Immunophenotypic profiles and inflammatory markers in Premature Ovarian Insufficiency
- PMID: 38776714
- DOI: 10.1016/j.jri.2024.104253
Immunophenotypic profiles and inflammatory markers in Premature Ovarian Insufficiency
Abstract
Premature Ovarian Insufficiency (POI), also known as Premature Ovarian Failure (POF), is a heterogeneous disorder characterized by the cessation of ovarian function before age 40. Clinical symptoms include menstrual disorders: amenorrhea/oligomenorrhea or symptoms of estrogen deficiency. This review aims to provide the most important summary of the immunophenotypic profile of premature ovarian failure syndrome, along with a review of the latest reports on the usefulness of inflammatory markers. The inflammatory microenvironment in POI applies to many levels. Concomitants of autoimmune ovarian inflammation and impaired cellular immune response may be a picture of impaired regulation in autoimmune ovarian disease. The serum concentration of pro-inflammatory cytokines, like IL-6, IL-8, IL-17, tumor necrosis factor α (TNF-α), and interferon-gamma (IFN-γ), tend to increase, whereas levels of the anti-inflammatory cytokine, IL-10, tend to decrease. In our review, we focus on whether the measured immunological parameters could help in the diagnosis and prognosis of the syndrome. Among the inflammatory markers, neutrophil-to-lymphocyte ratio (NLR) is noteworthy, as it is decreased in patients with POI. It is important to stress that besides case series, we need properly powered studies with randomization to answer which treatment is effective, and how to deal with concurrent autoimmunity. In this review, we emphasize the importance of the premature ovarian failure syndrome immunoprofile for a proper understanding of the complexity of this syndrome, potential diagnostic points, and therapeutic targets.
Keywords: Anti-ovarian antibodies; Autoimmunity; POI; Premature ovarian insufficiency.
Copyright © 2024 Elsevier B.V. All rights reserved.
Conflict of interest statement
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this work paper.
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