Polycystic Ovarian Syndrome (PCOS)

What is Polycystic Ovarian Syndrome (PCOS)?

The polycystic ovary syndrome is an endocrinological disease, characterized by the cardinal signs of: decreased menstruation frequency (Oligomenorrhea), absence of ovulation (anovulation) that can be identified with the absence of menstruation (amenorrhea), androgenic signs , and sonographic signs of cysts in the ovaries. In order to have an adequate definition of this syndrome, different criteria for its diagnosis have been proposed over the years that will be explained and shown below the article.

What is the prevalence and causes of PCOS?

The prevalence of this disease is between 4-12% of women of reproductive age, being the endocrine pathology more frequent in women, and affects all races and nationalities equally.


It must be taken into account that the cause of polycystic ovarian syndrome to date is of unknown origin, but it is believed to have a high genetic origin of multifactorial type, the prevalence increases from 32 to 66% in women with SOPs with PCOS and in 24 to 52% in mothers with the syndrome.

There is no single etiological factor, which is why several causes have been identified, such as:

  • The alteration in GnRH secretion
  • An increase in Luteinizing Hormone (LH)
  • Stimulation of teak cells for androgen production
  • A factor of hereditary character

What is the pathophysiology of polycystic ovarian syndrome?

As we have already mentioned on several occasions, it is not known exactly what is the cause of SOP, but it is known that:

  1. There is an alteration in the secretion of Gonadotropin-releasing Hormone (GnRH), this alteration generates the increased release at the pituitary level of LH compared to FSH.
  2. The disproportional increase between LH and FSH is 2: 1. The increased LH stimulates the secretion of Androgens (androstenedione) at the level of the ovary in the cells of the teak.
  3. The disproportionate reduction of FSH with respect to LH does not allow at the level of the ovary through aromatase the conversion of androgens (Androstenedione) to estrogens (Estradiol), this results in the increase of androgens.
  4. The increase of androgens generates: Follicular Atresia (Anovulation), alterations in lipid profiles, Hirsutism and acne
  5. Peripheral level androgens in the lipid tissue are converted into estrogen (Estrone), generating a feedback that maintains abnormal secretion in the hypothalamus and pituitary gland.
  6. Estrone maintains a stimulation of the endometrium which can cause endometrial hyperplasia.

Insulin resistance

The resistance to insulin is the decrease in the response of the uptake of glucose given by insulin. This resistance is associated with several disorders, such as: Diabetes Mellitus type 2, hypertension, dyslipidemia and cardiovascular disease.

What is sex hormone binding globulin (SHBG)?

It is a glycoprotein, produced by the liver, that allows the union of most sex steroids, causing only 1% of these steroids are free in blood and bioavailable. In women with Polycystic Ovarian Syndrome the synthesis of SHBG is diminished by the action of androgens, insulin, corticosteroids, progestins and growth hormone. Therefore, low levels of sex hormone binding globulin SHBG, does not allow its binding to steroids, making the latter, free in blood and biofunctional, manifesting in these women with clinical changes of hyperandrogen.

Keep in mind that blood will show normal testosterone levels, the difference is that this testosterone is free.

On the other hand, SHBG is related to the control of glucose through a mechanism that is not known until today, this lack of control that is generated in glucose by low levels of type 2 DM increases the risk that these patients also develop DM type 2


It is believed that the alteration in the release of GnRH that produces an altered release of gonadotropins has a direct relationship with the irregularity of menstruation, together with the increase in insulin resistance.

Signs and symptoms of Polycystic Ovarian Syndrome?

In order to identify the signs and symptoms in patients, the first thing to do is an excellent clinical history and physical examination of the patient identifying: Family history of PCOS in the mother and / or sisters, determine the date of last menstruation (FUM) ), observe physical signs of hyperandrogenism (signs of masculinization), obesity with androgenic redistribution, hirsutism, alopecia (loss of hair, baldness).

The main signs and symptoms of PCOS are:

Amenorrhea, oligomenorrhea, chronic anovulation.

These are the most frequent signs for which patients go to the doctor, it should be taken into account that 75% of the patients present a chronic anovulation, 85% -90% of the patients have oligomenorrhea and 30-40% of the patients have amenorrhea. Chronic anovulation manifests with oligomenorrhea and is defined as less than 9 menses per year.

How is polycystic ovarian syndrome diagnosed?

