Study Results
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
Get a concise snapshot of the trial, including recruitment status, study phase, enrollment targets, and key timeline milestones.
UNKNOWN
80 participants
OBSERVATIONAL
2019-01-01
2020-08-30
Brief Summary
Review the sponsor-provided synopsis that highlights what the study is about and why it is being conducted.
Healthy women pregnancy can be associated with resistance to the action of insulin on glucose uptake and utilization. Insulin Resistance (IR) is defined as decreased ability of target tissues such as liver, adipose tissue and muscle to respond to normal circulating concentrations of insulin. Insulin Resistance can be a result of a number of factors such as defective molecular structure of insulin, defective receptor functioning or defective signal transduction pathway .
Preeclampsia is associated with increased expression of Tumor necrosis Factor α and other inflammatory marker which causes Insulin Resistance. Increased Insulin Resistance leads to dyslipidemia that can worsen the placental ischemia leading to vicious cycle of ischemia-inflammation-Insulin Resistance-dyslipidemia-ischemia . Insulin resistance has also been hypothesized to contribute to the pathophysiology of preeclampsia. Compared to women who have normotensive pregnancies, women who develop preeclampsia are more insulin resistant prior to pregnancy .
The recognition that specific miRNAs are induced by hypoxia and are commonly dysregulated in preeclampsia raises the possibility that such miRNAs mediate the adverse effects of placental hypoxia in preeclampsia. MiRNAs present in maternal blood may have the potential to be used as biomarkers, as they are relatively stable and tissue specific . It was found that mir-210 is induced in patients with pre-eclampsia, whether mir-210 contributes to the pathogenesis of pre-eclampsia, a complex disorder widely believed to be associated with placental hypoxia .
Related Clinical Trials
Explore similar clinical trials based on study characteristics and research focus.
miRNA-452 in Patients With Preeclampsia and Its Correlation With MMP-9
NCT03258125
The Association Between Different Markers With Development of Maternal and Neonatal Complications in Women With Severe Preeclampsia
NCT07125599
Comparison Between Uterine Artery Doppler and Placental Vascular Indices in Prediction of Preeclampsia
NCT03838887
Knowledge and Attitude of Pregnant Women Towards Preeclampsia in Assiut Governorate
NCT05955690
The Outcomes of Hypertension in Obese Versus Non-obese Pregnant Women
NCT05673135
Detailed Description
Dive into the extended narrative that explains the scientific background, objectives, and procedures in greater depth.
In severe disease there may be red blood cell breakdown, a low blood platelet count, impaired liver function, kidney dysfunction, swelling, shortness of breath due to fluid in the lungs, or visual disturbances. Pre-eclampsia increases the risk of poor outcomes for both the mother and the baby . If left untreated, it may result in seizures at which point it is known as eclampsia or HELLP syndrome (hemolysis ,elevated liver enzymes , low platelets ) .
The clinical features of preeclampsia are caused by systemic maternal endothelial dysfunction resulting from a combination of preexisting maternal risk factors and abnormal placental development. Risk factors for pre-eclampsia include: obesity, prior hypertension, older age, and diabetes mellitus . It is also more frequent in a woman's first pregnancy and if she is carrying twins. The underlying mechanism involves abnormal formation of blood vessels in the placenta amongst other factors .
These maternal characteristics may contribute to oxidative stress, inflammation and vascular dysfunction, all of which have been implicated in the etiology of preeclampsia .
Healthy women pregnancy can be associated with resistance to the action of insulin on glucose uptake and utilization . Insulin Resistance is defined as decreased ability of target tissues such as liver, adipose tissue and muscle to respond to normal circulating concentrations of insulin. Insulin Resistance can be a result of a number of factors such as defective molecular structure of insulin, defective receptor functioning or defective signal transduction pathway .
Many maternal hormones and factors play role in causation of Insulin Resistance during pregnancy such as increased levels of serum cortisol, Tumor necrosis factor α , can interrupt the insulin signaling pathway and can lead to Insulin Resistance during normal pregnancy .
Women with increased Insulin Resistance are more prone to develop preeclampsia and gestational diabetes. Preeclampsia is associated with increased expression of Tumor necrosis factor α and other inflammatory marker which causes Insulin Resistance. Increased Insulin Resistance leads to dyslipidemia that can worsen the placental ischemia leading to vicious cycle of ischemia-inflammation-Insulin Resistance-dyslipidemia-ischemia .
Insulin resistance has also been hypothesized to contribute to the pathophysiology of preeclampsia. Compared to women who have normotensive pregnancies, women who develop preeclampsia are more insulin resistant prior to pregnancy .
Early reliable markers for preeclampsia development is the involvement of microRNA in the pathogenesis and its possible role as an early biomarker for disease development. MicroRNAs (miRNAs) are a series of small (18-24 nt) endogenous noncoding single-stranded RNAs, which can regulate gene expression post transcriptionally by a nonperfect pairing of 6-8 nucleotides with target mRNAs . It is currently estimated that up to 30% of human genes may contain miRNAs' binding sites, which suggested a potential role of microRNAs as central regulators in the control of gene expression .
