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Volume 24, Issue 9 (September 2026)
Int J Reprod BioMed. 2026, 24(9): 861-863 |
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Torkashvand H, Pilehvari S. Adding fuel to the fire? platelet-rich plasma -induced estrogen rise in endometriosis patients. , Int J Reprod BioMed.. 2026; 24 (9) :861-863
URL: http://ijrm.ir/article-1-3911-en.html
URL: http://ijrm.ir/article-1-3911-en.html
1- Fertility and Infertility Research Center, Avicenna Institute of Clinical Sciences, Hamadan University of Medical Sciences, Hamadan, Iran.
2- Fertility and Infertility Research Center, Avicenna Institute of Clinical Sciences, Hamadan University of Medical Sciences, Hamadan, Iran. ,sh.pilevar@umsha.ac.ir
2- Fertility and Infertility Research Center, Avicenna Institute of Clinical Sciences, Hamadan University of Medical Sciences, Hamadan, Iran. ,
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Dear Editor
Over recent years, the application of autologous platelet-rich plasma (PRP) has rapidly expanded in assisted reproductive technologies (1). In many infertility centers, off-label use of PRP for ovarian rejuvenation, enhancement of follicular development, improvement of oocyte quality, and endometrial regeneration has become increasingly common (2). Despite some clinical observations showing promising short-term results, such as an increase in antral follicle count in patients with poor ovarian response, as well as improved endometrial thickness in patients with thin endometrium (3), there are growing concerns regarding its safety in a specific subgroup of patients.
Endometriosis is one of the most common causes of infertility and is defined by the ectopic growth of tissue resembling the endometrial lining within the pelvis or abdomen. This condition is a chronic, estrogen-dependent inflammatory disease that affects a significant proportion of women of reproductive age.
One of the safety concerns raised in this context is the observation of a correlation between the intraovarian administration of PRP and a significant increase in serum estradiol levels (4). Given the estrogen-dependent nature of endometriosis, this PRP-induced estrogen surge has the potential to stimulate the proliferation of endometrial lesions, exacerbate pelvic inflammation, and lead to disease progression. Clinically, this effect may result in the exacerbation of the current condition in patients with known or suspected endometriosis and significantly increase the risk of disease advancement.
Several clinical observations, along with supporting histological and molecular data, raise serious concerns regarding this approach.
Intra-ovarian PRP injection has been associated with a marked elevation in serum estradiol levels, such that in some cases, this increase can be reported as significantly higher than the baseline level (5). In our clinical experience and in some published reports, it is widely recognized that increased endogenous estrogen exposure is associated with progression of endometriotic lesions, worsening of pelvic pain, dysmenorrhea, and recurrence of the disease. Histologically, endometriotic lesions are characterized by markedly elevated expression of estrogen receptors (ER), particularly ER-β (which can be over 100 times higher than in eutopic endometrium), along with significant expression of ER-α (6). These ectopic tissues also aberrantly overexpress the aromatase enzyme cytochrome P450 family 19 subfamily A member 1, enabling local estrogen biosynthesis from androgen precursors. This creates an estrogen-rich microenvironment that promotes lesion survival, proliferation, angiogenesis, and invasion of endometriotic implants (7). Moreover, at the molecular level, PRP was found to be rich in bioactive growth factors including vascular endothelial growth factor, platelet-derived growth factor, transforming growth factor beta, and insulin-like growth factor 1. These factors can upregulate aromatase activity and steroidogenic enzymes in endometriotic stromal cells, thereby increasing local and systemic estradiol production. Furthermore, estrogen, acting through overexpressed ER-β, activates multiple pro-inflammatory and pro-angiogenic pathways, including increased production of cytokines such as interleukin 6, interleukin 8, and tumor necrosis factor, as well as enhanced vascular endothelial growth factor -mediated angiogenesis. Platelets and their released mediators may also directly contribute to the pathogenesis of endometriosis by promoting inflammation, fibrosis, and epithelial-mesenchymal transition in ectopic endometrial tissue (8). Consequently, the intersection of these 2 biological realities raises a fundamental clinical concern; applying PRP in women with endometriosis may inadvertently amplify estrogen-dependent pathogenic processes.
Future well-designed prospective studies, particularly randomized clinical trials with long-term follow-up, are urgently needed to evaluate the safety of PRP treatment in women with endometriosis. Future research should involve systematic screening for endometriosis prior to PRP administration, serial monitoring of serum and follicular fluid estradiol levels, objective assessment of disease progression (via imaging or laparoscopy when feasible), and meticulous documentation of clinical outcomes such as pelvic pain, dysmenorrhea, and recurrence rates. Comparative studies between patients with and without endometriosis would be particularly valuable in elucidating the benefit-risk profile of this intervention.
