Przedłużona preeklampsja poporodowa – Patofizjologia i mechanizm

Przedłużona preeklampsja poporodowa
Patofizjologia i mechanizm

Przedłużona preeklampsja poporodowa to rzadkie, ale poważne schorzenie manifestujące się nadciśnieniem tętniczym oraz białkomoczem ≥300 mg/24h lub stosunkiem białka do kreatyniny ≥0,3, pojawiające się od 48 godzin do 6 tygodni po porodzie. Patogeneza jest wieloczynnikowa i obejmuje dysfunkcję śródbłonka naczyniowego spowodowaną zaburzeniem równowagi czynników angiogennych, w tym podwyższonym poziomem sFlt-1 oraz zwiększonym stosunkiem sFlt-1/PlGF. Nieprawidłowa inwazja trofoblastu i niedokrwienie łożyska prowadzą do uwalniania antyangiogennych mediatorów, co skutkuje nasilonym stresem oksydacyjnym i stanem zapalnym. Leki takie jak NLPZ (ibuprofen, indometacyna) oraz alkaloidy sporyszu mogą nasilać objawy poprzez mechanizmy naczynioskurczowe. Diagnostyka opiera się na kryteriach preeklampsji z uwzględnieniem czasu wystąpienia i obecności objawów narządowych, a leczenie obejmuje m.in. stosowanie siarczanu magnezu w profilaktyce drgawek.

Przedłużona preeklampsja poporodowa – patogeneza

Przedłużona preeklampsja poporodowa to rzadkie, ale poważne schorzenie charakteryzujące się wystąpieniem wysokiego ciśnienia tętniczego i białkomoczu lub objawów dysfunkcji narządowej po porodzie. Może wystąpić de novo w okresie poporodowym u kobiet, które nie doświadczyły nadciśnienia w czasie ciąży, lub stanowić kontynuację stanu przedrzucawkowego z okresu ciąży. Najczęściej rozwija się w ciągu 48 godzin po porodzie, ale może pojawić się do 6 tygodni po urodzeniu dziecka.¹²

Mimo że patogeneza przedłużonej preeklampsji poporodowej nie jest w pełni poznana, istnieją liczne hipotezy wyjaśniające mechanizm tego zjawiska, które kwestionują tradycyjne przekonanie, że poród i usunięcie łożyska leczy preeklampsję.³⁴

Patofizjologiczne mechanizmy przedłużonej preeklampsji poporodowej

Choć patogeneza przedłużonej preeklampsji poporodowej pozostaje nie w pełni wyjaśniona, mechanizmy leżące u jej podstaw wydają się złożone i wieloczynnikowe, podobnie jak w przypadku preeklampsji występującej w trakcie ciąży.⁵⁶ Dane naukowe sugerują, że przedłużona preeklampsja poporodowa może być odrębnym zespołem chorobowym lub podtypem preeklampsji występującej w okresie przedporodowym.

Czynniki angiogenne i dysfunkcja śródbłonka

Jednym z najważniejszych mechanizmów patogenetycznych w preeklampsji, w tym w jej postaci poporodowej, jest zaburzenie równowagi czynników angiogennych. Badania wykazały, że kobiety, u których rozwinęła się poporodowa preeklampsja de novo, miały znacząco wyższe poziomy rozpuszczalnej fms-podobnej kinazy tyrozynowej-1 (sFlt-1) oraz wyższy stosunek sFlt-1/PlGF (czynnik wzrostu łożyska) w porównaniu z kobietami, które pozostały normotensyjne po porodzie.⁷

sFlt-1 jest antyangiogennym czynnikiem, który wiąże się z naczyniowym czynnikiem wzrostu śródbłonka (VEGF) i PlGF, neutralizując ich działanie proangiogenne i prowadząc do dysfunkcji śródbłonka.⁸⁹ Dysfunkcja śródbłonka jest kluczowym elementem patogenezy przedłużonej preeklampsji poporodowej i stoi u podstaw zaburzenia równowagi mediatorów wazoaktywnych, co prowadzi do zwiększonej produkcji substancji naczynioskurczowych.¹⁰

Niedoskonałe przekształcanie tętnic spiralnych i hipoperfuzja łożyska

Podobnie jak w preeklampsji przedporodowej, nieprawidłowa implantacja łożyska i nieodpowiednia inwazja trofoblastu do tętnic macicznych może odgrywać rolę w patogenezie przedłużonej preeklampsji poporodowej. W normalnej ciąży cytotrofoblasty płodowe wnikają do macicznych tętnic spiralnych, przekształcając je w naczynia o dużej pojemności zdolne do zapewnienia odpowiedniego przepływu krwi przez łożysko.¹¹

W preeklampsji cytotrofoblasty płodowe nie różnicują się prawidłowo w fenotyp śródbłonkowy, co prowadzi do płytkiej inwazji tętnic spiralnych, które pozostają naczyniami o małej średnicy i wysokim oporze. Skutkuje to względnym niedokrwieniem łożyska, hipoksją, stresem oksydacyjnym i uwolnieniem czynników antyangiogennych do krążenia matczynego.¹²¹³

Ta patologia łożyskowa może przyczyniać się do wystąpienia objawów preeklampsji po porodzie, ponieważ proces złuszczania wyściółki macicy po porodzie może być związany z opóźnionym wystąpieniem objawów przedłużonej preeklampsji poporodowej.¹⁴

Stan zapalny i stres oksydacyjny

Profil immunologiczny i zapalny w momencie wystąpienia choroby znacząco różni się między preeklampsją poporodową a przedporodową.¹⁵ Preeklampsja, w tym jej postać poporodowa, charakteryzuje się nasilonym ogólnoustrojowym stanem zapalnym i niewłaściwą aktywacją śródbłonka.¹⁶

Stres oksydacyjny odgrywa istotną rolę w patogenezie preeklampsji. Nadmierna produkcja reaktywnych form tlenu (ROS) prowadzi do uszkodzenia lipidowej dwuwarstwy poprzez peroksydację, niszczenia komórek śródbłonka i odsłonięcia podśródbłonka, do którego przylegają płytki krwi, uwalniające tromboksan A2 i powodujące skurcz naczyń i agregację płytek.¹⁷

Wpływ leków i innych czynników na rozwój przedłużonej preeklampsji poporodowej

Niektóre leki mogą przyczyniać się do rozwoju przedłużonej preeklampsji poporodowej. Niesteroidowe leki przeciwzapalne (NLPZ), takie jak ibuprofen i indometacyna, mogą wywoływać przełom nadciśnieniowy w ciągu 2-10 godzin od ich przyjęcia. Wpływ NLPZ na ciśnienie krwi jest prawdopodobnie spowodowany zwiększoną syntezą naczynioskurczowych czynników nerkowych, a także zatrzymaniem sodu i wody.¹⁸

