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The Impact of Mitochondrial Dysfunction in human oocytes on Embryo quality and Conception rates in IVF patients with varying stages of Endometriosis

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Background: Endometriosis is a chronic, estrogen-dependent gynecological condition that is closely linked to infertility. Although significant progress has been made in assisted reproductive technologies (ART), including in vitro fertilization (IVF), women with endometriosis frequently encounter challenges such as poor oocyte quality, impaired embryo development, and lower pregnancy rates. Emerging evidence suggests that mitochondrial dysfunction, particularly through reduced ATP production and mitochondrial DNA (mtDNA) deletions, plays a critical role in the reproductive difficulties observed in these patients. Aim: The aim is to evaluate the impact of mitochondrial dysfunction on oocyte quality, embryo development, and IVF outcomes in women with endometriosis, comparing them with a control group of women without endometriosis. Methodology: A prospective cohort study was conducted over three years (2021-2024) at the Medical Health and Research Institute, involving 60 women aged 20-40 years. The cohort consisted of 42 women diagnosed with endometriosis (study group) and 42 women undergoing IVF treatment without endometriosis (control group). Mitochondrial function, including ATP content and mitochondrial DNA (mtDNA) integrity, was assessed in oocytes retrieved from both groups. The study compared the outcomes of oocyte maturation, fertilization rates, embryo development, implantation rates, and clinical pregnancy between the two groups. Results: The demographic and clinical characteristics of patients with endometriosis and controls revealed significant differences in age, body mass index (BMI), follicle-stimulating hormone (FSH) levels, and infertility duration. IVF outcomes showed no significant difference in clinical pregnancy rates (54.7% in endometriosis patients vs. 52.3% in controls), but endometriosis patients had slightly lower live birth rates (45.2% vs. 52.3%). Oocyte quality analysis indicated that endometriosis patients exhibited lower ATP content and mitochondrial number, particularly at the prophase I (PI) and metaphase I (MI) stages. Mitochondrial DNA deletions were found to have a significant negative impact on oocyte quality and IVF success, with all cycles involving oocytes with mtDNA deletions resulting in failure, including a biochemical pregnancy in a patient with moderate endometriosis. Conclusion: Mitochondrial dysfunction, characterized by reduced ATP levels and mtDNA deletions, adversely impacts oocyte quality and IVF outcomes in women with endometriosis. These results highlight the importance of personalized IVF protocols that focus on mitochondrial health, potentially enhancing reproductive outcomes. Further research is needed to explore targeted interventions to minimize mitochondrial damage and improve ART success in this population.
Title: The Impact of Mitochondrial Dysfunction in human oocytes on Embryo quality and Conception rates in IVF patients with varying stages of Endometriosis
Description:
Background: Endometriosis is a chronic, estrogen-dependent gynecological condition that is closely linked to infertility.
Although significant progress has been made in assisted reproductive technologies (ART), including in vitro fertilization (IVF), women with endometriosis frequently encounter challenges such as poor oocyte quality, impaired embryo development, and lower pregnancy rates.
Emerging evidence suggests that mitochondrial dysfunction, particularly through reduced ATP production and mitochondrial DNA (mtDNA) deletions, plays a critical role in the reproductive difficulties observed in these patients.
Aim: The aim is to evaluate the impact of mitochondrial dysfunction on oocyte quality, embryo development, and IVF outcomes in women with endometriosis, comparing them with a control group of women without endometriosis.
Methodology: A prospective cohort study was conducted over three years (2021-2024) at the Medical Health and Research Institute, involving 60 women aged 20-40 years.
The cohort consisted of 42 women diagnosed with endometriosis (study group) and 42 women undergoing IVF treatment without endometriosis (control group).
Mitochondrial function, including ATP content and mitochondrial DNA (mtDNA) integrity, was assessed in oocytes retrieved from both groups.
The study compared the outcomes of oocyte maturation, fertilization rates, embryo development, implantation rates, and clinical pregnancy between the two groups.
Results: The demographic and clinical characteristics of patients with endometriosis and controls revealed significant differences in age, body mass index (BMI), follicle-stimulating hormone (FSH) levels, and infertility duration.
IVF outcomes showed no significant difference in clinical pregnancy rates (54.
7% in endometriosis patients vs.
52.
3% in controls), but endometriosis patients had slightly lower live birth rates (45.
2% vs.
52.
3%).
Oocyte quality analysis indicated that endometriosis patients exhibited lower ATP content and mitochondrial number, particularly at the prophase I (PI) and metaphase I (MI) stages.
Mitochondrial DNA deletions were found to have a significant negative impact on oocyte quality and IVF success, with all cycles involving oocytes with mtDNA deletions resulting in failure, including a biochemical pregnancy in a patient with moderate endometriosis.
Conclusion: Mitochondrial dysfunction, characterized by reduced ATP levels and mtDNA deletions, adversely impacts oocyte quality and IVF outcomes in women with endometriosis.
These results highlight the importance of personalized IVF protocols that focus on mitochondrial health, potentially enhancing reproductive outcomes.
Further research is needed to explore targeted interventions to minimize mitochondrial damage and improve ART success in this population.

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