How Does Preeclampsia Affect The Liver – Background: Preeclampsia is a disease with far-reaching consequences that extend beyond the immediate postpartum period and have serious lifelong consequences. Preeclampsia affects most organ systems in the body. These sequelae are partially mediated by the incompletely understood pathophysiology of preeclampsia and associated vascular changes.
Contents: Current research focuses on elucidating the pathophysiology of preeclampsia with the goal of implementing accurate screening and treatment approaches as the disease develops and progresses. Preeclampsia causes significant short- and long-term maternal morbidity and mortality not only in the cardiovascular system but also in other organ systems throughout the body. These effects persist after pregnancy and immediately after giving birth.
- 1 How Does Preeclampsia Affect The Liver
- 2 Explainer: What Is Pre Eclampsia, And How Does It Affect Mums And Babies?
How Does Preeclampsia Affect The Liver
Summary: The objective of this review is to discuss the current understanding of how the pathophysiology of preeclampsia is associated with adverse health outcomes in patients with this disease and briefly discuss ways to improve overall outcomes.
How Pre Eclampsia Affects Pregnancy Outcomes In Pregnancy
Hypertensive disorders of pregnancy (HDP) are a major cause of pregnancy-related morbidity and mortality. These disorders have far-reaching consequences well beyond pregnancy and the postpartum period. According to the Centers for Disease Control (CDC), HDP, including preeclampsia, accounts for nearly 7% of all maternal deaths (1). HDP carries numerous diagnoses, including chronic hypertension, gestational hypertension, preeclampsia, severe preeclampsia, and eclampsia (2, 3). There is data to show that, similar to chronic hypertension, preeclampsia has serious consequences later in life. Therefore, a thorough understanding of the pathogenesis and prediction of HDP and its impact on short- and long-term health outcomes is important to provide optimal care to pregnant patients, especially those outside the postpartum period.
To improve long-term morbidity in pregnant patients, it is of utmost importance to minimize the onset and early diagnosis of diseases. There is no perfect prediction model that can accurately identify all patients who will develop HDP or define those at highest risk of long-term disease. However, risk factors for the disease have been identified. As determined by the American College of Obstetricians and Gynecologists (ACOG), risk factors for developing preeclampsia include prior preeclampsia, chronic hypertension, diabetes, kidney disease, autoimmune diseases such as lupus, and multiple pregnancies (2, 4, 5) . Black race has traditionally been identified as a risk factor for the development of HDP, as blacks have a significantly higher incidence of preeclampsia than whites (6). However, recent research on health inequities raises the question of whether race or ethnicity is a specific risk factor for HDP, or whether race and ethnicity simply reflect unequal access to care and adverse socioeconomic conditions that they exist in the healthcare system and in society. Done.
Preeclampsia and HDP have established guidelines to help clinicians make the diagnosis (Table 1). (2, 7) Chronic hypertension is defined as elevated blood pressure (≥ 140/90) diagnosed before pregnancy or twice at least 4 hours apart before the 20th week of pregnancy (8). Even if these patients were diagnosed with chronic hypertension before pregnancy, they remain at risk for worsening hypertension and developing preeclampsia. Gestational hypertension is diagnosed when blood pressure rises to ≥ 140/90 (defined as blood pressure in the mild range) on two occasions at least 4 hours apart after 20 weeks (2). Patients with this diagnosis are at high risk of developing preeclampsia but have no obvious signs and symptoms of preeclampsia. Patients diagnosed with early pregnancy are at a higher risk of developing preeclampsia, with 15–25% of patients eventually developing preeclampsia (9). The risk of this progression increases the earlier the disease is diagnosed, making careful monitoring of the patient necessary.
Several diagnostic challenges exist regarding the accurate diagnosis of preeclampsia, particularly in the context of overlapping disease and patient symptoms. People with chronic hypertension may experience worsening blood pressure during pregnancy, but this in itself does not guarantee a diagnosis of preeclampsia. Patient observation and evaluation are necessary to further characterize the diagnosis in this subgroup of patients. Furthermore, patients meeting criteria for preeclampsia with persistent symptoms represent a unique cohort. These symptoms require a comprehensive examination, and since the symptoms of preeclampsia are vague and nonspecific, evaluation is essential to rule out other causes of the symptoms (16).
Abnormal Placentation, Angiogenic Factors, And The Pathogenesis Of Preeclampsia.