Consequently, until robust safety data become available, we recommend a cautious approach when considering PRP treatment in infertile women with known or suspected endometriosis.
Acknowledgments
The authors acknowledge the use of ChatGPT, an AI-based language model, to improve the English language editing of this manuscript.
Conflict of Interest
The authors declare that there is no conflict of interest.
Over recent years, the application of autologous platelet-rich plasma (PRP) has rapidly expanded in assisted reproductive technologies (1). In many infertility centers, off-label use of PRP for ovarian rejuvenation, enhancement of follicular development, improvement of oocyte quality, and endometrial regeneration has become increasingly common (2). Despite some clinical observations showing promising short-term results, such as an increase in antral follicle count in patients with poor ovarian response, as well as improved endometrial thickness in patients with thin endometrium (3), there are growing concerns regarding its safety in a specific subgroup of patients.
Endometriosis is one of the most common causes of infertility and is defined by the ectopic growth of tissue resembling the endometrial lining within the pelvis or abdomen. This condition is a chronic, estrogen-dependent inflammatory disease that affects a significant proportion of women of reproductive age.
One of the safety concerns raised in this context is the observation of a correlation between the intraovarian administration of PRP and a significant increase in serum estradiol levels (4). Given the estrogen-dependent nature of endometriosis, this PRP-induced estrogen surge has the potential to stimulate the proliferation of endometrial lesions, exacerbate pelvic inflammation, and lead to disease progression. Clinically, this effect may result in the exacerbation of the current condition in patients with known or suspected endometriosis and significantly increase the risk of disease advancement.
Several clinical observations, along with supporting histological and molecular data, raise serious concerns regarding this approach.
Intra-ovarian PRP injection has been associated with a marked elevation in serum estradiol levels, such that in some cases, this increase can be reported as significantly higher than the baseline level (5). In our clinical experience and in some published reports, it is widely recognized that increased endogenous estrogen exposure is associated with progression of endometriotic lesions, worsening of pelvic pain, dysmenorrhea, and recurrence of the disease. Histologically, endometriotic lesions are characterized by markedly elevated expression of estrogen receptors (ER), particularly ER-β (which can be over 100 times higher than in eutopic endometrium), along with significant expression of ER-α (6). These ectopic tissues also aberrantly overexpress the aromatase enzyme cytochrome P450 family 19 subfamily A member 1, enabling local estrogen biosynthesis from androgen precursors. This creates an estrogen-rich microenvironment that promotes lesion survival, proliferation, angiogenesis, and invasion of endometriotic implants (7). Moreover, at the molecular level, PRP was found to be rich in bioactive growth factors including vascular endothelial growth factor, platelet-derived growth factor, transforming growth factor beta, and insulin-like growth factor 1. These factors can upregulate aromatase activity and steroidogenic enzymes in endometriotic stromal cells, thereby increasing local and systemic estradiol production. Furthermore, estrogen, acting through overexpressed ER-β, activates multiple pro-inflammatory and pro-angiogenic pathways, including increased production of cytokines such as interleukin 6, interleukin 8, and tumor necrosis factor, as well as enhanced vascular endothelial growth factor -mediated angiogenesis. Platelets and their released mediators may also directly contribute to the pathogenesis of endometriosis by promoting inflammation, fibrosis, and epithelial-mesenchymal transition in ectopic endometrial tissue (8). Consequently, the intersection of these 2 biological realities raises a fundamental clinical concern; applying PRP in women with endometriosis may inadvertently amplify estrogen-dependent pathogenic processes.
Future well-designed prospective studies, particularly randomized clinical trials with long-term follow-up, are urgently needed to evaluate the safety of PRP treatment in women with endometriosis. Future research should involve systematic screening for endometriosis prior to PRP administration, serial monitoring of serum and follicular fluid estradiol levels, objective assessment of disease progression (via imaging or laparoscopy when feasible), and meticulous documentation of clinical outcomes such as pelvic pain, dysmenorrhea, and recurrence rates. Comparative studies between patients with and without endometriosis would be particularly valuable in elucidating the benefit-risk profile of this intervention.
Consequently, until robust safety data become available, we recommend a cautious approach when considering PRP treatment in infertile women with known or suspected endometriosis.
Acknowledgments
The authors acknowledge the use of ChatGPT, an AI-based language model, to improve the English language editing of this manuscript.
Conflict of Interest
The authors declare that there is no conflict of interest.
Type of Study: Letter to Editor |
Subject:
Fertility & Infertility
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