartum revealed the degeneration had completely disappeared. The present case confirms the presence of a pathologic condition—transient degeneration in adenomyosis—which is triggered by pregnancy.

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