Inne leki, które mogą odgrywać rolę w rozwoju przedłużonej preeklampsji poporodowej, to alkaloidy sporyszu, takie jak ergotamina i metylergonowina, stosowane w leczeniu atonii macicy i zapobieganiu krwotokom macicznym. Leki te działają poprzez receptory alfa-adrenergiczne, powodując obwodowy skurcz naczyń i nie powinny być stosowane u osób z nadciśnieniem, ponieważ mogą zaostrzać epizody przełomu nadciśnieniowego.¹⁹

Mechanizmy molekularne i epigenetyczne

Badania sugerują znaczące zaburzenia epigenetyczne w łożysku pacjentek z przedłużoną preeklampsją poporodową. Wykazano, że nowo rozpoznana przedłużona preeklampsja poporodowa ma zarówno wspólne, jak i unikalne szlaki molekularne z klasyczną preeklampsją.²⁰²¹

Ostatnie badania zidentyfikowały również sygnatury RNA wolnokrążącego (cfRNA), które mogą być obiecujące w przewidywaniu preeklampsji na kilka tygodni przed wystąpieniem objawów. Odkryto zmniejszony sygnał w hepatocytach, nerkach, komórkach śródbłonka i mięśniach gładkich w trakcie rozwoju ciąży oraz zwiększony sygnał płytkowy przed 12. tygodniem ciąży dla preeklampsji, co jest zgodne z powszechną patogenezą preeklampsji.²²

Jedno interesujące, choć nieudowodnione, spostrzeżenie wskazuje, że surowica poporodowa może mieć efekt kompensacyjny w odniesieniu do formowania kanalików i migracji komórek, co może sugerować obecność czynników regeneracyjnych pojawiających się po porodzie.²³

Zmiany hormonalne i objętościowe po porodzie

Szybkie zmiany hormonalne po porodzie mogą wpływać na regulację ciśnienia krwi, potencjalnie prowadząc do nadciśnienia. W normalnej ciąży występuje zwiększenie objętości osocza nawet o 45%, aby sprostać większym potrzebom krążeniowym łożyska i narządów matczynych. Zwiększenie objętości osocza oznacza większe zatrzymanie wody i sodu, co powoduje proporcjonalny wzrost ciśnienia krwi.²⁴²⁵

Kliniczne implikacje patogenezy przedłużonej preeklampsji poporodowej

Zrozumienie patogenezy przedłużonej preeklampsji poporodowej ma kluczowe znaczenie dla wczesnej diagnostyki i skutecznego leczenia tego schorzenia, które może prowadzić do poważnych powikłań, jeśli nie zostanie szybko rozpoznane i leczone.

Diagnostyka i leczenie oparte na mechanizmach patogenetycznych

Kryteria diagnostyczne dla preeklampsji i przedłużonej preeklampsji poporodowej są takie same, mimo różnicy w czasie wystąpienia. W przypadku przedłużonej preeklampsji poporodowej początek przypada na 48 godzin do 6 tygodni po porodzie.²⁶

Przedłużona preeklampsja poporodowa różni się od poporodowego nadciśnienia tym, że obejmuje białkomocz wynoszący 300 mg lub więcej w 24-godzinnej zbiórce moczu, odczyt dipstick moczu wynoszący 2 lub więcej, lub stosunek białka do kreatyniny w moczu wynoszący 0,3 lub więcej.²⁷

W przypadku braku białkomoczu z nowo rozpoznanym nadciśnieniem, objawy mózgowe lub neurologiczne, takie jak ból głowy i zmiany widzenia, podwyższone transaminazy wątrobowe, małopłytkowość, dyskomfort w nadbrzuszu lub prawym górnym kwadrancie, obrzęk płuc i niewydolność nerek mogą wskazywać na preeklampsję.²⁸

Siarczan magnezu jest rozpoczynany przed porodem w celu zmniejszenia ryzyka drgawek matczynych (rzucawki). Większość protokołów zaleca kontynuację przez 24 godziny po porodzie, gdy ryzyko drgawek pozostaje wysokie. W niektórych okolicznościach, takich jak niepełna kontrola ciśnienia krwi lub niepokojący profil kliniczny, leczenie może przekraczać 24 godziny. Jeśli drgawki wystąpią po porodzie, określa się je jako rzucawkę poporodową.²⁹

Długoterminowe konsekwencje zdrowotne

Badania wykazały, że preeklampsja zwiększa ryzyko wystąpienia w ciągu życia przewlekłego nadciśnienia, choroby niedokrwiennej serca, cukrzycy typu 2, niewydolności serca, epizodów zakrzepowo-zatorowych i udaru. Pacjentki z przedłużoną preeklampsją poporodową są 4 razy bardziej narażone na udar niż przeciętna kobieta po porodzie.³⁰

Uważa się, że ryzyko rozwoju przewlekłego nadciśnienia zależy od ciężkości preeklampsji. W metaanalizie zaobserwowano kilka związków między zwiększonym ryzykiem chorób sercowo-naczyniowych a ciążą powikłaną preeklampsją. Związki te obejmowały około 4-krotny wzrost ryzyka późniejszego rozwoju nadciśnienia i około 2-krotny wzrost ryzyka choroby niedokrwiennej serca, żylnej choroby zakrzepowo-zatorowej i udaru.³¹

Obszary przyszłych badań nad patogenezą przedłużonej preeklampsji poporodowej

Przedłużona preeklampsja poporodowa pozostaje relatywnie słabo zbadanym zagadnieniem klinicznym. Przyszłe badania powinny skupić się na lepszym zrozumieniu jej patofizjologii i specyficznych czynników ryzyka.³²

Biomarkery i przewidywanie ryzyka

Identyfikacja biomarkerów umożliwiających wczesne przewidywanie przedłużonej preeklampsji poporodowej jest obiecującym obszarem badań. Zidentyfikowano nowe potencjalne biomarkery do wczesnego poporodowego przewidywania nowo powstałej przedłużonej preeklampsji poporodowej.³³³⁴

Badania nad angiogennymi czynnikami, profilami zapalnymi i patologią łożyska mogą być przydatne w ustaleniu, czy przedłużona preeklampsja poporodowa jest podtypem preeklampsji przedporodowej, czy stanowi odrębną jednostkę chorobową.³⁵