MicroRNAs have been implicated in a variety of human diseases, such as cardiovascular disease, primary muscular disorders, and cancer. In addition, miRNAs have been reported involved in regulating pregnancy process .
The human placenta exhibits a specific microRNA expression pattern that dynamically changes during pregnancy and is reflected in the maternal plasma .
The recognition that specific microRNAs are induced by hypoxia and are commonly dysregulated in preeclampsia raises the intriguing possibility that such microRNAs mediate the adverse effects of placental hypoxia in preeclampsia. The connection between microRNAs, adipose tissue, and insulin resistance may have a role in gestational diabetes mellitus pathophysiology. microRNAs present in maternal blood may have the potential to be used as biomarkers, as they are relatively stable and tissue specific .
MicroRNA 210 is identified as a unique hypoxia induced miRNA that is universally induced in various cell types. Using microRNA microarray it was found that microRNA 210 is overexpressed in placental tissue derived from patients with pre-eclampsia .
It was found whether microRNA 210 contributes to the pathogenesis of pre-eclampsia, a complex disorder widely believed to be associated with placental hypoxia. The results show that microRNA 210 is induced in patients with pre-eclampsia and in hypoxia treated trophoblast cells .
It has been found that microRNA 210 levels are dramatically increased in the placental tissue derived from patients with preeclampsia. In this issue, MicroRNA 210 levels in plasma from preeclampsia patients were significantly higher than those in gestational healthy controls. Furthermore, the expression levels of microRNA 210 seemed to correlate well with disease severity, suggesting a potential role of circulating microRNA 210 as novel biomarker for the diagnosis of preeclampsia.
Conditions
See the medical conditions and disease areas that this research is targeting or investigating.
Study Design
Understand how the trial is structured, including allocation methods, masking strategies, primary purpose, and other design elements.
CASE_CONTROL
CROSS_SECTIONAL
Eligibility Criteria
Check the participation requirements, including inclusion and exclusion rules, age limits, and whether healthy volunteers are accepted.
Inclusion Criteria
* Group 2: Healthy pregnant women as control group .
Exclusion Criteria
2- Past history of chemotherapy or surgical treatment of cancer. 3-Women who diagnosed as preeclamptic or diabetic
20 Years
40 Years
FEMALE
Yes
Sponsors
Meet the organizations funding or collaborating on the study and learn about their roles.
Assiut University
OTHER
Responsible Party
Identify the individual or organization who holds primary responsibility for the study information submitted to regulators.
Yousra M Farghaly
principal investigator
Locations
Explore where the study is taking place and check the recruitment status at each participating site.
ASSIUT University
Asyut, , Egypt
Assiut Unversity
Asyut, , Egypt
Countries
Review the countries where the study has at least one active or historical site.
Central Contacts
Reach out to these primary contacts for questions about participation or study logistics.
Facility Contacts
Find local site contact details for specific facilities participating in the trial.
Lobna
Role: primary
Lobna
Role: primary
References
Explore related publications, articles, or registry entries linked to this study.
Al-Jameil N, Aziz Khan F, Fareed Khan M, Tabassum H. A brief overview of preeclampsia. J Clin Med Res. 2014 Feb;6(1):1-7. doi: 10.4021/jocmr1682w. Epub 2013 Dec 13.
Bueno MJ, Perez de Castro I, Malumbres M. Control of cell proliferation pathways by microRNAs. Cell Cycle. 2008 Oct;7(20):3143-8. doi: 10.4161/cc.7.20.6833. Epub 2008 Oct 20.
Eiland E, Nzerue C, Faulkner M. Preeclampsia 2012. J Pregnancy. 2012;2012:586578. doi: 10.1155/2012/586578. Epub 2012 Jul 11.
Hypertension in pregnancy. Report of the American College of Obstetricians and Gynecologists' Task Force on Hypertension in Pregnancy. Obstet Gynecol. 2013 Nov;122(5):1122-1131. doi: 10.1097/01.AOG.0000437382.03963.88. No abstract available.
Morales Prieto DM, Markert UR. MicroRNAs in pregnancy. J Reprod Immunol. 2011 Mar;88(2):106-11. doi: 10.1016/j.jri.2011.01.004. Epub 2011 Feb 25.
Roberts JM, Lain KY. Recent Insights into the pathogenesis of pre-eclampsia. Placenta. 2002 May;23(5):359-72. doi: 10.1053/plac.2002.0819.
Steegers EA, von Dadelszen P, Duvekot JJ, Pijnenborg R. Pre-eclampsia. Lancet. 2010 Aug 21;376(9741):631-44. doi: 10.1016/S0140-6736(10)60279-6. Epub 2010 Jul 2.
Other Identifiers
Review additional registry numbers or institutional identifiers associated with this trial.
D V O MicroRNA210 I PET
Identifier Type: -
Identifier Source: org_study_id
More Related Trials
Additional clinical trials that may be relevant based on similarity analysis.