Polycystic ovary syndrome (PCOS) emerges as a widespread endocrine and metabolic disorder, notably impacting women in their reproductive years (Sirmans and Pate 2013). The reported prevalence of PCOS varies from 4% to 26%, contingent upon demographic factors and diagnostic criteria (Sirmans and Pate 2013). Diagnosis, based on the Rotterdam criteria, necessitates the presence of a minimum of two among the following features: oligo/anovulation, clinical or biochemical hyperandrogenism, or the identification of polycystic ovaries via ultrasound (Anon, 2004, Teede et al., 2018, Javidan et al., 2022). This intricate condition presents across a spectrum of clinical manifestations, with its complex pathogenesis intertwined with hormonal imbalances and hyperandrogenism (Mierzwicka and Bolanowski, 2016, Czerwińska et al., 2021). Despite considerable advancements, the precise etiology of PCOS remains elusive. Current insights propose a multifaceted interplay of genetic, environmental, metabolic, and immunological factors, possibly initiated during fetal development (Gawron et al. 2022). Concurrently, thyroid hormones are critical for maintaining reproductive health and regulating metabolism. Normal levels of these hormones are essential at all stages of the reproductive process (Farshchian et al., 2021, Bahreiny et al., 2024b).

This intricate interplay is susceptible to disruption, exemplified by the emergence of Autoimmune Thyroiditis (AIT), also recognized as "Hashimoto thyroiditis" or "chronic lymphocytic thyroiditis," which assumes prominence as a prevalent endocrine disorder in premenopausal women, affecting up to 5-20% of women during the Age of fertility. AIT prevalence underscores its significance, where immune dysfunction, characterized by T cell-mediated attacks on the thyroid gland, positions it as the primary cause of hypothyroidism (Artini et al., 2013, Kim et al., 2022). A deficiency of thyroid hormones can impair gonadal function and fertility and result in a delay in the onset of puberty and ovulation (Colicchia et al. 2014).

Diagnostic markers, such as anti-peroxidase antibodies (Anti-TPO), anti-thyroglobulin antibodies (Anti-TG), and thyroid gland hypo-echogenicity observed through ultrasound, yield crucial insights for accurate AIT diagnosis (Janssen et al., 2004, Cooper and Biondi, 2012, Benetti-Pinto et al., 2013).

Although the pathophysiological relationship between AIT and PCOS remains unclear, several studies suggest a possible link between the two conditions; however, it is not clear whether the common features of these syndromes are due to some common factors that predispose an individual to both disorders or whether there is a pathophysiological link between them.

In the context of this knowledge gap, our study aims to investigate the correlation and potential variations in AIT, with a specific emphasis on Hashimoto thyroiditis, among individuals diagnosed with PCOS. Through a systematic review and meta-analysis, we aspire to provide a nuanced and comprehensive understanding of the intricate relationship between these prevalent endocrine disorders and their contributing factors. This research seeks not only to address the current knowledge gap but also to make a substantive contribution to the existing body of knowledge on this subject.