Badania nad mechanizmem molekularnym

Dalsze badania powinny koncentrować się na tym, jak profile ekspresji genów mogą być wpływane przez ekspozycję na surowicę pacjentek, oraz wykorzystywać techniki edycji genów do badania efektu genotyp-fenotyp w rozwoju preeklampsji.³⁶

Badania nad profilem immunologicznym i zapalnym są również potrzebne, aby lepiej zrozumieć różnice między preeklampsją poporodową a przedporodową.³⁷

Spersonalizowane podejście do leczenia

Lepsze zrozumienie patogenezy przedłużonej preeklampsji poporodowej może prowadzić do opracowania spersonalizowanych podejść do leczenia, które uwzględniają specyficzne mechanizmy leżące u podstaw choroby u poszczególnych pacjentek.³⁸

Chociaż istnieją obiecujące badania podstawowe badające potencjał terapeutyczny obniżenia poziomu sFlt-1 lub podwyższenia poziomu PlGF, istnieje niewiele dowodów klinicznych, że modulowanie czynników angiogennych poprawia wyniki matczyne lub okołoporodowe u kobiet z preeklampsją.³⁹

Implikacje kliniczne i wnioski

Przedłużona preeklampsja poporodowa to potencjalnie zagrażający życiu stan, który wymaga natychmiastowego rozpoznania i leczenia. Mimo że dokładny mechanizm jej rozwoju nie jest w pełni poznany, podstawowym procesem patologicznym wydaje się być dysfunkcja śródbłonka naczyniowego będąca wynikiem zaburzenia równowagi czynników angiogennych.⁴⁰⁴¹

Lepsze zrozumienie patogenezy przedłużonej preeklampsji poporodowej jest niezbędne dla opieki nad pacjentką i poradnictwa, przewidywania przed wypisem ze szpitala i ma kluczowe znaczenie dla zmniejszenia zachorowalności i śmiertelności matek w okresie poporodowym.⁴²

Przyszłe badania powinny koncentrować się na patofizjologii i specyficznych czynnikach ryzyka przedłużonej preeklampsji poporodowej, aby lepiej zrozumieć, czy jest to odrębna jednostka chorobowa od preeklampsji z początkiem przedporodowym, czy też stanowi jej podtyp.⁴³⁴⁴

