A new review provides a comprehensive picture of how endometriosis makes the female reproductive environment hostile and to what extent this can be partially counteracted by a fertility programme. The authors - a team from the University of Medicine in Lublin and the Bocian Reproduction Centre - combined molecular biology with data from assisted reproductive technologies. The picture is both sobering and hopeful: the multi-level damaging effects of endometriosis do not disappear once fertilisation is "out" of the body's inflammatory milieu, yet the laboratory environment can overcome more obstacles and offer a chance of success, especially if a more personalised strategy tailored to the triggering mechanisms is used.
The central claim of the study is that the infertility effects of endometriosis do not occur at a single point, but along the entire reproductive chain. Persistent, low-grade inflammation, oxidative stress, immunological imbalance and mitochondrial damage remodel the microclimate of the ovaries and pelvic organs; in addition, structural abnormalities - adhesions, endometriomas - mechanically complicate spontaneous conception. In an inflammatory-oxidative environment, oocytes are at higher risk of DNA damage, the composition of follicular fluid is altered and ovarian reserve may be reduced. This affects every step from the chance of fertilisation to early embryo development.
However, in vitro fertilisation can improve the odds because it avoids the damaging effects of some of the pelvic environment: fertilisation and embryo culture take place in a controlled, less inflammatory environment. However, practical experience has shown that the picture is more nuanced. The bottleneck to success is usually the oocyte itself: the quality of the egg determines the outcome In vitro fertilisation can still improve the chances of success because it avoids the damaging effects of part of the pelvic environment: fertilisation and embryo culture take place in a controlled, less inflammatory environment. However, practical experience has shown that the picture is more nuanced. The bottleneck to success is mostly in the oocyte itself: the quality of the oocyte is the main determinant of embryo viability and final outcome. The receptivity of the endometrium, on the other hand, is often preserved, meaning that the difference is not primarily due to the endometrium. The overall picture reported is that in endometriosis, the survival rate of IVF treatments is on average 10-15% lower compared to unaffected controls - not a dramatic but consistent disadvantage, explained mainly by oocyte-derived factors.most importantly embryo viability and final outcome. In contrast, the receptivity of the endometrium is preserved in many cases, i.e. the difference is not primarily due to the endometrium. The overall picture reported is that in endometriosis, the survival rate of fertility treatments is on average 10-15% lower in endometriosis compared to unaffected controls - not a dramatic but consistent disadvantage, mainly explained by oocyte-derived factors.
This has several implications for clinical practice. There may be value in pre-treatments aimed at reducing inflammation and oxidative stress: some data show a benefit with GnRH agonists and antioxidants, although the level of evidence and the exact target population need to be refined. On the laboratory side, advances in embryo selection and monitoring are promising: time-lapse imaging, analysis of morphokinetic patterns, non-invasive metabolomics/'multi-omics' approaches and artificial intelligence-based embryo screening all point in the direction of increasingly tailoring the decision to the biological profile of the patient and the specific embryo.
Research is currently working on detailed mapping of processes at the cellular and tissue level: single-cell transcriptomic analyses, immunomodulatory strategies and experimental exosome-based interventions are mapping possible pathways for the future. However, the message is cautionary: these technologies are mostly in the development phase and their large-scale clinical validation is not yet complete.
Endometriosis often creates a hostile environment for conception, and IVF offers a temporary "in vitro refuge". But the technique is not a magic wand. The success of reproduction is crucially determined by oocyte competence, redox balance and immune homeostasis.
Precision reproductive medicine is the promise of the future: protocols in which AI, metabolomics and immunoprofiling are not separate stunts, but part of a translational ecosystem that works in harmony. Thus, rather than being "better" in itself, fombics are more precisely adapted to the dynamic biological equilibrium disrupted by disease.
The authors are not silent about the limitations of the evidence. The available literature is heterogeneous, there is a paucity of good quality data on stage-specific, long-term IVF outcomes, and many personalised interventions are still only theoretical possibilities. This raises caution about generalisability and calls for further well-designed prospective studies.
The practical message for a woman with endometriosis is twofold. On the one hand, it is worth starting the treatment with realistic expectations: fombies can bypass certain obstacles, but they cannot prevent oocyte-derived harm overnight.
On the other hand, the success rate can be increased by paying attention to reducing inflammation/oxidative stress, proper preparation and by using embryo selection methods that reveal as much information as possible about the biological characteristics of the patient and embryo. The path to a solution is not a single procedure, but a mindset: a series of personalised clinical decisions based on an understanding of the molecular nature of the disease. In this framework, IVF is not just a technique, but a bridge between the lab and the bedside - and the stronger the two pillars of the bridge, the greater the chance that hope will turn into tangible results.
Source : https://pubmed.ncbi.nlm.nih.gov/40906150/
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