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Pravastatin suppresses inflammatory cytokines and endothelial activation in patients at risk of developing
Muhammad Ilham Aldika Akbar1,2,3, Angelina Yosediputra2, Raditya Ery Pratama2
1Department Obstetrics & Gynecology, Faculty of Medicine, Universitas Airlangga, Surabaya, Indonesia.
Insights
Pravastatin significantly reduced inflammatory markers Interleukin-6 (IL-6) and Endothelin-1 (ET-1) in high-risk pregnant women. This suggests pravastatin may help prevent preeclampsia by improving endothelial function and reducing inflammation.
Area of Science:
- Obstetrics and Gynecology
- Cardiovascular Research
- Pharmacology
Background:
- Preeclampsia is a leading cause of maternal and fetal morbidity worldwide.
- Identifying effective preventative strategies for high-risk pregnancies is crucial.
- Endothelial dysfunction and inflammation are key pathological features of preeclampsia.
Purpose of the Study:
- To evaluate the effect of pravastatin on circulating inflammatory and endothelial markers in high-risk pregnancies.
- To assess pravastatin's potential role in preeclampsia prevention.
Main Methods:
- A nested cohort study within the INOVASIA randomized controlled trial.
- 38 high-risk pregnant women received pravastatin (40mg/day) plus standard care (aspirin, calcium) or standard care alone.
- Vascular Endothelial Growth Factor (VEGF), Interleukin-6 (IL-6), Endothelin-1 (ET-1), and Nitric Oxide (NO) levels were measured pre- and post-treatment.
Main Results:
- Pravastatin significantly decreased IL-6 and ET-1 levels (p<0.05).
- Nitric Oxide (NO) levels increased significantly in the pravastatin group (p=0.044) but decreased in the control group (p=0.002).
- VEGF levels showed no significant difference between groups.
Conclusions:
- Pravastatin administration improved NO levels and reduced IL-6 and ET-1.
- These biomarker changes suggest a potential beneficial role for pravastatin in preeclampsia prevention.
- Further research is warranted to confirm pravastatin's efficacy in preventing preeclampsia.
Introduction:
The Indonesian INOVASIA study is an ongoing multicentre randomized, open controlled trial of pravastatin for the prevention of preeclampsia in patients deemed to be high risk. Here we evaluate the effects of pravastatin on circulating inflammatory and endothelial markers, i.e. Vascular Endothelial Growth Factor (VEGF), Interleukin-6 (IL-6), Endothelin-1 (ET-1), and Nitric Oxide (NO).
Methods:
Pregnant women deemed to be at a high risk of developing preeclampsia women were recruited based on the Fetal Medicine Foundation preeclampsia screening test or a history of preterm preeclampsia, or clinical risk factors in combination with an abnormal uterine artery Doppler flow pattern at 11-20 week's gestation. This is a nested cohort study within the larger trial (INOVASIA); 38 patients were consecutively recruited and assigned to the pravastatin group and the control group. Participants in the pravastatin group received pravastatin (2 × 20 mg p.o) in addition to a standard regimen of aspirin (80 mg p.o) and calcium (1 g p.o), from 14 to 20 weeks until delivery. Blood samples to measure the various biomarkers were obtained in consecutive patients before starting the research medication and just before delivery (pre and post-test examination).
Result:
The number of samples on the 2 time points for the various biomarkers was: VEGF: 38, IL-6: 30, ET-1: 38, and NO: 35. IL-6 levels decreased significantly in the pravastatin group (mean ± SD): (191.87 ± 82.99 vs. 151.85 + 48.46, p = .013), while levels in the control group did not change significantly (median (interquartile range)) (144.17 (53.91) vs. 140.82 (16.18), p = .177). ET-1 levels decreased significantly in the pravastatin group (3.64 ± 0.85 vs. 3.01 ± 0.74, p = .006) while the control group had more or less stable levels (3.57 ± 1.12 vs. 3.78 ± 0.73 p = .594). NO was the only serum marker that showed significant changes in both groups. NO levels increased in pravastatin group (11.30 (17.43) vs. 41.90 (53.18), p = .044) and decreased in control group (38.70 (34.80) vs. 10.03 (26.96), p = .002). VEGF levels appeared to follow opposite trends in the 2 groups (NS) (Pravastatin: 3.22 (0.62) vs. 3.28 (0.75), p = .402. Control: 3.38 (0.83) vs. 3.06 (0.74), p = .287).
Conclusion:
Administration of 40 mg pravastatin resulted in an improvement in NO levels, and a decrease in IL-6 and endothelin (ET-1) levels. The direction of the effect of pravastatin on these biomarkers appears to underpin the potential for a beneficial effect of pravastatin in the prevention of preeclampsia.
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