Pre-eclampsia ( PE ) is a pregnancy disorder characterized by the onset of high blood pressure and often a significant amount of protein in the urine. When it appears, the condition begins after 20 weeks of pregnancy. In severe disease there may be damage to red blood cells, low blood platelet count, liver function impairment, renal dysfunction, swelling, breathlessness due to fluid in the lungs, or visual impairment. Pre-eclampsia increases the risk of poor outcomes for both mother and baby. If left untreated, it can cause seizures at a point known as eclampsia.
Risk factors for pre-eclampsia include obesity, previous hypertension, older age, gestational diabetes, and diabetes mellitus. It is also more common in a woman's first pregnancy and if she is pregnant with twins. The underlying mechanism involves the formation of abnormal blood vessels in the placenta among other factors. Most cases are diagnosed before delivery. Rarely, pre-eclampsia can begin in the postpartum period. While historically both high blood pressure and protein in urine are needed to make the diagnosis, some definitions also include those with hypertension and related organ dysfunction. Blood pressure is defined high when greater than 140 mmHg systolic or 90 mmHg diastolic at two separate times, more than four hours apart in women after twenty weeks of pregnancy. Pre-eclampsia is routinely screened during prenatal care.
Recommendations for prevention include: aspirin in those at high risk, calcium supplementation in areas with low intake, and treatment of previous hypertension with drugs. In those who deliver babies and pre-eclampsia placentas is an effective treatment. When delivery becomes recommended depends on how severe pre-eclampsia and how far in a woman's pregnancy. Blood pressure drugs, such as labetalol and methyldopa, can be used to improve the condition of the mother before delivery. Magnesium sulfate can be used to prevent eclampsia in those with severe disease. Bedrest and salt intake have not been found to be beneficial for treatment or prevention.
Pre-eclampsia affects 2-8% of pregnancies worldwide. Hypertensive disorders of pregnancy (which includes pre-eclampsia) is one of the most common causes of pregnancy-related death. They produce 46,900 deaths by 2015. Pre-eclampsia usually occurs after 32 weeks; However, if it happens earlier, it is associated with a worse outcome. Women who have experienced preeclampsia have a greater risk of heart disease and stroke later in life. The word eclampsia comes from the Greek term for lightning. The first description known about this condition was by Hippocrates in the 5th century BC.
Video Pre-eclampsia
Signs and symptoms
Swelling (especially in the hands and face) was initially considered an important sign for the diagnosis of pre-eclampsia. However, since swelling is a common occurrence in pregnancy, its usefulness as a differentiating factor in preeclampsia is not high. Pitting edema (unusual swelling, especially on the hands, feet, or face, can be detected by leaving the grooves when pressed) can be significant, and should be reported to the doctor.
In general, there are no signs of specific preeclampsia, and even seizures in pregnancy are more likely to have other causes than eclampsia in modern practice. Furthermore, symptoms such as epigastric pain can be misinterpreted as heartburn. The diagnosis, therefore, depends on the coincident discovery of some pre-eclampsia features, the final proof is their regression after childbirth.
Maps Pre-eclampsia
Cause
There is no known cause of pre-eclampsia, although it may be related to a number of factors. Some of these factors include:
- Placentation abnormal (formation and development of placenta)
- Immunological factors
- Previous or previous maternal pathology - pre-eclampsia is seen more in higher incidence in individuals with pre-existing hypertension, obesity, antiphospholipid antibody syndrome, and those with a history of pre-eclampsia
- Food factors, e.g. calcium supplementation in areas where dietary low calcium intake has been shown to reduce the risk of pre-eclampsia
- Environmental factors, e.g. air pollution
Those with long-term high blood pressure had a 7 to 8 times higher risk than those who did not.
Physiologically, studies have linked preeclampsia with the following physiological changes: changes in the interaction between maternal and placental immune responses, placental injury, endothelial cell injury, vascular reactivity changes, oxidative stress, imbalance between vasoactive substances, intravascular volume depletion, and intravascular coagulation disseminated.
While the exact cause of pre-eclampsia remains unclear, there is strong evidence that the predisposing cause of women susceptible to pre-eclampsia is abnormally planted placentas. This abnormally planted placenta may result in poor uterine and placental perfusion, resulting in hypoxic states and increased oxidative stress and release of anti-angiogenic proteins along with inflammatory mediators into maternal plasma. The main consequence of this sequence of events is general endothelial dysfunction. Abnormal implantation may be derived from the maternal immune system response to the placenta, in particular the lack of immunologic tolerance established in pregnancy. Endothelial dysfunction results in hypertension and many other symptoms and complications associated with pre-eclampsia. Those with pre-eclampsia may have a lower risk of developing breast cancer.
