Category: Basic Science
Poster Session II
To determine if high sensitivity C-reactive protein (hsCRP) serum concentrations changed significantly between the first and third trimesters in subpopulations exposed to different doses of aspirin (LDA) prophylaxis stratified by BMI.
Study Design:
This is a secondary analysis from an open-label randomized control study of 81 vs 162 mg LDA prophylaxis with patients enrolled based on USPSTF major criteria (pooled cohort of all aspirin-exposed defined as the high-risk group). A third convenience, low-risk control population was also simultaneously recruited. Serum samples were obtained prior to aspirin initiation and at 28-32 weeks’ gestation. Analysis included groupings based on LDA exposure to any dose vs controls; and also based on specific dose, 0 vs 81 mg vs 162 mg. hsCRP levels were analyzed using an enzyme immunoassay test kit (BioCheck, Inc, Foster City, CA; Cat # BC-1119) utilizing quantitative sandwich enzyme immunoassay technique (ELISA). Statistical analysis included oneway ANOVA and pooled T-test.
Results:
171 subjects were grouped based on LDA exposure: 81mg (n= 69), 162mg (n= 75), and no LDA / control (“low risk”, n= 65). Serial first and third hsCRP results were available for 129 patients (76%). Groups were similar with regard to age and race; see Table 1. Women in the high-risk group were more likely to be obese (p=0.0003). Women who received 162mg LDA were more likely to report tobacco use (p=0.0037). At baseline a significant difference in hsCRP was not identified between 3 subgroups stratified by aspirin exposure (p=0.09); however, in the third trimester, this biomarker did differ significantly between these groups (p=0.048). No difference in hsCRP concentrations in the third trimester or change in hsCRP from baseline to third trimester was evident in subgroups stratified by BMI; see Table 2.
Conclusion:
Although variation in hsCRP was evident in third trimester between high-risk aspirin exposed subgroups and low-risk patients, BMI was not clearly associated as an explanatory variable for this difference suggesting a potential mechanism for LDA on inflammation.
Ashley Boerrigter, MD
University of Kentucky
Lexington, Kentucky, United States
Katherine Vignes, MD
MFM Faculty
Ochsner Clinic Foundation
Lafayette, Louisiana, United States
Hong Huang, MD, PhD
Department of Pediatrics, University of Kentucky College of Medicine
Lexington, Kentucky, United States
Asmita Shrestha, MPH
University of Kentucky
Lexington, Kentucky, United States
Wendy Whitley, RN
University of Kentucky
Lexington, Kentucky, United States
Cynthia Cockerham, BS, RN
Department of OBGYN, Division of Maternal Fetal Medicine, University of Kentucky
Lexington, Kentucky, United States
Aarthi Srinivasan, MD, MS
University of Kentucky
Lawrenceville, New Jersey, United States
Arnold J. Stromberg, MS, PhD
Department of Statistics, University of Kentucky
Lexington, Kentucky, United States
John O'Brien, MD
Chandler Medical Center, University of Kentucky
Lexington, Kentucky, United States