Patients with preeclampsia typically have some degree of elevated blood pressure (17). You may have persistent headaches, right upper abdominal pain, or changes in vision. Sometimes patients may complain of increased swelling in the lower extremities which, although not diagnostic of preeclampsia, should certainly raise concerns about the development of the disease. If no symptoms are present, the doctor should be alerted to the suspicion by referral to a laboratory for signs that may indicate the development of preeclampsia. Patients typically have their blood pressure checked at each appointment, and overall blood pressure trends are important because patients diagnosed with preeclampsia often have elevated blood pressure during pregnancy (18). In addition to the patient’s symptoms, the fetus often presents a pathology compatible with preeclampsia. Although not specified in the American College of Obstetricians and Gynecologists (ACOG) US guidelines, international organizations recommend that the diagnosis of preeclampsia include fetal growth restriction and other signs of uteroplacental insufficiency (7). Therefore, any changes in the growth or health of the fetus requires a thorough evaluation by the doctor.
A more in-depth discussion of diagnostic modalities and criteria is beyond the scope of this article, but it is important to recognize the signs and symptoms of HDP if diagnosed early in pregnancy. This is because if diagnosed early in pregnancy, there is a greater risk of it progressing to a more serious disease and leading to long-term illness. Term morbidity (9).
The pathophysiology of HDP is not fully understood, but proposed contributors include immunologic changes resulting from placental dysfunction and poor uteroplacental perfusion (Figure 1). Importantly, the underlying mechanisms thought to contribute to vascular dysfunction in preeclampsia are similar to those of cardiovascular and atherosclerotic disease in non-pregnant individuals. These similarities may help explain why preeclampsia is associated with an increased risk of cardiovascular disease later in life.
Figure 1. Two-step model of the pathogenesis of preeclampsia. Stage 1 consists of the preclinical stage and is characterized by an abnormal placenta, resulting in the release of soluble factors into the maternal circulation, leading to systemic endothelial dysfunction and hypertension (stage 2).
Explainer: What Is Pre Eclampsia, And How Does It Affect Mums And Babies?
In normal pregnancy, cytotrophoblasts invade the myometrium and spiral arteries, creating a rich network of vascular anastomoses that ultimately perfuse the placenta and fetus ( 19 ). In patients with preeclampsia, cytotrophoblasts fail to develop the invasive phenotype necessary to create a robust anastomosis, resulting in decreased and less intravascular invasion of the spiral arteries (20-22). These abnormal blood vessels have narrow calibers, leading to placental ischemia and inefficient oxygen supply (23). This is demonstrated in step 1 of Figure 1. Furthermore, it has been shown that higher levels of a variety of proinflammatory molecules, including natural killer cells and other nonspecific markers of inflammation, are present in patients with preeclampsia (5, 24). In normal pregnancy, there is “immune tolerance” due to changes in the maternal immune system surrounding T cells (24). In pregnancies without preeclampsia, Th1 and Th2 cells coexist in harmony to prevent excessive inflammation and fetal rejection. In models of preeclampsia, this balance is disrupted and many T cells switch to the Th1 phenotype, similar to patients with chronic autoimmune diseases ( 19 , 24 ). Th1 cells promote inflammation through increases in proinflammatory cytokines, autoantibodies, and oxidative stress, which further exacerbates the damage and ischemia observed in preeclampsia ( 24 ).
The complex process of development of preeclampsia may be promoted by the combination of an abnormal placenta and ischemia, leading to the release of proinflammatory and antiangiogenic proteins into the maternal circulation and, ultimately, to endothelial dysfunction, leading to the clinical syndrome observed in Fare . Patients with preeclampsia. In particular, the two most studied and relevant biomarkers for the development of preeclampsia are soluble FMS-like tyrosine kinase-1 (sFlt-1) and placental growth factor (PlGF) (5). sFlt-1 is an antiangiogenic factor that inhibits angiogenesis (25). Higher levels of sFlt-1 are found in the placentas of preeclamptic and posteclamptic patients ( 25 , 26 ). In patients with preeclampsia, PlGF levels are lower and the ratio of sFlt-1 to PlGF is increased (26, 27). This is illustrated in step 2 of Figure 1.
Overall, the pathogenesis of preeclampsia is very complex and probably multifactorial. The major principles proposed in the development involve abnormal placentation leading to inappropriate remodeling of the spiral artery, resulting in tissue hypoxia causing endothelial damage leading to hypertensive pathology. Meanwhile, changes in the maternal immune system in patients with preeclampsia promote chronic low-level inflammation, continuing to perpetuate the cycle of endothelial damage. This combination may result in an imbalance between proangiogenic and antiangiogenic factors. The complex interaction between placental pathology, inflammation, and angiogenic changes ultimately causes the clinical syndrome known as preeclampsia and contributes to adverse patient health outcomes during pregnancy and postpartum ( 28 , 29 ).
Preeclampsia can cause serious harm to patients’ health during pregnancy, immediately after giving birth, and beyond. Understanding the risk of preeclampsia and the pathophysiology of the disease process can help prevent maternal morbidity and mortality. The spectrum of these adverse outcomes is discussed in detail.
Preeclampsia: Risk Factors, Symptoms, & Treatment
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