The abnormal chromosomal microRNA cluster (C19MC) damages invasion of extravellular trophoblast cells into the spiral arteries, leading to high resistance, low blood flow, and low nutrient supply to the fetus.
Risk factors
Known risk factors for pre-eclampsia include:
- Having never given birth before
- Diabetes mellitus
- Kidney disease
- Chronic hypertension
- Pre-eclampsia history before
- Family history of pre-eclampsia
- Mother age (& gt; 35 years)
- Obesity
- Antiphospholipid antibody syndrome
- Double pregnancy
- After donating the kidney.
- Have subclinical hypothyroidism or thyroid antibodies
- Placental abnormalities such as placental ischemia.
Pathogenesis
Although much research on the mechanism of pre-eclampsia has occurred, the exact pathogenesis remains uncertain. Pre-eclampsia is thought to result from abnormal placenta, the elimination of which ends the disease in many cases. During normal pregnancy, the placenta vascularization to allow the exchange of water, gas, and solutes, including nutrients and wastes, between maternal and fetal circulation. Abnormal development of the placenta causes poor placental perfusion. The placenta of women with pre-eclampsia is abnormal and is characterized by a poor trophoblast invasion. It is thought that this produces oxidative stress, hypoxia, and release of factors that promote endothelial dysfunction, inflammation, and other possible reactions.
Clinical manifestations of pre-eclampsia are associated with generalized endothelial dysfunction, including vasoconstriction and end-organ ischemia. Implied in this generalized endothelial dysfunction may be an imbalance of angiogenic and anti-angiogenic factors. Both levels of circulation and placenta of fms-like tyrosine kinase-1 (sFlt-1) are higher soluble in women with pre-eclampsia than in women with normal pregnancies. sFlt-1 is an anti-angiogenic protein that antagonizes vascular endothelial growth factor (VEGF) and placental growth factor (PIGF), both of which are proangiogenic factors. The soluble endoglin (sEng) has also been shown to increase in women with pre-eclampsia and has anti-angiogenic properties, such as sFlt-1.
Both sFlt-1 and saturated in all pregnant women to some extent, support the idea that hypertensive disease in pregnancy is a normal, chaotic adaptation of pregnancy. Since natural killer cells are closely involved in placentation and placentation involves maternal immune tolerance for foreign placenta, it is not surprising that the maternal immune system may respond more negatively to the arrival of multiple placentas under certain circumstances, such as placenta. which is more invasive than usual. Early maternal rejection of the placental cytotrophoblast may be the cause of spiral artery that is not modeled in the case of preeclampsia associated with shallow implantation, leading to downstream hypoxia and the appearance of maternal symptoms in response to sFlt-1 and regulated saturation.
Oxidative stress can also play an important part in the pathogenesis of pre-eclampsia. The main source of reactive oxygen species (ROS) is the enzyme xanthine oxidase (XO) and this enzyme mainly occurs in the liver. One hypothesis is that increased purine catabolism from placental hypoxia results in increased ROS production in the liver of the mother and release into the maternal circulation that causes endothelial cell damage.
Abnormalities in the maternal immune system and inadequate gestational immune tolerance appear to play a major role in preeclampsia. One of the major differences found in pre-eclampsia is a shift toward the response of Th 1 and the production of IFN-?. The origin of IFN-? not clearly identified and can be a natural uterine cell killer, placental dendritic cells modulate helper T helper response, changes in synthesis or response to regulatory molecules, or changes in regulatory T cell function in pregnancy. Immature immune responses promoting preeclampsia may also be caused by changes in fetal consciousness or inflammatory triggers. It has been documented that fetal cells such as fetal erythroblasts and cell-free fetal DNA increase in the maternal circulation in women who develop preeclampsia. These findings have led to the hypothesis that pre-eclampsia is a disease process by which placental lesions such as hypoxia allow increased fetal material into the maternal circulation, which in turn leads to immune responses and endothelial damage, and which ultimately results in preeclampsia and eclampsia.
