Published online Jul 15, 2019. doi: 10.4239/wjd.v10.i7.396
Peer-review started: March 22, 2019
First decision: May 31, 2019
Revised: June 10, 2019
Accepted: June 21, 2019
Article in press: June 21, 2019
Published online: July 15, 2019
Processing time: 118 Days and 3.9 Hours
Pregnancy induced hypertension and diabetes are an increasing threat to the wellbeing of both mother and the baby. The basic pathophysiological link to disease predisposition is attributed to the functionality of epidermis and angiogenesis. Several genetic studies have provided evidence that epidermal growth factor dysfunction can lead to hypertension and its complications in preg-nancy.
Materno-fetal mortality is on the rise in lower middle income countries; predominantly due to lack of primary prevention of non-communicable diseases. This led us to investigate one of the route cause i.e. genetic modification as a risk for development of disease.
Explore any association of SNP rs17337023 with the development of gestational hypertension in pregnant females with gestational diabetes.
A case-control study was conducted recruiting 202 pregnant women at 28 wk of gestation. Their blood pressure, blood glucose levels were measures and genotyping of EGFR SNP rs17337023 was performed via tetra arms PCR.
No difference was seen in the EGFR rs17337023 polymorphism genotype frequency among both normotensive and hypertensive groups in this study.
This pilot study indicates that polymorphisms in rs17337023 may not be involved in the pathophysiology of gestational hypertension in gestational diabetes. Further large-scale studies should explore polymorphism in epidermal growth factor receptor and other genes in this regard.
This study has shown some negative results linking a specific area of the gene EGFR; however, it should be noted that other factors may also be in play such as obesity and family history that can be a contributing factor along with genetic predisposition for hypertension. This opens up new avenues for researchers to perform prospective studies to identify the causal link between genetic and environmental factors.