Systemic immune-inflammation index in ovarian reserve, polyendocrine metabolic ovarian syndrome, and assisted reproductive technology outcomes: a narrative review

Background The systemic immune-inflammation index (SII) has emerged as a composite marker integrating platelet, neutrophil, and lymphocyte counts, reflecting both proinflammatory and immunoregulatory pathways. While increasing clinical evidence links the SII to ovarian reserve and assisted reproductive technology (ART) outcomes, a comprehensive synthesis of its clinical utility and underlying mechanisms is lacking. This narrative review summarizes the evidence linking the SII to anti-Müllerian hormone (AMH) levels, ovarian reserve, polyendocrine metabolic ovarian syndrome (PMOS), and ART outcomes, while proposing a unified “inflammation–oxidative stress–fibrosis” model for ovarian damage. Key findings Large cohort studies have demonstrated a robust negative correlation between the SII and the AMH/antral follicle count, independent of age and body mass index. In PMOS patients, the SII is associated with hyperandrogenism, insulin resistance, and dyslipidemia, and predicts embryo arrest and a reduced available embryo rate with clear threshold effects (SII > 733, log SII > 6.72). Mechanistically, an elevated SII reflects a dual imbalance: increased neutrophil‑platelet activation drives follicular inflammation and neutrophil extracellular trap formation (NETosis), while relative lymphopenia weakens immune tolerance at the maternal–fetal interface. This imbalance triggers oxidative stress and TGF‑β1‑mediated fibrosis, forming a vicious cycle of ovarian dysfunction and follicular atresia. Lifestyle and pharmacological interventions targeting this pathway, such as weight loss, metformin, and melatonin, show promise for improving fertility outcomes. Conclusion The SII is a low‑cost, accessible marker with strong potential for risk stratification in fertility management. Prospective trials are needed to validate SII‑guided interventions.