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Materiały źródłowe

#1 Postpartum Preeclampsia: Causes, Symptoms & Treatment
https://my.clevelandclinic.org/health/diseases/17733-postpartum-preeclampsia
Postpartum preeclampsia is a rare but serious condition related to high blood pressure after you give birth. Its most common within 48 hours of delivery but can occur up to six weeks after your baby is born. Postpartum preeclampsia can lead to strokes, seizures and other complications if not promptly treated. […] The exact cause is unknown. Healthcare providers know that certain factors increase your risk. […] Postpartum preeclampsia can lead to serious complications without treatment, including: Permanent damage to your brain, liver and kidneys. Seizures. Excess fluid in your lungs (pulmonary edema). Stroke. Blood clots. HELLP syndrome. Death. […] Knowing the signs of postpartum preeclampsia can save your life. Pay attention to your body and how you feel after your baby is delivered. Tell your healthcare provider if you have symptoms of postpartum preeclampsia like headaches, swelling and blurred vision. While postpartum preeclampsia is rare, its very serious and can lead to permanent organ damage, stroke or death. Early detection and prompt treatment with medication is the best way to ensure a full recovery.
#2 Postpartum Preeclampsia: Clinical Overview of Hypertensive Crisis
https://www.clinicaladvisor.com/features/postpartum-preeclampsia-overview/
Other medications that are thought to play a role in postpartum preeclampsia include the ergot alkaloids such as ergotamine and methylergonovine for treatment of uterine atony and prevention of uterine hemorrhage. […] These medications work through alpha adrenergic receptors that cause peripheral vasoconstriction and should not be used in people with hypertension as it can exacerbate an episode of hypertensive crises. […] The diagnostic criteria for preeclampsia and postpartum preeclampsia are the same despite the difference in time of onset. […] In terms of postpartum preeclampsia, the onset occurs 48 hours to 6 weeks following delivery of a newborn. […] Postpartum preeclampsia differs from postpartum hypertension in that it includes proteinuria of 300 mg or more within a 24-hour urine collection, urine dipstick reading of 2 or more, or urine protein/creatinine ratio of 0.3 or greater.
#3 Postpartum Preeclampsia
https://www.preeclampsia.org/postpartum-preeclampsia
Delivery is not the cure for preeclampsia. […] It’s important to know that delivery is not the cure for preeclampsia. Any woman can develop preeclampsia after her baby is born, or postpartum preeclampsia, whether she experienced high blood pressure during her pregnancy or not. […] Thereâs no definitive cause of preeclampsia. Delivery, in most cases, is the acute treatment, not a cure. âIt takes time for the uterus to shed its lining after birth, so this process may be behind the delay thatâs sometimes seen in [postpartum preeclampsia] after delivery,” says James N. Martin, MD, past president of the American College of Obstetricians and Gynecologists and member of the Preeclampsia Foundation Medical Advisory Board. Itâs also possible this condition begins during pregnancy but doesnât show signs or symptoms until after the baby has arrived.
#4
https://pmc.ncbi.nlm.nih.gov/articles/PMC8857508/
We believe further study is needed to determine if new-onset postpartum preeclampsia/eclampsia is a distinct entity from preeclampsia with antepartum-onset; that said, we recommend that this condition be highlighted here and in national/international guidelines as it is under-recognized by providers. […] The traditional adage in obstetrics has always been that delivery of the placenta cures preeclampsia, thus the onset of preeclampsia days to weeks after placental delivery raises questions about whether delayed postpartum preeclampsia is a sub-type of antepartum preeclampsia or whether it represents a separate disease entity. […] Studies of angiogenic factors, inflammatory profiles and placental pathology have been useful in informing this distinction. […] A prospective study that collected blood samples prior to cesarean section noted that women who developed new onset postpartum preeclampsia had significantly higher sFlt1 levels and a higher sFlt1 / PlGF ratio compared with women who remained normotensive postpartum.
#5
https://pmc.ncbi.nlm.nih.gov/articles/PMC8857508/
In contrast, the immune and inflammatory profile at the time of disease seems to differ significantly between postpartum and antepartum preeclampsia. […] Overall, it is clear from the limited data that the etiology of postpartum preeclampsia as well as whether it is a subtype of antepartum preeclampsia remain unanswered.
#6 Postpartum preeclampsia – Symptoms & causes – Mayo Clinic
https://www.mayoclinic.org/diseases-conditions/postpartum-preeclampsia/symptoms-causes/syc-20376646
Postpartum preeclampsia is a rare condition that occurs when you have high blood pressure and excess protein in your urine soon after childbirth. […] The causes of postpartum preeclampsia and preeclampsia that occurs during pregnancy aren’t well understood.
#7
https://pmc.ncbi.nlm.nih.gov/articles/PMC8857508/
We believe further study is needed to determine if new-onset postpartum preeclampsia/eclampsia is a distinct entity from preeclampsia with antepartum-onset; that said, we recommend that this condition be highlighted here and in national/international guidelines as it is under-recognized by providers. […] The traditional adage in obstetrics has always been that delivery of the placenta cures preeclampsia, thus the onset of preeclampsia days to weeks after placental delivery raises questions about whether delayed postpartum preeclampsia is a sub-type of antepartum preeclampsia or whether it represents a separate disease entity. […] Studies of angiogenic factors, inflammatory profiles and placental pathology have been useful in informing this distinction. […] A prospective study that collected blood samples prior to cesarean section noted that women who developed new onset postpartum preeclampsia had significantly higher sFlt1 levels and a higher sFlt1 / PlGF ratio compared with women who remained normotensive postpartum.
#8 Preeclampsia/Eclampsia Associated Retinopathy – EyeWiki
https://eyewiki.org/Preeclampsia/Eclampsia_Associated_Retinopathy
Research has demonstrated that excess quantities of the antiangiogenic factors soluble fms-like tyrosine kinase-1 (sFlt1) and soluble endoglin (sEng) are released by the placenta into maternal blood, causing widespread endothelial dysfunction that results in hypertension, proteinuria, and other systemic manifestations of preeclampsia. […] The two important antiangiogenic factors implicated in preeclampsia are soluble vascular endothelial growth factor (VEGF) and soluble endoglin. Nitric oxide signaling is involved in vascular relaxation and is reduced in preeclampsia. The molecular basis for placental dysregulation of these pathogenic factors remains unknown.
#9 SciELO Brazil – Preeclampsia: Vascular Pathophysiological Mechanism and the Basis for Early Diagnosis and Treatment Preeclampsia: Vascular Pathophysiological Mechanism and the Basis for Early Diagnosis and Treatment
https://www.scielo.br/j/rbgo/a/cGDhnvFQd6PWDFdSTggPhqv/?lang=en
Placental hypoxia generates the production of soluble fms-like tyrosine kinase receptor-1 (sFlt-1), which binds to the vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) that are responsible for the maintenance of endothelial integrity. […] The pathophysiology of other signs and symptoms, such as headache, tinnitus, scotoma, vomiting, nausea, epigastric and right upper quadrant pain, oliguria, hyperreflexia, and convulsions involves an imbalance between thromboxane and prostacyclin and the consequences of subsequent hypoxia and ischemia resulting from the obstruction of blood flow. […] It is important to note that in the brain there is a significant increase in the production of excitatory amino acids such as glutamate, which binds to the N-methyl D-aspartate (NMDA) receptor, allowing the opening of calcium channels in the cell membrane, with calcium entry into hypoxic cells triggering the typical tonic-clonic convulsions of eclampsia. […] In view of the aforementioned considerations, we can see that progress is being made in the understanding of the pathophysiology of preeclampsia that allows us to explore new fields of scientific research, seeking therapeutic interventions to achieve success in the management of the disease.