One hypothesis for susceptibility to preeclampsia is maternal-fetal conflicts between maternal and fetal organisms. After the first trimester trophoblast enters the maternal spiral artery to alter the spiral artery and thus gain more access to maternal nutrition. Sometimes there is a trophoblast invasion disorder that causes inadequate changes to the uterine spiral artery. It is hypothesized that the developing embryo releases biochemical signals that cause the woman to develop hypertension and pre-eclampsia so that the fetus may benefit from the large amount of maternal nutrient circulation as the increase of blood flow to the placenta is impaired. This results in a conflict between maternal and fetal fitness and survival because the fetus is invested solely in survival and fitness while the mother is invested in this and subsequent pregnancy.
Another evolutionary hypothesis for susceptibility to preeclampsia is the idea of ​​ensuring the bond between mother and father and father's investment in the fetus. The researchers presume that pre-eclampsia is an adaptation for the mother to stop investing in a fetus who may have an unavailable father donor, as determined by recurrent cement exposure from the father's donor to the mother. Studies show that women who are often exposed to partner sperm before conception have a reduced risk of pre-eclampsia. Also, subsequent pregnancies by the same father donor had a reduced risk of pre-eclampsia while subsequent pregnancies by different fathers donors had a higher risk for developing pre-eclampsia.
In normal early embryonic development, the outer epithelial layer contains cytotrophoblastic cells, a type of stem cell found in trophoblasts that subsequently differentiate into fetal placenta. These cells differentiate into many types of placental cells, including extravard trophoblast cells. Extravili trophoblast cells are a type of invasive cell that overhauls the maternal spiral artery by replacing the maternal epithelium and smooth muscle lining the spiral arteries that cause arterial dilatation. It prevents maternal vasoconstriction in the spiral arteries and allows for continued blood supply and nutrients to the growing fetus with low resistance and high blood flow.
In pre-eclampsia, the abnormal expression of the chromosome 19 microRNA cluster (C19MC) in the placental cell pathway reduces the migration of the extraviliated trophoblast. Specific microRNAs in this cluster that may cause invasion of the abnormal spiral arteries include miR-520h, miR-520b, and 520c-3p. This disrupts the invasion of extravillus trophoblast cells into the maternal spiral artery, leading to high resistance and low blood flow and low nutrient supply to the fetus.
Diagnosis
Tests for preeclampsia are recommended throughout pregnancy through measurement of a woman's blood pressure.
Diagnostic criteria
Pre-eclampsia is diagnosed when a pregnant woman develops:
- Blood pressure> = 140 mm Hg systolic or> = 90 Âμm Hg diastolic on two separate readings taken at least four to six hours after 20 weeks' gestation in an individual with previously normal blood pressure.
- In women with essential hypertension beginning before 20 weeks' gestation, the diagnostic criteria are: increased systolic blood pressure (SBP)> 30mmHg or increased diastolic blood pressure (DBP)> = 15 mmHg./li>
- Proteinuria> = 0.3 grams (300 mg) or more protein in a 24-hour urine sample or urinary SPOT protein for creatinine ratio> = 0.3 or urinary dipstick readings of 1 or greater (dipstick reading should only be used if other quantitative methods are not available).
Suspicions for pre-eclampsia should be maintained in complicated pregnancies by high blood pressure, even in the absence of proteinuria. Ten percent of individuals with other signs and symptoms of pre-eclampsia and 20% of individuals diagnosed with eclampsia do not exhibit proteinuria. In the absence of proteinuria, the presence of new-onset hypertension (high blood pressure) and new onset of one or more of the following is suggestive of the diagnosis of pre-eclampsia:
- Evidence of renal dysfunction (oliguria, elevated creatinine levels)
- Liver function impairment (noted by liver function tests)
- Thrombocytopenia (platelet count & lt; 100,000/microliter)
- Pulmonary edema
- Ankle edema (pitting type)
- Cerebral or visual impairments
Pre-eclampsia is a progressive disorder and signs of organ dysfunction are indicative of severe pre-eclampsia. Systolic blood pressure> = 160 or diastolic blood pressure> = 110 and/or proteinuria & gt; 5g in 24 hours is also an indication of severe preeclampsia. Clinically, individuals with severe preeclampsia may also have right epigastric/right right quadrant abdominal pain, headache, and vomiting. Severe pre-eclampsia is a significant risk factor for intrauterine fetal death.
