The results of the present study indicate that the antioxidant lycopene has no benefit in prevention of pre-eclampsia in healthy primigravidas. Rather, there is an increased incidence of the adverse effects of preterm labor and low birthweight babies.

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It is believed that the mechanism underlying vascular endothelial cell damage in preeclampsia is associated with the formation of lipid peroxides and other reactive free radical oxygen species generated from persistent placental underperfusion. Support for the role of oxidative stress (free radical-mediated lipid peroxidation) in the pathophysiology of preeclampsia is provided by biochemical evidence that the plasma serum of patients with the disorder has a high concentration of lipid peroxidation products and is deficient in endogenous antioxidants. One clinical trial showed that oral administration of lycopene, a strong antioxidant and free radical scavenger, significantly reduced the risk of preeclampsia and intrauterine growth retardation in low-risk primigravidas. Because of this and other evidence, it was expected that lycopene would prevent preeclampsia in a similar low-risk population.This randomized double blind placebo-controlled trial evaluated the effectiveness of antioxidant supplementation with lycopene for the prevention of preeclampsia in 159 healthy singleton primigravidas between 12 and 20 weeks of gestation. The study subjects were randomized to receive oral daily doses of lycopene 2 mg (n ϭ 77) or a placebo (n ϭ 82) and were followed until delivery for the development of preeclampsia.There was no difference between the 2 groups in the percentage of patients who developed preeclampsia (18% in both groups). However, women who received lycopene had a significantly higher incidence of preterm labor than the placebo (10.4% vs. 1.2%, P ϭ 0.02), and more low birth weight (Ͻ2.5 kg) babies (22.1% vs. 9.8%, P ϭ 0.05).These findings indicate that the antioxidant lycopene is not effective for prevention of preeclampsia in healthy primigravidas and may be associated with an increased incidence of adverse effects such as preterm labor and low birth weight babies.

Background: Changes in the hemostatic system are observed in both normal and hypertensive pregnant patients. Although the exact pathophysiology of pregnancy induced hypertension is not completely understood, numerous pathophysiological mechanisms, alone or in combination, have been suggested to be responsible for the diverse subsets of PIH.Methods: This was a prospective case control study conducted on 100 pregnant females (50 PIH and 50 normotensive) at Holy Family Hospital, New Delhi, from October 2020 to May 2021. platelet count and platelet indices (mean platelet volume and ratio of platelet count to mean platelet volume) at 32 weeks and at time of delivery were checked and Outcomes were compared.Results: For predicting PIH, platelet count showed sensitivity of 82% and specificity of 54%, MPV sensitivity of 54% and specificity of 82%, PC/MPV sensitivity of 82% and specificity of 62%. For predicting pre-eclampsia without severe symptoms, platelet count showed sensitivity of 89.47% and specificity of 47.62%, mean platelet volume sensitivity of 47.37% and specificity of 76.19%, platelet count/mean platelet volume sensitivity of 31.58% and specificity of 100%. We also found that in predicting pre-eclampsia with severe symptoms platelet count showed a sensitivity of 100% and specificity of 26.32%, whereas, mean platelet volume showed equal sensitivity and specificity of 55.56%, platelet count/mean platelet volume with sensitivity of 44.44% and specificity of 84.21%.Conclusions: We found that platelet count and platelet count/mean platelet volume decreases while mean platelet volume increases with severity of pregnancy induced hypertension.

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