#10 Modern concepts of etiology, pathogenesis and risk factors for preeclampsia – Abramova – Journal of obstetrics and women’s diseases
https://journals.eco-vector.com/jowd/article/view/77046
Endothelial dysfunction is central to the maternal syndrome pathogenesis of PE and underlies the imbalance of vasoactive mediators, which induces a shift toward increased vasoconstrictor production. […] An endogenous antiangiogenic factor (endostatin), sFlt1, is a potent VEGF antagonist that is significantly elevated in PE. […] Increased expression of sFlt1 (in vitro) induces glomerular endotheliosis with the disappearance of fenestras, which histologically resembles renal damage in PE. […] Matrix metalloproteinases (MMPs) are of great importance in the formation of endothelial dysfunction in PE. […] A decreased expression of various MMP groups, together with increased endogenous MMP inhibitor synthesis, induces endothelial damage and increases vascular reactivity, which leads to pronounced vasoconstriction. […] Evidence on the involvement of the renin-angiotensin-aldosterone system in PE pathogenesis has been obtained. […] One of the potential mechanisms for increasing sensitivity to angiotensin II is the expression of autoantibodies to AT2R1 in PE women, which are produced in response to placental ischemia and systemic inflammation.
#11 Hypertensive Disorders of Pregnancy – OpenAnesthesia
https://www.openanesthesia.org/keywords/hypertensive-disorders-of-pregnancy/
The pathogenesis of preeclampsia is abnormal placentation due to impaired angiogenesis of spiral arteries (terminal branches of the uterine artery), leading to placental ischemia and release of antiangiogenic factors to maternal circulation, leading to systemic endothelial dysfunction. […] During normal placental development, fetal cytotrophoblasts invade the maternal spiral arteries, converting them into large caliber capacitance vessels capable of providing adequate placental perfusion to sustain fetal growth. […] In preeclampsia, the fetal cytotrophoblasts fail to differentiate into the invasive endothelial phenotype. The end result is a shallow invasion of the maternal spiral arteries, which remain small-caliber, high-resistance vessels. […] This results in relative placental under perfusion, hypoxia, oxidative stress, and release of antiangiogenic factors into the maternal circulation, causing widespread systemic maternal endothelial dysfunction.
#12 Preeclampsia: Background, Pathophysiology, Etiology
https://emedicine.medscape.com/article/1476919-overview
Placental implantation with abnormal trophoblastic invasion of uterine vessels is a major cause of hypertension associated with preeclampsia syndrome. In fact, studies have shown that the degree of incomplete trophoblastic invasion of the spiral arteries is directly correlated with the severity of subsequent maternal hypertension. This is because the placental hypoperfusion resulting from the incomplete invasion leads by an unclear pathway to the release of systemic vasoactive compounds that cause an exaggerated inflammatory response, vasoconstriction, endothelial damage, capillary leak, hypercoagulability, and platelet dysfunction, all of which contribute to organ dysfunction and the various clinical features of the disease. […] Data show that an imbalance of proangiogenic and antiangiogenic factors produced by the placenta may play a major role in mediating endothelial dysfunction. Angiogenesis is critical for successful placentation and the normal interaction between trophoblasts and endothelium. […] Evidence also suggests that oxidative stress, circulatory maladaptation, inflammation, and humoral, mineral, and metabolic abnormalities contribute to the endothelial dysfunction and pathogenesis of preeclampsia.
#13 Hypertensive Disorders of Pregnancy – OpenAnesthesia
https://www.openanesthesia.org/keywords/hypertensive-disorders-of-pregnancy/
The pathogenesis of preeclampsia is abnormal placentation due to impaired angiogenesis of spiral arteries (terminal branches of the uterine artery), leading to placental ischemia and release of antiangiogenic factors to maternal circulation, leading to systemic endothelial dysfunction. […] During normal placental development, fetal cytotrophoblasts invade the maternal spiral arteries, converting them into large caliber capacitance vessels capable of providing adequate placental perfusion to sustain fetal growth. […] In preeclampsia, the fetal cytotrophoblasts fail to differentiate into the invasive endothelial phenotype. The end result is a shallow invasion of the maternal spiral arteries, which remain small-caliber, high-resistance vessels. […] This results in relative placental under perfusion, hypoxia, oxidative stress, and release of antiangiogenic factors into the maternal circulation, causing widespread systemic maternal endothelial dysfunction.
#14 Postpartum Preeclampsia
https://www.preeclampsia.org/postpartum-preeclampsia
Delivery is not the cure for preeclampsia. […] It’s important to know that delivery is not the cure for preeclampsia. Any woman can develop preeclampsia after her baby is born, or postpartum preeclampsia, whether she experienced high blood pressure during her pregnancy or not. […] Thereâs no definitive cause of preeclampsia. Delivery, in most cases, is the acute treatment, not a cure. âIt takes time for the uterus to shed its lining after birth, so this process may be behind the delay thatâs sometimes seen in [postpartum preeclampsia] after delivery,” says James N. Martin, MD, past president of the American College of Obstetricians and Gynecologists and member of the Preeclampsia Foundation Medical Advisory Board. Itâs also possible this condition begins during pregnancy but doesnât show signs or symptoms until after the baby has arrived.
#15
https://pmc.ncbi.nlm.nih.gov/articles/PMC8857508/
In contrast, the immune and inflammatory profile at the time of disease seems to differ significantly between postpartum and antepartum preeclampsia. […] Overall, it is clear from the limited data that the etiology of postpartum preeclampsia as well as whether it is a subtype of antepartum preeclampsia remain unanswered.
#16 Diagnosis and Management of Preeclampsia | AAFP
https://www.aafp.org/pubs/afp/issues/2004/1215/p2317.html
Preeclampsia is a pregnancy-specific multisystem disorder of unknown etiology. […] Although the exact cause of preeclampsia remains unclear, many theories center on problems of placental implantation and the level of trophoblastic invasion. It is important to remember that although hypertension and proteinuria are the diagnostic criteria for preeclampsia, they are only symptoms of the pathophysiologic changes that occur in the disorder. One of the most striking physiologic changes is intense systemic vasospasm, which is responsible for decreased perfusion of virtually all organ systems. Perfusion also is diminished because of vascular hemoconcentration and third spacing of intravascular fluids. In addition, preeclampsia is accompanied by an exaggerated inflammatory response and inappropriate endothelial activation. Activation of the coagulation cascade and resultant microthrombi formation further compromise blood flow to organs.
#17 SciELO Brazil – Preeclampsia: Vascular Pathophysiological Mechanism and the Basis for Early Diagnosis and Treatment Preeclampsia: Vascular Pathophysiological Mechanism and the Basis for Early Diagnosis and Treatment
https://www.scielo.br/j/rbgo/a/cGDhnvFQd6PWDFdSTggPhqv/?lang=en
