AR is a steroid hormone receptor that regulates various genes' expression and affects cellular proliferation and differentiation. Androgens interact with AR, exert their paracrine action on granulosa cells and regulate gonadotropin synthesis, follicle development, oocyte maturation and corpus luteum function. Estrogens increase AR mRNA and testosterone binding site in uterine endometrium and leiomyoma. In human cancer cells, low estradiol increases AR levels, suggesting the estrogen/androgen ratio as a predictor of sex steroid response. AR mRNA expression is, also, regulated by progesterone. Although AR mRNA is expressed in the female reproductive tissues, its expression has never been studied in peripheral blood.

Inclusion Criteria:

• Women with poor ovarian response according to bologna criteria

  1. Advanced maternal age (≥40 years) or any other risk factor for poor ovarian response
  2. A previous poor ovarian response (≤3 oocytes with a conventional stimulation protocol)
  3. Abnormal ovarian reserve test, (AFC ˂5-7 follicles or AMH ˂0.5-1.1 ng/ml).

• Women with normal ovarian response with normal menstrual cycles, normal astral follicle count and normal hormonal assay.

Exclusion Criteria:

• Not more than 43 years old.
• No history of malignancies, endometriosis or polycystic ovary syndrome.
• Underlying genetic cause of infertility
• History of severe cardiac, hepatic or renal disease.
• History of systemic disease or treatment during the last three (3) months
• Participation in another interventional study and a likelihood of being unavailable for follow-up.

Forty normal responders and twenty-seven poor responders according to Bologna criteria, undergoing IVF/ICSI. Ovarian stimulation was performed with 200 IU recombinant follicle stimulating hormone (rFSH) and gonadotrophin releasing hormone (GnRH) antagonists. Triggering of final oocyte maturation was performed by recombinant human chorionic gonadotrophic (rhCG)