title: [Premature ovarian failure after chemotherapy for breast cancer].
abstract: About a quarter of breast cancers occur before menopause. Most breast cancer types occurring in young women require adjuvant treatments that can partially or definitively affect the reproductive function. Risk factors of chemotherapy-induced ovarian failure (CIOF) include woman's age, type, dose and schedule of chemotherapy. Cyclophosphamide-based regimens, notably when high doses are used, confer the highest rates of CIOF (especially for patients older than 40). A continual decline in ovary function follows cyclophosphamide-based regimens. By contrast, anthracycline-based regimens confer lower rates of CIOF and ovarian function recovers in half of the cases. The role of more recently reported adjuvant chemotherapy strategies in CIOF, such as alternative schedules (for example, dose-dense therapy), newer agents (for example, taxanes) or the addition of new therapies such as trastuzumab, is still controversial or unknown. Ovarian suppression through gonadotropin releasing hormone (Gn-RH) agonists treatment during chemotherapy to avoid CIOF is still under evaluation. Until the publication of prospective clinical trials results, "non-controlled" use of Gn-RH agonists should not be encouraged, notably for patients with a hormonosensible tumor, since there is insufficient evidence regarding their safety and effectiveness on female fertility preservation. More recent data suggest that an individual woman's risk of developing CIOF could be determined by the exploration of some genetic variants like CYP2C19. Before treatment strategy determination, the desire to preserve fertility should be systematically taken into account. Likewise, the early loss of ovarian function induced by treatments has to be explained to young patients diagnosed with a breast cancer and can sometimes lead to therapeutic options associated with less ovary dysfunction.
authors.affiliation: Service de gynécologie-obstétrique, CHRU, 1, place de l'Hôpital, 67091 Strasbourg. Carole.Mathelin@chru-strasbourg.fr
authors.forename: Carole
authors.initials: C
authors.lastname: Mathelin
authors.forename: Jean-Philippe
authors.initials: JP
authors.lastname: Brettes
authors.forename: Pierre
authors.initials: P
authors.lastname: Diemunsch
mesh_terms: D000328:Adult; D000367:Age Factors; D000911:Antibodies, Monoclonal / Q000009:adverse effects; D061067:Antibodies, Monoclonal, Humanized; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000009:adverse effects*; D001943:Breast Neoplasms / Q000188:drug therapy*; D017024:Chemotherapy, Adjuvant / Q000009:adverse effects; D003276:Contraceptives, Oral / Q000627:therapeutic use; D003520:Cyclophosphamide / Q000009:adverse effects; D005260:Female; D020022:Genetic Predisposition to Disease; D007987:Gonadotropin-Releasing Hormone / Q000819:agonists*; D006801:Humans; D007247:Infertility, Female / Q000209:etiology / Q000517:prevention & control; D009376:Neoplasms, Hormone-Dependent / Q000188:drug therapy; D010053:Ovary / Q000187:drug effects*; D016649:Primary Ovarian Insufficiency / Q000139:chemically induced* / Q000150:complications / Q000517:prevention & control; D011379:Prognosis; D012307:Risk Factors; D013629:Tamoxifen / Q000009:adverse effects; D043823:Taxoids / Q000009:adverse effects; D000068878:Trastuzumab
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D003276:Contraceptives, Oral; D043823:Taxoids; D013629:Tamoxifen; D007987:Gonadotropin-Releasing Hormone; D003520:Cyclophosphamide; D000068878:Trastuzumab