The baseline blood pressure rise (TD) of 30 mmHg or diastolic systolic 15 mmHg, while not meeting the absolute criteria of 140/90, is important to note but not considered diagnostic.
Predictive test
There are many assessment tests aimed at predicting preeclampsia, although no single biomarker adequately predicts the disorder. Assessed predictive tests include those associated with placental perfusion, vascular resistance, renal dysfunction, endothelial dysfunction, and oxidative stress. Examples of well-known tests include:
- Doppler ultrasound from the uterine artery to investigate inadequate signs of placental perfusion. This test has a high negative predictive value among people with previous pre-eclampsia history. Increased serum uric acid (hyperuricemia) is used by some to "define" pre-eclampsia, although it has been found to be a poor predictor of the disorder. Increased levels in the blood (hyperuricemia) are likely due to reduced urinary acid clearance secondary to impaired renal function.
- angiogenic proteins such as vascular endothelial growth factor (VEGF) and placental growth factor (PIGF) and anti-angiogenic proteins such as insoluble fy-tyrosine kinase-1 (sFlt-1) have shown hope for potential clinical use in diagnosing pre-eclampsia, although sufficient evidence to recommend clinical use for this marker.
- Recent research has shown that looking for podocytes (kidney special cells) in the urine has the potential to help predict preeclampsia. Studies have shown that finding podocytes in urine may serve as an early marker and diagnostic testing for preeclampsia.
- Because poor invasion of the extrapulmonary trophoblast into the uterus may be involved in the pathogenesis of preeclampsia, the factors released by these cells may be useful as predictive markers. It has been shown that the enzyme diamine oxidase oxidase, which is released by extraval trophoblasts into the maternal blood circulation, is lowered in early pregnancy in women who then develop early-onset preelampsia later in pregnancy.
Differential diagnosis
Pre-eclampsia can mimic and become confused with many other diseases, including chronic hypertension, chronic kidney disease, primary seizure disorders, gall bladder disease and pancreas, thrombocytopenic purpura or immune thrombotic, antiphospholipid syndrome and hemolytic-uremic syndrome. It should be considered likely in pregnant women beyond 20 weeks of pregnancy. It is very difficult to diagnose when pre-existing conditions such as hypertension are present. Women with acute fatty liver pregnancy may also present with high blood pressure and protein in the urine, but in contrast to the extent of liver damage. Other disorders that can cause high blood pressure include thyrotoxicosis, pheochromocytoma, and drug abuse.
Prevention
Precautions against pre-eclampsia have been studied in depth. Because the pathogenesis of pre-eclampsia is not fully understood, prevention remains a complex issue. Below are some of the recommendations currently accepted.
Diet
Supplementation with protein and a balanced energy diet does not seem to reduce the risk of pre-eclampsia. Furthermore, there is no evidence that changing salt intake has an effect.
Supplementation with antioxidants such as vitamin C, D and E has no effect on the incidence of pre-eclampsia; Therefore, supplementation with vitamins C, E, and D is not recommended to reduce the risk of pre-eclampsia.
Calcium supplements of at least 1 gram per day are recommended during pregnancy because it prevents preeclampsia where dietary calcium intake is low, especially for those at high risk. Low selenium status is associated with higher incidence of pre-eclampsia.
Aspirin
Taking aspirin is associated with a 1% to 5% reduction in preeclampsia and a 1% to 5% reduction in preterm delivery in high-risk women. The World Health Organization recommends low-dose aspirin for the prevention of pre-eclampsia in women at high risk and recommends it to begin before 20 weeks of gestation. The US Preventive Services Task Force recommends low-dose regimens for women at high risk starting at week 12. The benefits are less if it starts after 16 weeks.
Physical activity
There is not enough evidence to recommend either strenuous exercise or bedding as a precautionary measure of pre-eclampsia.
Smoking cess
In low-risk pregnancies, the association between smoking and decreased risk of pre-eclampsia has been consistent and can be reproduced throughout epidemiological studies. High-risk pregnancies (those with pregestational diabetes, chronic hypertension, preeclampsia history in previous pregnancies, or multifetal pregnancies) do not show significant protective effects. The reasons for this difference are not known for certain; the study supports the speculation that underlying pathology increases the risk of preeclampsia to some degree so that any measured risk reduction due to smoking is disguised. However, the damaging effects of smoking on health and overall pregnancy outweigh the benefits in reducing the incidence of preeclampsia. It is advisable to stop smoking before, during and after pregnancy.