Preeclampsia is a multifactorial disease caused by environmental factors that act over a genetic base, permitting the occurrence of this disorder. […] The interaction of risk factors and multiple polymorphic genes induces the synthesis of several proteins with effects differing from their original function, leading to the impairment of placental perfusion and the consequent production of mediators that damage the endothelium. […] Physiologically, in order to promote vascular remodeling, the changes of the decidua also occur in the inner area of the myometrium. […] The onset of the circulation is normally a progressive periphery-center phenomenon, and high levels of oxidative stress in the periphery may induce the formation of the chorion laeve. […] Superoxide ion, hydroxyls and hydrogen peroxide damage the lipid bilayer through peroxidation, destroying endothelial cells and exposing the subendothelium to which platelets adhere and release thromboxane A2, causing vasoconstriction and platelet aggregation.
#18 Postpartum Preeclampsia: Clinical Overview of Hypertensive Crisis
https://www.clinicaladvisor.com/features/postpartum-preeclampsia-overview/
Timely recognition and treatment of postpartum preeclampsia is essential to improving morbidity and mortality in postpartum patients. […] The exact development of postpartum preeclampsia is not completely understood; however, during normal pregnancy, an increase of up to 45% of plasma volume occurs to meet the greater circulatory needs of the placenta and maternal organs. […] An increase in plasma volume means further retention of water and sodium that causes a proportional increase in blood pressure. […] The NSAIDs discussed were ibuprofen and indomethacin and the time between taking the NSAID and onset of hypertensive crises ranged from 2 to 10 hours. […] This influence of NSAIDs on blood pressure is thought to be caused by the increase in synthesis of renal vasoconstrictors as well as retention of sodium and water.
#19 Postpartum Preeclampsia: Clinical Overview of Hypertensive Crisis
https://www.clinicaladvisor.com/features/postpartum-preeclampsia-overview/
Other medications that are thought to play a role in postpartum preeclampsia include the ergot alkaloids such as ergotamine and methylergonovine for treatment of uterine atony and prevention of uterine hemorrhage. […] These medications work through alpha adrenergic receptors that cause peripheral vasoconstriction and should not be used in people with hypertension as it can exacerbate an episode of hypertensive crises. […] The diagnostic criteria for preeclampsia and postpartum preeclampsia are the same despite the difference in time of onset. […] In terms of postpartum preeclampsia, the onset occurs 48 hours to 6 weeks following delivery of a newborn. […] Postpartum preeclampsia differs from postpartum hypertension in that it includes proteinuria of 300 mg or more within a 24-hour urine collection, urine dipstick reading of 2 or more, or urine protein/creatinine ratio of 0.3 or greater.
#20 New-onset postpartum preeclampsia: epigenetic mechanism and prediction.
https://scholarlyworks.beaumont.org/pathology_laboratory_medicine_articles/123/
OBJECTIVE: Placental cytosine (CpG) methylation was measured to predict new-onset postpartum preeclampsia (NOPP) and interrogate its molecular pathogenesis. […] CONCLUSIONS: There was significant placental epigenetic dysregulation in NOPP. NOPP shared both common and unique molecular pathways with classic preeclampsia. Finally, we have identified novel potential biomarkers for the early post-partum prediction of NOPP.
#21
https://tandf.figshare.com/articles/journal_contribution/New-onset_postpartum_preeclampsia_epigenetic_mechanism_and_prediction/15141430
Placental cytosine (CpG) methylation was measured to predict new-onset postpartum preeclampsia (NOPP) and interrogate its molecular pathogenesis. […] There was significant placental epigenetic dysregulation in NOPP. NOPP shared both common and unique molecular pathways with classic preeclampsia. Finally, we have identified novel potential biomarkers for the early post-partum prediction of NOPP.
#22 Preeclampsia, Genomics and Public Health | Blogs | CDC
https://blogs.cdc.gov/genomics/2022/10/25/preeclampsia/
A recent study identified a cell free RNA (cfRNA) signature that was promising in predicting pre-eclampsia several weeks before the onset of symptoms. […] Though rarer, preeclampsia may also develop during the post-partum period. […] Studies have shown that genetic factors are associated with pregnancy complications, such as preeclampsia. […] Additionally, they found a decreased signal in hepatocyte, kidney, endothelial cell, and smooth muscle signatures across pregnancy development, and an increased platelet signal before 12 weeks of pregnancy for preeclampsia, which is consistent with common preeclampsia pathogenesis and with the specific diagnoses. […] Moufarrej and colleagues suggested that a series of clinical tests can be used to help to identify and stratify the pathogenesis of preeclampsia in real time, thus meeting important objectives for obstetric care, such as characterizing and stratifying the development of preeclampsia in real time. […] More studies need to be done on preeclampsia and genetics.
#23 Stanford researchers share new findings on preeclampsia pathogenesis, the effects of wildfires on preterm birth and hypertensive disorders at SMFM23 | Dunlevie Maternal-Fetal Medicine | Stanford Medicine
https://dunleviemfm.stanford.edu/news/stanford-researchers-share-new-findings-on-preeclampsia-pathogen.html
One interesting but unproven observation was that the postpartum sera had a compensating effect in regard to tube formation and cell migration, which could hint at restorative factors that come after giving birth. […] Whats next is that we would like to look further into how gene expression profiles would be impacted by exposure to patients sera and use gene editing techniques to explore the genotype-phenotype effect in the development of preeclampsia, Wu said.
#24 Postpartum Preeclampsia: Clinical Overview of Hypertensive Crisis
https://www.clinicaladvisor.com/features/postpartum-preeclampsia-overview/
Timely recognition and treatment of postpartum preeclampsia is essential to improving morbidity and mortality in postpartum patients. […] The exact development of postpartum preeclampsia is not completely understood; however, during normal pregnancy, an increase of up to 45% of plasma volume occurs to meet the greater circulatory needs of the placenta and maternal organs. […] An increase in plasma volume means further retention of water and sodium that causes a proportional increase in blood pressure. […] The NSAIDs discussed were ibuprofen and indomethacin and the time between taking the NSAID and onset of hypertensive crises ranged from 2 to 10 hours. […] This influence of NSAIDs on blood pressure is thought to be caused by the increase in synthesis of renal vasoconstrictors as well as retention of sodium and water.
#25 Postpartum Preeclampsia: A Silent, But Serious Condition | ColumbiaDoctors
https://www.columbiadoctors.org/news/postpartum-preeclampsia-silent-serious-condition
Postpartum preeclampsia happens when a womans blood pressure goes above 140/90 after childbirth. […] We dont know exactly what causes postpartum preeclampsia, but experts believe there are a few contributing factors. Quick changes in hormonal levels and fluids can affect blood pressure. […] Hormonal changes: The rapid hormonal shifts after childbirth can affect blood pressure regulation, potentially leading to hypertension. […] Studies show that the development of postpartum preeclampsia increases a womans risk of having heart disease or stroke later in life, so while it is important for all women to lead a heart-healthy lifestyle, it is even more important for women who experience hypertensive disorders of pregnancy, cautions Dr. Tolani.
#26 Postpartum Preeclampsia: Clinical Overview of Hypertensive Crisis
https://www.clinicaladvisor.com/features/postpartum-preeclampsia-overview/
Other medications that are thought to play a role in postpartum preeclampsia include the ergot alkaloids such as ergotamine and methylergonovine for treatment of uterine atony and prevention of uterine hemorrhage. […] These medications work through alpha adrenergic receptors that cause peripheral vasoconstriction and should not be used in people with hypertension as it can exacerbate an episode of hypertensive crises. […] The diagnostic criteria for preeclampsia and postpartum preeclampsia are the same despite the difference in time of onset. […] In terms of postpartum preeclampsia, the onset occurs 48 hours to 6 weeks following delivery of a newborn. […] Postpartum preeclampsia differs from postpartum hypertension in that it includes proteinuria of 300 mg or more within a 24-hour urine collection, urine dipstick reading of 2 or more, or urine protein/creatinine ratio of 0.3 or greater.
