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DOI 10.3390/ph16121696

Медицинская библиотека · Pharmaceuticals (Basel, Switzerland) · 2023

Gut Microbiota and Endometriosis: Exploring the Relationship and Therapeutic Implications.

Xholli Anjeza, Cremonini Francesca, Perugi Isabella, Londero Ambrogio Pietro, Cagnacci Angelo

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Аннотация

Endometriosis is a common inflammatory disease affecting women of reproductive age, characterized by the growth of endometrial tissue beyond the uterus. In addition to gynecological manifestations, many endometriosis patients experience gastrointestinal symptoms, indicating a potential association between gut health and the disease. Recent studies have revealed alterations in the gut microbiota of individuals with endometriosis, including reduced diversity, microbial composition imbalances, and pathogenic bacteria. These changes can disrupt immune function, increase inflammation, and contribute to the chronic inflammatory state observed in endometriosis. Moreover, dysregulation of intestinal permeability may further exacerbate gastrointestinal symptoms in affected individuals. Understanding the role of the gut microbiota and intestinal permeability in endometriosis can provide valuable insights into disease pathogenesis, aid in non-invasive diagnostic approaches, and open new avenues for therapeutic interventions. Probiotics, in particular, have shown promise in improving endometriosis-associated pain symptoms and reducing endometriotic lesions in animal models. This review suggests that additional research and well-designed clinical trials are necessary to validate the potential diagnostic and therapeutic benefits of manipulating the gut microbiota in managing endometriosis and its gastrointestinal symptoms, thereby improving the quality of life for those affected.

Для цитирования: Xholli Anjeza, Cremonini Francesca, Perugi Isabella, Londero Ambrogio Pietro, Cagnacci Angelo. Gut Microbiota and Endometriosis: Exploring the Relationship and Therapeutic Implications.. Pharmaceuticals (Basel, Switzerland). 2023. DOI: 10.3390/ph16121696.
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