Does asporin have a role in polycystic ovary syndrome? A pilot study

AUTOR(ES)
FONTE

Revista da Associação Médica Brasileira

DATA DE PUBLICAÇÃO

2022

RESUMO

SUMMARY OBJECTIVE: Asporin is secreted by theca cells in the mouse ovaries and is an effective marker at the gonadotropin-independent stage in secondary follicle development. It has an inhibitory effect on transforming growth factor beta and bone morphogenic proteins, which are involved in androgenesis process. Our aim was to compare serum asporin levels of polycystic ovary syndrome and control groups and examine the relationship between asporin and hyperandrogenism. METHODS: A total of 60 patients, i.e., 30 polycystic ovary syndrome group and 30 controls, were included in the study. The demographic characteristics, hormonal status, and serum asporin levels of patients were evaluated and compared for each group. In addition, polycystic ovary syndrome patients were analyzed according to the presence of hyperandrogenism. Receiver operating characteristic curve analysis was performed for asporin levels in order to distinguish polycystic ovary syndrome patients from controls. RESULTS: Body mass index, serum asporin and androgen levels, free androgen index, and insulin resistance values were statistically significantly higher in polycystic ovary syndrome group. Serum asporin levels were statistically significantly higher in hyperandrogenic polycystic ovary syndrome patients compared to non-hyperandrogenic polycystic ovary syndrome women (p=0.010). Receiver operating characteristic curve analysis was done for serum asporin levels to distinguish between polycystic ovary syndrome patients and healthy controls (area under the curve=0.676, standard error: 0.070, 95%CI: 0.539–0.812, p=0.019, 63.3% sensitivity, and 70% specificity). CONCLUSION: The elevation of serum asporin levels in patients with polycystic ovary syndrome may be associated with the pathogenesis of this syndrome, or it may be the consequence of the disease. This relationship may be explained through the androgen mechanism.

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