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Case Profile A 33-year-old female presented to the clinic for the evaluation of infertility and had obesity (Type 1), menstrual irregularities, and amenorrhea. She was married for the last 8 years with a history of abortion, 7 years earlier. She did not receive any hormonal treatment but was on metformin for 2 months which was … Continue reading “An Obese Woman with PCOS Trying to Conceive”
A 33-year-old female presented to the clinic for the evaluation of infertility and had obesity (Type 1), menstrual irregularities, and amenorrhea. She was married for the last 8 years with a history of abortion, 7 years earlier. She did not receive any hormonal treatment but was on metformin for 2 months which was discontinued due to abdominal discomfort. She was a non-smoker and a non-drinker with no family history of PCOS or any other hormonal disease. Both her parents were of normal weight. The patient also had the following
1) Had severe abdominal pain during periods
2) Had high intra-abdominal fat and hyperandrogenism
3) Sedentary lifestyle with mild acne
4) Acanthosis nigricans was mildly present
Detailed physical and laboratory assessments revealed the following:
– The patient was obese, weighing 81.0 kg and having a BMI of 32.3 kg/m2 & Her height was 158cm.
– Pregnancy test was negative and semen analysis of her husband was normal.
– Blood pressure: 140/90 mmHg
– Mild acanthosis nigricans and acne & Follicle-stimulating hormone – 2.51 IU/L
– Serum luteinizing hormone – 9.88 IU/L
– Testosterone – 2.23 nmol/L
– Estradiol – 210 pmol/L
– 17-OH progesterone – 1.30 nmol/L
– Thyroid stimulating hormone – 0.96 mU/L
– Serum prolactin – 12.55 µg/L
– Fasting blood glucose – 130 mg/dL
USG of the pelvis revealed tiny follicles in the periphery of the ovaries, suggestive of polycystic ovaries.
Secondary amenorrhea, mid-abdominal fat retention with elevated glucose and testosterone levels, together with the appearance of polycystic ovaries on ultrasound established the diagnosis of PCOS.
The patient was assessed by a nutritional therapist and was advised to reduce her current weight by incorporating a low glycaemic diet with an increase in physical activity. She was advised to shed at least 7-10% of her current weight.
The combination of myo-inositol (MI), d-chiro inositol (DCI) and Vitamin D was recommended to be taken twice daily for a period of 6 months, for improving her hormonal parameters, glucose tolerance and to establish regularity in her menstrual cycles. She was also advised to take folic acid 400 mg for pre-conception readiness.
She lost 5 kgs of body weight within 6 months leading to a reduction in her BMI to 30.2 kg/m2.
Another 2 months later, she further reduced 3 kg and regular menstruation cycles were established.
1) Fasting blood glucose – 92 mg/dL
2) Follicle-stimulating hormone – 5.9 IU/L
3) Serum luteinizing hormone – 7.0 IU/L
4) Testosterone – 1.5 nmol/L
5) Estradiol – 200 pmol/L
6) 17-OH progesterone – 2.9 nmol/L
7) Serum prolactin – 9.1 µg/L
After 9 months of treatment, the patient conceived naturally. Her pregnancy was uneventful and she delivered a healthy baby at 38 weeks.
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder among reproductive women aged between 18 and 44 years and it affects approximately 5% to 10% of this age group. The mechanism of anovulation in PCOS is uncertain, but there is an evidence of arrested antral follicle development in women with PCOS. Also, endocrine disruption such as changed levels of gonadotropin-releasing hormone, and hyperinsulinemia may also directly decrease fertility in these women.
PCOS is associated with obesity in 80% of cases; and metabolic syndrome with insulin resistance in 30–40% of cases, which can aggravate PCOS. The management of this insulin resistance is therefore essential in the treatment of PCOS, and is based on nutritional rules, physical activity and other molecules including myo-inositol (MI).
Myo-inositol is the most abundant inositol isomer in the human body; DCI is synthesized by an insulin-dependent epimerase that converts MI into DCI. In PCOS, a defect of MI utilization impairs FSH and insulin signalling. In the ovary, DCI is responsible for an excess production of insulin- dependent testosterone, whereas MI enhances the action of FSH, via anti-Müllerian hormone (AMH). MI has been found in follicular fluid and appears to improve oocyte and embryo quality. Usually, the MI/DCI ratio is 100:1, whereas in PCOS it is 0.2:1. When the concentration of MI is reduced in the follicular fluid (which is the case of PCOS, where it is reduced by 500 times), epimerase activation is excessive leading to an excess of DCI, an increase in insulin resistance and an increase in LH levels. The adequate MI/DCI ratio for supplementation is 40:1.
MI is responsible for a decrease in LH, in the LH/FSH ratio and in testosterone and androstenedione. When ovulation is induced in PCOS women with hyperinsulinism, MI reduces the risk of multifollicular development.
Therefore, MI reduces androgen levels, corrects the LH/FSH ratio, restores normal menstrual cycles and induces ovulation, thereby facilitating spontaneous pregnancies by adequate luteal phase progesterone production.
Merviel P, James P, Bouée S. et al. Impact of myo-inositol treatment in women with polycystic ovary syndrome in assisted reproductive technologies. Reprod Health. 2021;18:13.