In the US, pre-eclampsia occurs in approximately 8.9 per 1,000 pregnant women who deliver a live child. There is no significant increase in pre-eclampsia when comparing obstetric practices from low-risk and high-risk populations. A multicenter nationwide study is needed to determine the epidemiology of pre-eclampsia.
Despite large studies, there are few conclusive therapies to prevent or treat pre-eclampsia. Treatment options include: anti-hypertensive, glucocorticoid, or magnesium supplementation, aspirin, and the use of protein antagonists. There is currently not enough evidence to show that any therapy work in prevention, so there is no evidence that pre-eclampsia can be cured.
Pre-eclampsia is thought to be caused by an underlying autoimmune response to antigens found within the placenta. However, this explanation remains elusive as it is only a partial cause of the disease. For the most part, the cause of pre-eclampsia is thought to be genetically inherited or a combination of several factors. Studies have linked factors such as infections, toxins, and stress to the development of pre-eclampsia. However, an underlying genetic predisposition for this disease is not yet apparent and the underlying genetics are unknown.
What is not clear from the available research is whether pre-eclampsia should be considered in terms of treating associated co-morbid disorder. The evidence suggests that treating these comorbid disorders such as hypertension during pregnancy may reduce the burden of pre-eclampsia. Antispasmodics such as Phenytoin may be used to control pre-eclampsia associated hypertension, however these do not have proven benefits and may lead to premature delivery. Antihypertensive agents such as folic acid are also effective and safe in managing pre-eclampsia mellitus.
Pre-eclampsia is a multi-system disorder affecting the kidneys and vasculature, and other organs as well. Significant renal insufficiency is a sign of severe pre-eclampsia. Symptoms of pre-eclampsia may include pain or discomfort in the back, abdominal pain, swelling in the hands and feet, skin changes, visual disturbances. These are nonspecific symptoms which are common with many disease processes and should prompt a thorough medical history. A history and physical examination combined with special investigations such as blood tests and ultrasound can help delineate the cause of the patient's signs and symptoms.
The main defining characteristics of pre-eclampsia that are easily identifiable in a clinical setting are pre-existing hypertension and proteinuria. However, other signs are also frequently identifiable, and these include elevated levels of creatinine in pregnant women with eclampsia, abnormal liver enzyme levels, or raised blood pressure in the pre-pregnant woman. The presence of these signs should prompt consideration of pre-eclampsia when there is new-onset pre-pregnancy hypertension. The diagnosis of pre-eclampsia during pregnancy can be made by measuring high levels of protein in the urine of pregnant women and by ultrasound detection of vascular malformations or placental abnormalities.
The aetiology of pre-eclampsia was most likely multifactorial. The aetiology was more difficult to define if the patient developed eclampsia or not. The aetiology of pre-eclampsia is difficult to define, however, this study does bring new knowledge and data to this field.
In the management of pre-eclampsia, treatment with labetalol is effective. It is relatively inexpensive in comparison with other antihypertensive drugs. Labetalol has significant adverse drug reactions in comparison with other antihypertensives, in particular tachycardia and dizziness. Labetalol is a beta-blocker; therefore the side effects are beta-blocker-like. In particular, labetalol has been reported to increase blood plasma levels of norepinephrine and epinephrine, which may cause symptoms like anxiety, palpitations, and tremors.
Labetalol is a commonly used drug in combination with other treatments. However, the use of labetalol alone appears to be rare in a clinical setting. Results from a recent paper also found that the labetalol has similar efficacy to nifedipine.
Nifedipine combined with labetalol in hypertensive pregnant women resulted in a reduction in heart rate and mean arterial pressure. On the other hand, beta blockade by labetalol appeared to result in a reduction in systolic blood pressure. All of these side effects were associated with high plasma drug concentrations.
Data from a recent study confirms that HRQoL improves in PE patients who are given nifedipine. It shows that HRQoL is not impaired after initiation of nifedipine. Nifedipine offers good HRQoL gains in patients who have PE. These patients had the highest HRQoL before initiating treatment with nifedipine and, therefore, should be considered for treatment with nifedipine as a first-line therapy.
In this large study, labetalol was not associated with increases in blood pressure. Furthermore, labetalol was also not associated with increased fetal heart rates in the short or long term in pregnant women. Although this study had shortcomings, it suggests that labetalol is safe for use by pregnant women in early pregnancy.