Published in:
30-05-2022 | Fertility | Meta- Analysis
Assessment of ovarian reserve in patients with type 1 diabetes: a systematic review and meta-analysis
Authors:
Wenjia Yang, Chu Lin, Mengqian Zhang, Fang Lv, Xingyun Zhu, Xueyao Han, Xiaoling Cai, Linong Ji
Published in:
Endocrine
|
Issue 2/2022
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Abstract
Purpose
Current knowledge about the ovarian reserve in patients with type 1 diabetes is inconsistent and based on studies with small sample size. This meta-analysis aimed to produce a comprehensive evaluation on the ovarian reserve of type 1 diabetes female patients and to analyze the associated factors with the ovarian reserve.
Methods
Systematic searches were conducted for studies published from the inception to December 2021. Original human observational studies either with case-control, cross-sectional, or longitudinal design evaluating ovarian reserve markers between type 1 diabetes patients and healthy controls were included. Levels of anti-müllerian hormone (AMH), follicle-stimulating hormone (FSH), and estradiol (E2) were extracted.
Results
It was indicated that women with type 1 diabetes were associated with decreased levels of AMH compared with healthy controls (weighted mean difference [WMD] −0.70 ng/ml, 95% confidence intervals [CI] −1.05 to −0.34 ng/ml, P = 0.0001). Subgroup analyses stratified by age showed that adult patients with type 1 diabetes were associated with decreased levels of AMH (WMD −0.70 ng/ml, 95% CI −1.06 to −0.34 ng/ml, P = 0.0001) and FSH (WMD −1.07 IU/L, 95% CI −1.75 to −0.39 IU/L, P = 0.002) compared with healthy controls. Meta-regression analysis showed no significant correlation between AMH, FSH, and clinical factors, while level of E2 was negatively correlated with daily insulin doses and glycosylated hemoglobin A1c (HbA1c) values.
Conclusion
According to this meta-analysis, type 1 diabetes might be associated with decreased AMH levels. Further studies using different markers and fertility outcomes focus on the ovarian reserve of women with type 1 diabetes are urgently needed.