Association between the histidine-rich glycoprotein (HRG) C633T single nucleotide polymorphism (SNP) and recurrent miscarriage was investigated in a case-control study. The cases constituted 187 women with recurrent miscarriage that were compared with 395 controls who had delivered a child and had no history of miscarriage. Blood samples were collected from each woman, genomic DNA was extracted and genotyped for the HRG C633T SNP. In the whole study population, the percentage of miscarriage was the same, regardless of genotype (C/C 31.2%, C/T 32.9% and T/T 32.5%). However, an association between homozygous T/T carriers and recurrent miscarriage was detected in a subgroup of women with primary recurrent miscarriage (odds ratio 2.44, 95% CI 1.01-5.92). Our results indicate an important role for the HRG C633T SNP in the occurrence of recurrent miscarriage.

Download full-text PDF

Source
http://dx.doi.org/10.1111/aogs.12155DOI Listing

Publication Analysis

Top Keywords

recurrent miscarriage
24
hrg c633t
12
histidine-rich glycoprotein
8
miscarriage
8
c633t snp
8
recurrent
6
glycoprotein gene
4
gene polymorphism
4
polymorphism patients
4
patients recurrent
4

Similar Publications

Recurrent pregnancy loss (RPL) is the occurrence of two or more consecutive miscarriages before 20 weeks of gestation. Recent research has increasingly focused on the role of oxidative stress in RPL, providing insights into its underlying mechanisms and potential therapeutic targets. Oxidative stress arises from an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, leading to cellular damage and inflammation.

View Article and Find Full Text PDF

AMPK-mTOR pathway modulates glycolysis reprogramming in unexplained recurrent spontaneous abortion.

BMC Pregnancy Childbirth

December 2024

Department of Obstetrics and Gynecology, The First Affiliated Hospital, Fujian Medical University, 20 Chazhong Road, Fuzhou, Fujian, 350005, P.R. China.

Background: Recurrent spontaneous abortion (RSA), whose underlying cause has yet to be fully elucidated, is often classified as unexplained recurrent spontaneous abortion (URSA). Promoting the differentiation of CD4 T cells into Tregs may be the key to prevent URSA. The differentiation of CD4 T cells was controlled by mTOR, but the regulatory mechanism is still unclear.

View Article and Find Full Text PDF

Background: Maternal infections caused by the ToRCH complex, comprising Toxoplasma gondii (T.gondii), Rubella Virus (RV), Cytomegalovirus (CMV), and Herpes Simplex Virus (HSV), are significant contributors to Bad Obstetric History (BOH). These infections can vertically transmit through the placental barrier, leading to complications in fetal development.

View Article and Find Full Text PDF

Haemolytic disease of the foetus and newborn (HDFN) due to Rhesus D (RhD) antigen mismatch between the mother and foetus has been a significant cause of neonatal jaundice, recurrent miscarriage and stillbirth throughout history. Anti-RhD prophylaxis using polyclonal immunoglobulin G (RhD-pIgG) derived from the plasma of RhD-negative donors immunised with RhD-positive red blood cells (RBCs), has reduced the incidence of HDFN, but this approach is currently restricted to developed countries. Monoclonal antibodies (mAbs) offer a promising alternative to address this pressing need, but prior attempts to develop effective anti-RhD mAbs have failed, in some cases due to differences in fucosylation patterns between mAbs produced in cell lines and RhD-pIgG.

View Article and Find Full Text PDF

The emerging role of long non-coding RNA SOX2-OT in cancers and non-malignant diseases.

J Physiol Biochem

December 2024

Hubei Key Laboratory of Tumor Microenvironment and Immunotherapy, China Three Gorges University, Yichang, 443002, China.

SOX2 overlapping transcript (SOX2-OT) is a long non-coding RNA located at chromosome 3q26.33 in humans. Convincing data confirm that SOX2-OT is evolutionarily conserved and plays a significant role in various malignant and non-malignant diseases.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!