#27 Postpartum Preeclampsia: Clinical Overview of Hypertensive Crisis
https://www.clinicaladvisor.com/features/postpartum-preeclampsia-overview/
Other medications that are thought to play a role in postpartum preeclampsia include the ergot alkaloids such as ergotamine and methylergonovine for treatment of uterine atony and prevention of uterine hemorrhage. […] These medications work through alpha adrenergic receptors that cause peripheral vasoconstriction and should not be used in people with hypertension as it can exacerbate an episode of hypertensive crises. […] The diagnostic criteria for preeclampsia and postpartum preeclampsia are the same despite the difference in time of onset. […] In terms of postpartum preeclampsia, the onset occurs 48 hours to 6 weeks following delivery of a newborn. […] Postpartum preeclampsia differs from postpartum hypertension in that it includes proteinuria of 300 mg or more within a 24-hour urine collection, urine dipstick reading of 2 or more, or urine protein/creatinine ratio of 0.3 or greater.
#28 Postpartum Preeclampsia: Clinical Overview of Hypertensive Crisis
https://www.clinicaladvisor.com/features/postpartum-preeclampsia-overview/
In the absence of proteinuria with new-onset hypertension, cerebral or neurologic symptoms such as headache and vision changes, impaired liver transaminases double the normal value, thrombocytopenia with a platelet count less than 100,000/L, epigastric or right upper quadrant discomfort, pulmonary edema, and renal insufficiency with a creatinine greater than 1.1 mg/dL or doubling of serum creatinine are all indicative of preeclampsia. […] A Danish study evaluated the long-term effects of preeclampsia. […] Researchers discovered preeclampsia increases an individuals lifetime risk for chronic hypertension, ischemic heart disease, type 2 diabetes, congestive heart failure, thromboembolic events, and stroke. […] Patients with postpartum preeclampsia are 4 times more likely to suffer from stroke than the average postpartum person. […] It is thought the risk for development of chronic hypertension is dependent on the severity of preeclampsia.
#29 Postpartum Preeclampsia
https://www.preeclampsia.org/postpartum-preeclampsia
The early postpartum period (up to seven days after delivery) is when women who experience preeclampsia are at highest risk — much of this risk can be lessened with effective blood pressure control. […] Magnesium sulfate is started prior to delivery to reduce the risks of maternal seizures, eclampsia. Most protocols recommend continuation for 24 hours postpartum when the risk for seizures remains high. In some circumstances such as incomplete blood pressure control or a concerning clinical profile, treatment may exceed 24 hours. If a seizure occurs after delivery, it is referred to as postpartum eclampsia.
#30 Postpartum Preeclampsia: Clinical Overview of Hypertensive Crisis
https://www.clinicaladvisor.com/features/postpartum-preeclampsia-overview/
In the absence of proteinuria with new-onset hypertension, cerebral or neurologic symptoms such as headache and vision changes, impaired liver transaminases double the normal value, thrombocytopenia with a platelet count less than 100,000/L, epigastric or right upper quadrant discomfort, pulmonary edema, and renal insufficiency with a creatinine greater than 1.1 mg/dL or doubling of serum creatinine are all indicative of preeclampsia. […] A Danish study evaluated the long-term effects of preeclampsia. […] Researchers discovered preeclampsia increases an individuals lifetime risk for chronic hypertension, ischemic heart disease, type 2 diabetes, congestive heart failure, thromboembolic events, and stroke. […] Patients with postpartum preeclampsia are 4 times more likely to suffer from stroke than the average postpartum person. […] It is thought the risk for development of chronic hypertension is dependent on the severity of preeclampsia.
#31 Preeclampsia: Background, Pathophysiology, Etiology
https://emedicine.medscape.com/article/1476919-overview
Preeclampsia is characterized by endothelial dysfunction in pregnant women. Therefore, the possibility exists that preeclampsia may be a contributor to future cardiovascular disease. In a meta-analysis, several associations were observed between an increased risk of cardiovascular disease and a pregnancy complicated by preeclampsia. These associations included an approximately 4-fold increase in the risk of subsequent development of hypertension and an approximately 2-fold increase in the risk of ischemic heart disease, venous thromboembolism, and stroke. Moreover, women who had recurrent preeclampsia were more likely to have hypertension later in life. […] The mechanisms by which preeclampsia occurs is not certain, and numerous maternal, paternal, and fetal factors have been implicated in its development. The factors considered to be the most important include the following: Maternal immunologic intolerance, Abnormal placental implantation, Genetic, nutritional, and environmental factors, Cardiovascular and inflammatory changes.
#32
https://pmc.ncbi.nlm.nih.gov/articles/PMC8857508/
High blood pressure in the postpartum period is most commonly seen in women with antenatal hypertensive disorders but it can develop de novo in the postpartum timeframe. […] New-onset postpartum preeclampsia is an understudied disease entity with few evidence-based guidelines to guide diagnosis and management. […] Older maternal age, black race, and maternal obesity as well as cesarean delivery are all associated with a higher risk of postpartum preeclampsia. […] Postpartum preeclampsia may be associated with a higher risk of maternal morbidity than preeclampsia with antepartum-onset, yet remains a significantly understudied disease process. […] Future research should focus on the pathophysiology and specific risk factors. […] A better understanding is imperative for patient care and counseling, anticipatory guidance prior to hospital discharge and is critically important for reduction of maternal morbidity and mortality in the postpartum period.
#33 New-onset postpartum preeclampsia: epigenetic mechanism and prediction.
https://scholarlyworks.beaumont.org/pathology_laboratory_medicine_articles/123/
OBJECTIVE: Placental cytosine (CpG) methylation was measured to predict new-onset postpartum preeclampsia (NOPP) and interrogate its molecular pathogenesis. […] CONCLUSIONS: There was significant placental epigenetic dysregulation in NOPP. NOPP shared both common and unique molecular pathways with classic preeclampsia. Finally, we have identified novel potential biomarkers for the early post-partum prediction of NOPP.
#34
https://tandf.figshare.com/articles/journal_contribution/New-onset_postpartum_preeclampsia_epigenetic_mechanism_and_prediction/15141430
Placental cytosine (CpG) methylation was measured to predict new-onset postpartum preeclampsia (NOPP) and interrogate its molecular pathogenesis. […] There was significant placental epigenetic dysregulation in NOPP. NOPP shared both common and unique molecular pathways with classic preeclampsia. Finally, we have identified novel potential biomarkers for the early post-partum prediction of NOPP.
#35
https://pmc.ncbi.nlm.nih.gov/articles/PMC8857508/
We believe further study is needed to determine if new-onset postpartum preeclampsia/eclampsia is a distinct entity from preeclampsia with antepartum-onset; that said, we recommend that this condition be highlighted here and in national/international guidelines as it is under-recognized by providers. […] The traditional adage in obstetrics has always been that delivery of the placenta cures preeclampsia, thus the onset of preeclampsia days to weeks after placental delivery raises questions about whether delayed postpartum preeclampsia is a sub-type of antepartum preeclampsia or whether it represents a separate disease entity. […] Studies of angiogenic factors, inflammatory profiles and placental pathology have been useful in informing this distinction. […] A prospective study that collected blood samples prior to cesarean section noted that women who developed new onset postpartum preeclampsia had significantly higher sFlt1 levels and a higher sFlt1 / PlGF ratio compared with women who remained normotensive postpartum.
