Letter regarding decreased anti-Müllerian hormone in women with superficial peritoneal endometriosis by Griffiths et al.

Dear Editor,We read with interest the article by Griffiths et al. published in this journal. The article concluded, using a retrospective design, that for the first time, infertile patients with peritoneal endometriosis were linked to a drop in the serum anti-Müllerian hormone levels (Griffiths et al. 2026). However, we have some important considerations to raise.The first report in the scientific literature on the decrease in anti-Müllerian hormone (AMH) in women with peritoneal endometriosis was published by my research group in 2008, using a prospective design (Lemos et al. 2008). Afterwards, we explored the dynamics of this hormone in the follicular fluid of this group of women and found that infertile patients with peritoneal endometriosis have follicular fluid AMH concentrations similar to those of control subjects after natural IVF.Moreover, recently, we have published an analysis of intraovarian physiology with a study of various cellular messengers (gene expression of the genes for ligands AMH, BMP-6, GDF-9, INHA, INHBB, and TGFβ; receptors AMHR2, BMPR2, and TGFβ; and intracellular signalling: SMAD3 and SMAD4) in the TGFβ signalling pathway (of which AMH is a part) and demonstrated that the SMAD4 and BMP-6 pathways were altered in these patients.We had also already addressed the role of the AMH gene polymorphism and demonstrated that it showed statistical significance, with the polymorphic allele associated with infertility in endometriosis (De Conto et al. 2021).Therefore, the authors’ findings do not surprise us and, unfortunately, are nothing new in the medical literature. We were surprised that they did not recognise or cite our previous research establishing this link between peritoneal endometriosis and a decreased ovarian reserve, as well as a series of molecular mechanisms which we clearly demonstrated and continue to study.The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the work reported.This research did not receive any specific grant from any funding agency in the public, commercial, or not-for-profit sector.