Treatment
The definitive treatment for pre-eclampsia is delivery of infants and placentas. Delivery time should balance the desire for optimal results for the baby while reducing the risk for the mother. The severity of the disease and the maturity of the baby is a major consideration. These specific considerations for the situation and management will vary according to the situation, location, and institution. Treatment can range from pregnant management to delivery that is accelerated by induction of labor or part of cesarean, in addition to drugs. Important in management are assessment of the maternal organ system, management of severe hypertension, and prevention and treatment of eclamptic seizures. Separate interventions aimed at babies may also be needed. Bed rest has not been found to be useful and thus not recommended routinely.
Blood pressure
The World Health Organization recommends that women with severe hypertension during pregnancy should receive treatment with an anti-hypertensive agent. Severe hypertension is generally considered TD systolic at least 160 or BP diastolic at least 110. Evidence does not support the use of one anti-hypertensive over another. The choice of agent used should be based on the experience of a doctor prescribed with a particular agent, cost, and availability. Diuretics are not recommended for the prevention of preeclampsia and its complications. Labetolol, Hydralazine and Nifedipine are commonly used as antihypertensive drugs for hypertension in pregnancy. ACE inhibitors and angiotensin receptor blockers are contraindicated because they affect the development of the fetus.
The goal of treating severe hypertension in pregnancy is to prevent cardiovascular, renal, and cerebrovascular complications. Target blood pressure has been proposed to be 140-160 mmHg systolic and 90-105 mmHg diastolic, although its value varies.
Prevention of eclampsia
Administration of intrapartum and magnesium sulfate pascapartum is recommended in severe preeclampsia for the prevention of eclampsia. Furthermore, magnesium sulfate is recommended for the treatment of eclampsia rather than other anticonvulsants. Magnesium sulfate acts by interacting with NMDA receptors.
Epidemiology
Pre-eclampsia affects about 2-8% of all pregnancies worldwide. Incidence of pre-eclampsia has increased in the United States since the 1990s, possibly as a result of an increased prevalence of predisposing disorders, such as chronic hypertension, diabetes, and obesity.
Pre-eclampsia is one of the major causes of maternal and perinatal morbidity and mortality worldwide. Almost one-tenth of all maternal deaths in Africa and Asia and a quarter in Latin America are associated with hypertensive disease in pregnancy, a category that includes pre-eclampsia.
Pre-eclampsia is much more common in women who are pregnant for the first time. Women who had previously been diagnosed with pre-eclampsia were also more likely to have preeclampsia in subsequent pregnancies. Pre-eclampsia is also more common in women with hypertension, obesity, diabetes, autoimmune diseases such as lupus, various inherited thrombophilia such as Factor Leiden, kidney disease, multiple pregnancies (twins or multiple births), and advanced maternal age. Women living at high altitudes are also more likely to have pre-eclampsia. Preeclampsia is also more common in some ethnic groups (eg African-Americans, Sub-Saharan Africans, Latin America, Caribbean Africa, and the Philippines). Changes in paternity in subsequent pregnancies have implications as an adverse risk, except in those with a family history of pregnancy hypertension
Eclampsia is a major complication of pre-eclampsia. Eclampsia affects 0.56 per 1000 pregnant women in developed countries and nearly 10-30 times as many women in low-income countries as in developed countries.
Complications
Complications of preeclampsia can affect the mother and fetus. Acutely, preeclampsia may be complicated by eclampsia, development of HELLP syndrome, hemorrhagic or ischemic stroke, liver damage and dysfunction, acute renal injury, and acute respiratory distress syndrome (ARDS).
Pre-eclampsia is also associated with increased caesarean section frequency, premature birth, and placental abruption. In addition, an increase in blood pressure can occur in some individuals during the first postpartum week due to volume expansion and fluid mobilization. Fetal complications include fetal growth restriction and potential fetal or perinatal deaths.
Long-term, an individual with preeclampsia at increased risk for recurrence of pre-eclampsia in subsequent pregnancies.
Eclampsia
Eclampsia is a new development of seizures in pre-eclampsia patients who may not be associated with other causes. This is a sign that the underlying pre-eclampsia condition is very severe and is associated with high rates of perinatal morbidity and mortality and mothers. Warning symptoms for eclampsia in individuals with current preeclampsia may include headache, visual impairment, and upper right abdominal pain or epigastrium, with the most consistent headache symptoms. Magnesium sulfate is used to prevent seizures in cases of severe preeclampsia.
