Preeclampsia (PE) is a serious and potentially fatal complication of pregnancy. It is a
placental disease characterized by an elevated blood pressure in the 3rd trimester with
multisystem involvement (proteinuria, elevated liver enzymes, low platelet count and/or
neurologic symptoms). PE can cause pulmonary edema, seizures, or stroke and is a leading
cause of maternal mortality. The pregnancy outcomes are further worsened if PE develops
before term. Women who have a history of PE in a prior pregnancy, diabetes, preexisting
hypertension, kidney disease, multifetal gestation or autoimmune diseases are at an
increased risk to develop PE in a subsequent pregnancy.
Clinical trials evaluating the benefits of low-dose aspirin (ASA) have used a wide range
of doses from 60mg to 150mg orally daily with low-dose being defined as less than 325mg
per day. Taking ASA (as opposed to placebo) is thought to reduce the risk of preeclampsia
by 17%, without increasing the risk of major obstetric bleeding. The number needed to
treat is only 19 women. ASA is currently the only prophylactic therapy for PE in
high-risk women to be recognized by the US Preventive Task Force and should be initiated
early in the second trimester of pregnancy, before 16 weeks of gestation.
There has also been more awareness that the efficacy of ASA in preventing preeclampsia is
limited by the poor adherence of patients to this therapy. Indeed, a cross-sectional
study has estimated that up to 46% of women (n=42) on ASA therapy may not be compliant to
it, as determined by a validated Simplified Medication Adherence Questionnaire (SMAQ).
Adherence is essential to the efficacy of ASA in preventing preterm preeclampsia. It
would therefore be of interest to obtain more information about adherence to ASA in women
who need this therapy.
Assessing molecular pathways in the development of PE may allow opportunity for earlier
diagnosis, specific triaging of patients to closer monitoring and further development of
preventative or curative treatment strategies. Samples will be biobanked for biomarker
discovery in the future.
The current literature is lacking in evidence to recommend a specific daily dose of ASA.
Recent meta-analyses have suggested that there may be a dose response in the protective
effect of ASA for PE. As compared to 60mg per day, an ASA dose of 100mg per day was
associated with a lower relative risk of PE (0.44 vs 0.57, p=0.36). A large study of 1776
women has compared a slightly higher dose of ASA (150mg per day) to placebo and found a
decrease in preterm delivery (before 37 weeks) due to PE (OR 0.38, p=0.004).
Meta-analyses have shown that any dose of ASA above 60mg per day is protective and should
be used to prevent PE in high risk pregnancies.
To date, there has not been any studies comparing lower doses of ASA (such as 81mg, the
traditional "baby aspirin" dose sold in the US) to higher "low-dose" ASA regimens (such
as 162mg) in their ability to prevent preterm or severe PE in women who are at a high
risk for this devastating disease.