#36 Stanford researchers share new findings on preeclampsia pathogenesis, the effects of wildfires on preterm birth and hypertensive disorders at SMFM23 | Dunlevie Maternal-Fetal Medicine | Stanford Medicine
https://dunleviemfm.stanford.edu/news/stanford-researchers-share-new-findings-on-preeclampsia-pathogen.html
One interesting but unproven observation was that the postpartum sera had a compensating effect in regard to tube formation and cell migration, which could hint at restorative factors that come after giving birth. […] Whats next is that we would like to look further into how gene expression profiles would be impacted by exposure to patients sera and use gene editing techniques to explore the genotype-phenotype effect in the development of preeclampsia, Wu said.
#37
https://pmc.ncbi.nlm.nih.gov/articles/PMC8857508/
In contrast, the immune and inflammatory profile at the time of disease seems to differ significantly between postpartum and antepartum preeclampsia. […] Overall, it is clear from the limited data that the etiology of postpartum preeclampsia as well as whether it is a subtype of antepartum preeclampsia remain unanswered.
#38
https://pmc.ncbi.nlm.nih.gov/articles/PMC8857508/
High blood pressure in the postpartum period is most commonly seen in women with antenatal hypertensive disorders but it can develop de novo in the postpartum timeframe. […] New-onset postpartum preeclampsia is an understudied disease entity with few evidence-based guidelines to guide diagnosis and management. […] Older maternal age, black race, and maternal obesity as well as cesarean delivery are all associated with a higher risk of postpartum preeclampsia. […] Postpartum preeclampsia may be associated with a higher risk of maternal morbidity than preeclampsia with antepartum-onset, yet remains a significantly understudied disease process. […] Future research should focus on the pathophysiology and specific risk factors. […] A better understanding is imperative for patient care and counseling, anticipatory guidance prior to hospital discharge and is critically important for reduction of maternal morbidity and mortality in the postpartum period.
#39 Pathophysiology of preeclampsia: an angiogenic imbalance and long-lasting systemic vascular dysfunction | Hypertension Research
https://www.nature.com/articles/hr2016152
The mechanisms regulating sFlt1 production by trophoblastic cells are largely unknown. […] A placenta-derived soluble TGF- coreceptor, endoglin (sEng), also induces a preeclampsia-like syndrome in concert with sFlt1 in pregnant rats. […] As described above, preeclampsia can be characterized as a systemic vascular disorder with generalized endothelial dysfunction caused by a maternal antiangiogenic state. […] Despite promising basic research investigating the therapeutic potential of reducing sFlt1 levels or raising PlGF levels, there is little clinical evidence that modulating angiogenic factors improves maternal or perinatal outcomes in women with preeclampsia. […] A maternal antiangiogenic state induced by placental antiangiogenic factors has emerged as one of the most important mechanisms for systemic vascular dysfunction, a central feature of preeclampsia.
#40 Postpartum Preeclampsia: Clinical Overview of Hypertensive Crisis
https://www.clinicaladvisor.com/features/postpartum-preeclampsia-overview/
Timely recognition and treatment of postpartum preeclampsia is essential to improving morbidity and mortality in postpartum patients. […] The exact development of postpartum preeclampsia is not completely understood; however, during normal pregnancy, an increase of up to 45% of plasma volume occurs to meet the greater circulatory needs of the placenta and maternal organs. […] An increase in plasma volume means further retention of water and sodium that causes a proportional increase in blood pressure. […] The NSAIDs discussed were ibuprofen and indomethacin and the time between taking the NSAID and onset of hypertensive crises ranged from 2 to 10 hours. […] This influence of NSAIDs on blood pressure is thought to be caused by the increase in synthesis of renal vasoconstrictors as well as retention of sodium and water.
#41 Postpartum Preeclampsia: Causes, Symptoms & Treatment
https://my.clevelandclinic.org/health/diseases/17733-postpartum-preeclampsia
Postpartum preeclampsia is a rare but serious condition related to high blood pressure after you give birth. Its most common within 48 hours of delivery but can occur up to six weeks after your baby is born. Postpartum preeclampsia can lead to strokes, seizures and other complications if not promptly treated. […] The exact cause is unknown. Healthcare providers know that certain factors increase your risk. […] Postpartum preeclampsia can lead to serious complications without treatment, including: Permanent damage to your brain, liver and kidneys. Seizures. Excess fluid in your lungs (pulmonary edema). Stroke. Blood clots. HELLP syndrome. Death. […] Knowing the signs of postpartum preeclampsia can save your life. Pay attention to your body and how you feel after your baby is delivered. Tell your healthcare provider if you have symptoms of postpartum preeclampsia like headaches, swelling and blurred vision. While postpartum preeclampsia is rare, its very serious and can lead to permanent organ damage, stroke or death. Early detection and prompt treatment with medication is the best way to ensure a full recovery.
#42
https://pmc.ncbi.nlm.nih.gov/articles/PMC8857508/
High blood pressure in the postpartum period is most commonly seen in women with antenatal hypertensive disorders but it can develop de novo in the postpartum timeframe. […] New-onset postpartum preeclampsia is an understudied disease entity with few evidence-based guidelines to guide diagnosis and management. […] Older maternal age, black race, and maternal obesity as well as cesarean delivery are all associated with a higher risk of postpartum preeclampsia. […] Postpartum preeclampsia may be associated with a higher risk of maternal morbidity than preeclampsia with antepartum-onset, yet remains a significantly understudied disease process. […] Future research should focus on the pathophysiology and specific risk factors. […] A better understanding is imperative for patient care and counseling, anticipatory guidance prior to hospital discharge and is critically important for reduction of maternal morbidity and mortality in the postpartum period.
#43
https://pmc.ncbi.nlm.nih.gov/articles/PMC8857508/
We believe further study is needed to determine if new-onset postpartum preeclampsia/eclampsia is a distinct entity from preeclampsia with antepartum-onset; that said, we recommend that this condition be highlighted here and in national/international guidelines as it is under-recognized by providers. […] The traditional adage in obstetrics has always been that delivery of the placenta cures preeclampsia, thus the onset of preeclampsia days to weeks after placental delivery raises questions about whether delayed postpartum preeclampsia is a sub-type of antepartum preeclampsia or whether it represents a separate disease entity. […] Studies of angiogenic factors, inflammatory profiles and placental pathology have been useful in informing this distinction. […] A prospective study that collected blood samples prior to cesarean section noted that women who developed new onset postpartum preeclampsia had significantly higher sFlt1 levels and a higher sFlt1 / PlGF ratio compared with women who remained normotensive postpartum.
#44
https://pmc.ncbi.nlm.nih.gov/articles/PMC8857508/
In contrast, the immune and inflammatory profile at the time of disease seems to differ significantly between postpartum and antepartum preeclampsia. […] Overall, it is clear from the limited data that the etiology of postpartum preeclampsia as well as whether it is a subtype of antepartum preeclampsia remain unanswered.