Long-term health in women of age more than 40years with polycystic ovary syndrome

Introduction

Polycystic ovary syndrome (PCOS) is the most common endocrinopathy, affecting women in reproductive age. The manifestations of this condition consist of ovulatory, metabolic, aesthetic, psychological, and possibly an elevated risk of cancer as well. Authorities have published guidelines on the management and consequences of PCOS in younger women .

A growing body of evidence focused on identifying the prevalence and describing the manifestations of PCOS in reproductive-aged or postmenopausal women. However, the investigation of PCOS in older women remains challenging due to the lack of available diagnostic criteria to describe the syndrome in aging women. The overall prevalence seems to differ according to the diagnostic criteria implemented, and has been estimated as 6% based on the National Institute of Health criteria, as high as 10% based on Rotterdam criteria, and 10% based on androgen excess-PCOS criteria .

The aim of this review is to present a guide on the manifestations of PCOS in women over 40 years and to summarize the most indicated management pathways.

The aging PCOS phenotypes

The manifestations of PCOS in reproductively active women have been clustered into four distinct phenotypes, namely, Type A (hyperandrogenism, ovulatory dysfunction, and presence of ovaries with polycystic morphology), Type B (hyperandrogenism and ovulatory dysfunction), Type C (hyperandrogenism and presence of ovaries with polycystic morphology), and Type D (ovulatory dysfunction and presence of ovaries with polycystic morphology) .

The age-related changes in ovarian morphology and ovarian function result into amelioration of the PCOS phenotypes defined during reproductive age . Women with PCOS are found to undergo menopause up to 2 years later as opposed to normo-ovulatory women . This finding might either be related with greater ovarian reserve during the reproductive years, with either increased number of germ cells at birth or reduced loss of germ cells . In clinical terms, women of older reproductive age with PCOS have a lower number of follicles compared to younger women with PCOS, and consequently lower levels of inhibin B, which in turn prevents the suppression of follicle stimulating hormone (FSH) levels. Normalization of serum levels of FSH is now inducing follicular growth and ovulation with a normalized frequency, so that older women with PCOS are more likely to experience regular ovulatory cycles ( Fig. 1 ).

Aging per se is associated with a progressive decrease in androgen production and a relative decline in ovarian volume and follicle count . The PCOS-related hyperandrogenemia (HA) tends to improve with aging; however, few biochemical and clinical features are likely to persist up to the menopause . The declining androgen levels will theoretically result into some improvement of insulin resistance; however, the possible beneficial implications of decreased androgens on cardiometabolic risk factors seem to be counterregulated by the hormonal changes triggered secondarily to ovarian senescence. Results from a 20-year longitudinal analysis have shown that levels of insulin seem to remain stable throughout the years, irrespective of altered levels of androgens in women with PCOS . The alterations in biochemical parameters of women with PCOS in parallel with aging are presented in Fig. 2 .

Diagnosis of PCOS in menopause

The diagnosis of PCOS after the menopausal transition remains challenging. The latest guidelines advise that the diagnosis could be considered provided:

• A previous diagnosis of PCOS documented during the reproductive years or report of a long-term history of menstrual irregularity accompanied by clinical and/or biochemical hyperandrogenism and/or presence of ovaries with polycystic morphology during the reproductive life.