Causal relationship between OHSS and immune cells: A Mendelian randomization study.
J Reprod Immunol
; 165: 104314, 2024 Sep.
Article
in En
| MEDLINE
| ID: mdl-39173334
ABSTRACT
OBJECTIVE:
To confirm the causal relationship between immune cells and Ovarian Hyperstimulation Syndrome.DESIGN:
Obtaining data, collecting single nucleotide polymorphisms, detecting instrumental variables heterogeneity, assessing causality, and assessing bidirectional causality.SUBJECTS:
A two sample Mendelian study to confirm the causal relationship between immune cells and Ovarian Hyperstimulation Syndrome. EXPOSURE Immune cell phenotype (including 22 million SNPs from GWAS on 3757 European individuals). MAIN OUTCOMEMEASURES:
Inverse variance weighting, one-sample analysis, MR-Egger, weighted median and weighted mode are used to assess the causal relationship between 731 immunophenotypes and Ovarian Hyperstimulation Syndrome. The weighted median and Mendelian Randomization multi-effect residuals and Mendelian Randomization multi-effect residuals and outlier tests are used to assess bidirectional causality between this two.RESULTS:
After False Discovery Rate correction, 9 immunophenotypes were found to be significantly associated with the risk of Ovarian Hyperstimulation Syndrome. B cell panel IgD+ AC (OR, 0.90) ãCD19 on CD24+ CD27+ (OR, 0.86) ãBAFF-R on CD20- CD38 (OR, -1.22); Mature T cell group panel EM DN (CD4 -CD8-) AC (OR, 1.46); Myeloid cell panel Mo MDSC AC (OR, 1.13) ãCD45 on CD33br HLA-DR+ (OR, 0.87); Monocyte panel HLA-DR on monocyte (OR, 0.86) ãCCR2 on CD14+ CD16+ monocyte (OR, 1.15) ãcDC panel HLA-DR on myeloid DC (OR, 0.89).CONCLUSION:
This study shows the potential link between OHSS and immune cells by genetic means, providing new ideas for future clinical and basic research.Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Ovarian Hyperstimulation Syndrome
/
Polymorphism, Single Nucleotide
/
Mendelian Randomization Analysis
Limits:
Female
/
Humans
Language:
En
Journal:
J Reprod Immunol
Year:
2024
Document type:
Article
Affiliation country:
Country of publication: