Introduction
Preeclampsia is a multisystem progressive disorder characterized by the
new onset of hypertension and proteinuria or the new onset of
hypertension and significant end-organ dysfunction with or without
proteinuria in the last half of pregnancy or postpartum
[1]. It is estimated to complicate
approximately 4.6% of pregnancies worldwide
[2]. Its pathophysiology is complex
and not fully understood yet. Both maternal and placental factors are
involved. Abnormal placentation and remodeling of spiral arteries may
lead to placental hypo-perfusion, hypoxia, ischemia and the release of
various antiangiogenic factors into the maternal circulation, causing
systemic endothelial dysfunction [3].
In addition, immunological and genetic factors have been proposed.
Preeclampsia can be characterized as early onset (<34 weeks of
gestation) and late onset (≥34 weeks of gestation). Early-onset disease
is associated with worse prognosis and poorer maternal and fetal
outcomes, such as fetal growth restriction and preterm birth
[4, 5].
Severe preeclampsia (or preeclampsia with severe features) is diagnosed
when there is severe hypertension (systolic BP ≥160 mmHg or diastolic BP
≥110 mmHg) and/or specific signs or symptoms of significant end-organ
dysfunction: thrombocytopenia (< 100,000 platelets/microL),
impaired liver function that is not accounted for by alternative
diagnoses and as indicated by abnormally elevated blood concentrations
of liver enzymes (to more than twice the upper limit normal
concentrations), or by severe persistent right upper quadrant or
epigastric pain unresponsive to medications, renal insufficiency (serum
creatinine > 1.1 mg/dL or a doubling of the serum
creatinine concentration in the absence of other renal disease),
pulmonary edema, new-onset headache unresponsive to medication and not
accounted for by alternative diagnoses, visual disturbances
[1].
Preeclampsia is associated with an increased risk for life-threatening
obstetric or medical complications, intrauterine growth restriction,
oligohydramnios and preterm labor. It is estimated that 10-15% of
direct maternal deaths are associated with preeclampsia and eclampsia
[6]. Therefore, it is essential to
estimate the risk of preeclampsia early in pregnancy and identify high
risk women that need frequent surveillance and prophylactic
administration of low-dose aspirin. Although various laboratory and
imaging tests have been proposed for preeclampsia prediction, the
optimal screening model to be widely used in clinical practice remains a
matter of debate [7].
Lactate dehydrogenase (LDH) is a cytoplasmic enzyme that catalyzes the
interconversion of pyruvate and lactate acid and is present in tissues
throughout the body. It is released into circulation following cellular
death and tissue injury. LDH is a highly sensitive marker for tissue
breakdown, but it is nonspecific as it is also elevated in many clinical
disorders. It is a marker of hemolysis, liver dysfunction and has been
used as a marker of myocardial infarction as well as a biomarker of
inflammation [8-10]. Several studies
have associated serum LDH levels with severity of preeclampsia, adverse
maternal and perinatal outcomes
[11-13].
The aim of this systematic review is to assess the usefulness of LDH as
a prognostic biomarker in preeclampsia, as well as to provide a summary
effect estimate concerning its effectiveness in predicting preeclampsia
complications and adverse maternal and neonatal outcomes.