HELLP Syndrome
HELLP syndrome is defined as hemolysis (microangiopathy), elevated liver enzymes (liver dysfunction), and low platelets (thrombocytopenia). This condition can occur in 10-20% of patients with severe pre-eclampsia and eclampsia and is associated with increased maternal and fetal morbidity and mortality. In 50% of cases, HELLP syndrome develops prematurely, while 20% of cases occur in late pregnancy and 30% during the postpartum period.
Long run
There is also an increased risk of cardiovascular complications, including hypertension and ischemic heart disease, and kidney disease. Other risks include stroke and venous thromboembolism. It appears that pre-eclampsia does not increase the risk of cancer.
Lowering the blood supply to the fetus in pre-eclampsia causes reduced nutritional supply, which can lead to intrauterine growth restriction (IUGR) and low birth weight. The fetal origin hypothesis states that fetal malnutrition is associated with coronary heart disease later in adulthood due to disproportionate growth.
Because preeclampsia causes a mismatch between maternal energy supply and fetal energy requirements, preeclampsia can cause IUGR in developing fetuses. Infants who suffer from IUGR tend to suffer from poor neurological development and in increased risk for adult disease according to the Barker hypothesis. Fetal-associated adult illness due to IUGR including, but not limited to, coronary artery disease (CAD), type 2 diabetes mellitus (T2DM), cancer, osteoporosis, and various psychiatric illnesses.
The risk of preeclampsia and the development of placental dysfunction has also been shown to be repeated across generations on the mother's side and most likely on the father's side. Fetuses born to mothers who are born small for gestational age (SGA) are 50% more likely to develop preeclampsia while fetuses born from both SGA parents are three times more likely to develop preeclampsia in subsequent pregnancies.
History
The word eclampsia comes from the Greek term for lightning. The first description known about this condition was by Hippocrates in the 5th century BC.
An outdated medical term for pre-eclampsia is pregnancy toxemia, a term derived from a false belief that the condition is caused by toxins.
Research
Several studies have pointed out the importance of a woman's immunological tolerance to her baby's father, since infants and fathers share genetics. There is transient evidence that continuous exposure by either vaginal or oral sex to the same semen that leads to pregnancy lowers the risk of pre-eclampsia. As one preliminary study described, "although pre-eclampsia is a disease in the first pregnancy, the protective effect of multiparity disappears with the change in pairs". The study also concluded that although women with couples who switched are strongly advised to use condoms to prevent sexually transmitted diseases, "a certain period of exposure to sperm in stable relationships, when pregnancy is directed to, is associated with protection against pre-eclampsia."
Several other studies have since been investigating the decline in pre-eclampsia in women who have received blood transfusions from their partners, those with previous long sex histories without barrier contraception, and in women who have regularly oral sex.
After knowing the importance of a woman's immunological tolerance for her baby-father's gene, some Dutch reproductive biologists decided to take their research a step further. Consistent with the fact that the human immune system tolerates better things as they enter the body through the mouth, Dutch researchers conduct a series of studies that confirm a very strong correlation between the incidence of reduced pre-eclampsia and the practice of oral sex women, and notes that the effect the strongest protective if she swallows her partner's semen. A team from the University of Adelaide has also been investigating to see if men who have fathered pregnancies ending in miscarriage or preeclampsia have low seminal rates of critical immune modulation factors such as TGF-Beta. The team has found that certain men, nicknamed "dangerous men", are several times more likely for pregnancy fathers who will end up either pre-eclampsia or miscarriage. Among other things, most of the "dangerous men" seem to lack the level of adequate seminal immune factors needed to induce the immune tolerance of their partners.
Because the theory of immune intolerance as a cause of pre-eclampsia has been accepted, women with recurrent pre-eclampsia, miscarriage, or in vitro fertilization failure are potentially given key immune factors such as TGF-beta along with foreign proteins of the father. , may be either orally, as sublingual spray, or as a vaginal gel to apply to the vaginal wall prior to intercourse.
References
External links
- Pre-eclampsia in Curlie (based on DMOZ)
- MedlinePlus goes into high blood pressure in pregnancy
- Mayo Clinic - fact sheets about pre-eclampsia
Source of the article : Wikipedia
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