4.4 Article

Glucose/insulin metabolism and vitamin D in women with recurrent pregnancy loss

Journal

Publisher

WILEY
DOI: 10.1111/aji.13505

Keywords

glucose; insulin resistance; insulin; miscarriage; recurrent pregnancy loss; vitamin D

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This study found a significant correlation between insulin and insulin resistance in women with recurrent pregnancy loss, while a negative but non-significant correlation was observed between vitamin D levels and insulin. Vitamin D may play additional roles in the pathogenesis of recurrent pregnancy loss beyond its immunomodulatory role.
Objective Glucose/insulin metabolism has been related to recurrent pregnancy loss (RPL) through mechanisms not really clarified. Also, vitamin D deficiency seems to be associated to RPL. The purpose of our study was to evaluate the correlation between glucose/insulin metabolism parameters and vitamin D levels in women with history of RPL. Study design Observational retrospective study on RPL women. The correlation among vitamin D levels and fasting glucose (FG), fasting insulin (FI), Homeostatic model assessment of insulin resistance (HOMA-IR) index, area under glucose curve (AUC-Glyc) and area under insulin curve (AUC-Ins), was evaluated. Results One-hundred and twenty-seven RPL women were classified into three subgroups (0-1-2) according to the levels of FI. We found a statistically significant linear Pearson correlation between FI and HOMA-IR (r = .840; P = .001). An, inverse, but non-significant correlation both between vitamin D and FI (R = -.202, ns) and vitamin D levels and AUC-Ins (R = -.288, ns) was observed. The variables vitamin D, HOMA-IR and AUC-Ins were statistically significant in the considered subgroups (Vitamin D: ANOVA + Bonferroni test: 0 vs. 1; P = .001; 0 vs. 2; P = .010; 1 vs. 2; P = .657; HOMA-IR: ANOVA + Bonferroni test: 0 vs. 1; P = .014; 0 vs. 2; P = .001; 1 vs. 2; P = .001; AUC-Ins: ANOVA + Bonferroni test: 0 vs. 1; P = .010; 0 vs. 2; P = .206; 1 vs. 2; P = .980). Conclusions Vitamin D might play additional roles in the pathogenesis of RPL, beyond its well known immunomodulatory role.

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