Illustration of a uterus model beside sample tubes in a research laboratory
Illustration created with generative AI (ChatGPT, OpenAI).

Polish researchers compared 33 patients with endometriosis and 14 controls. Differences in galectin proteins and inflammatory markers in women with both deep endometriosis and adenomyosis raise questions about the immune environment. Their relevance to fertility requires further study.

Endometriosis and adenomyosis are distinct conditions, yet both can occur in the same woman. They can cause severe menstrual and pelvic pain and, for some women, difficulty conceiving. Why do they sometimes coexist? Researchers in Poland looked for clues in immune regulation and inflammation. Their preliminary findings suggest that the overlap could involve a complex biological environment as well as structural changes in reproductive organs.

How endometriosis and adenomyosis differ

In endometriosis, tissue resembling the uterine lining occurs outside the uterus, for example on the ovaries or peritoneum. Deep endometriosis extends beneath the peritoneal surface and can cause severe pelvic pain, painful bowel movements and pain during intercourse.

In adenomyosis, similar tissue occurs within the uterine muscle. The uterus may enlarge, and periods may become heavier or more painful. The conditions arise in different locations but share features including chronic inflammation, hormonal responses and tissue remodeling. When they coexist, pain or menstrual symptoms can overlap. Fertility evaluation may need to consider both ovarian function and the uterine environment.

Why the team studied galectins

Galectins are proteins that bind to sugar structures on cell surfaces. They participate in cell interactions, immune responses and the regulation of inflammation. Different galectins can stimulate or inhibit immune cells depending on the surrounding tissue. A change in a galectin level may therefore offer a clue about the local immune environment.

The researchers analyzed galectins and inflammatory markers in 47 participants, with particular attention to women with both deep endometriosis and adenomyosis. They observed differences in some markers when the two conditions coexisted. The study could not determine whether the changes contributed to disease development or arose in response to existing lesions.

How might chronic inflammation relate to fertility?

Immune cells and signaling molecules help coordinate implantation and placental development in a normal pregnancy. Their balance matters. In endometriosis, researchers are investigating whether inflammation around lesions or changes in immune-cell activity affect eggs, fertilization or embryo development. Work on adenomyosis has also raised questions about uterine muscle changes, endometrial function and the conditions for implantation.

The study adds observations that could guide research into how the conditions relate to infertility. It measured proteins and inflammatory signals. It did not assess IVF pregnancy or live-birth rates. A high or low protein level cannot be used to predict a particular woman's chance of pregnancy.

Do changed markers justify immune treatment?

Women who have experienced repeated implantation failure or miscarriage may wonder whether their immune system is involved. Finding a difference in an immune marker and showing that a treatment helps are separate research questions. The study did not test whether changing a marker improves pregnancy rates. Its findings cannot support routinely recommending steroids or other immune-modifying treatments.

Symptoms, lesion location, ovarian function, uterine findings, age and pregnancy plans remain relevant to an individual clinical assessment.

What might explain the overlap?

With only 47 participants, these findings cannot be generalized to all women or all infertility patients. The relationships between the observed markers and disease severity, pain or pregnancy outcomes also need verification. Larger studies that follow changes in galectins and inflammatory signals alongside disease progression and treatment outcomes may clarify why the disorders coexist.

The results offer a clue about potentially connected inflammatory and immune responses. Translating that clue into a diagnostic test or fertility treatment would require further research.

Source: Preliminary Polish study published in Frontiers in Endocrinology, October 13, 2026. DOI: 10.3389/fendo.2026.1920315. PMID: 42947782.

Related reading: Adenomyosis pattern and live birth: a review of 19,510 women.

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