The diagnosis for polycystic ovarian syndrome today remains a controversy because three groups of criteria are still used: “The National Institutes of Health (NIH) conference in 1990”, “Rotterdam ESHRE / ASRM-PCOS Consortium Consensus Workshop Group, 2004 “and The Androgen Excess and PCOS Society (AE-PCOS) 2006”. These criteria have special characteristics that differentiate them from one another as follows:

The conference of the National Institutes of Health (NIH) in 1990

In these criteria they defined SOP without taking into account the appearance of ovarian ultrasound.

It should include: Oligoamenorrhea / Anovulation and polycystic ovaries

The Rotterdam Rotterdam ESHRE / ASRM-PCOS Consensus Workshop Group, 2004

To be able to make the diagnosis through these criteria, patients must meet two of three criteria, it must be an exclusion criterion because other pathologies such as congenital adrenal hyperplasia, androgen secreting tumors and hyperprolactinemia also lead to oligo-uvulation and / or androgen excess. This is an Exclusion Diagnosis.

It must include 2 of the following:

  • Clinical and / or biochemical hyperandrogenism
  • Oligomenorrhea / anovulation
  • Polycystic ovaries

The Androgen Excess y PCOS Society (AE-PCOS) 2006

It must include both:

  • Clinical and / or biochemical hyperandrogenism
  • Oligomenorrhea / anovulation and / or polycystic ovaries

Depending on the characteristics of the patients, different phenotypes can be differentiated as shown in the following table.

Fenotipos del Síndrome de Ovario Poliquistico
Table taken from the class of Dr. S. Moreno Ortega

Laboratories that must be requested

  • FSH.
  • LH
  • Prolactin
  • TSH
  • 17 OH progesterone.
  • Free and total testosterone
  • Progesterone luteal phase.

Complications or consequences of Polycystic Ovarian Syndrome

There are complications or consequences of PCOS in the short and long term.

Short-term consequences:

  • Obesity
  • Infertility
  • Depression
  • Sleep apnea
  • Irregular menstruation
  • High abnormal lipid profile
  • Non-alcoholic fatty liver disease
  • Hirsutism, acne, androgenic alopecia
  • Resistance to insulin and acanthosis nigricans

Long-term consequences

  • Mellitus diabetes
  • Endometrial cancer
  • Cardiovascular diseases

What is the treatment of PCOS?

The treatment for these women depends on which are the objectives they have and the severity of endocrine dysfunction.

Conservative treatment

Women who have regular cycle intervals such as (8 to 12 menstruations per year) may not be treated, but metabolic control must be taken because Diabetes Melitus and metabolic syndrome may be present.

Lifestyle changes

All women with PCOS who are obese are advised to lose weight, this weight loss can restore normal menstrual cycles. In addition to preventing other types of diseases that can be triggered in the long term such as diabetes mellitus type 2 and cardiovascular diseases.

  • Decrease glucose consumption
  • Exercise Aerobic Journal
  • Evaluate mood

Treatment for amenorrhea

For women who do not even want to have children, but as a method of prophylaxis for endometrial hyperplasia, is given as a first line treatment is the use of oral contraceptives (ACO), these induce menstrual cycles.


  • Increased hepatic production of SHBG
  • Modification / Suppression of LH production


  • Competitive inhibition of the androgen receptor
  • Decrease in ovarian steroid biosynthesis
  • Decrease in adrenal steroid biosynthesis
  • Increased hepatic metabolism of steroid hormones
  • Reduction in the peripheral activity of 5 alpha reductase.


Metformin therapy should be considered in overweight and obese women. This medication can improve menstrual cycles and the chances of pregnancy.


  • Cyproterone
  • Spironolactone, doses greater than 100mg / day. Effects similar to progestogens.
  • Flutamide
    • Non-steroidal antiandrogen
    • Hepatic toxicity.

Other agents

  • Finasteride
    • Competitive inhibitor of 5 alpha reductase
    • Cutaneous manifestations in the pilosebacea unit.


  • David A. Ehrmann, M.D. Polycystic Ovary Syndrome, N Engl J Med 2005;352:1223-36.
  • P.C.M. de Groot, O.M. Dekkers, J.A. Romijn, S.W.M. Dieben, and F.M. Helmerhorst. PCOS, coronary heart disease, stroke and the influence of obesity: a systematic review and meta-analysis. Human Reproduction Update, Vol.17, No.4 pp. 495–500, 2011.
  • Moran LJ1, Hutchison SK, Norman RJ, Teede HJ. Lifestyle changes in women with polycystic ovary syndrome. Cochrane Database Syst Rev. 2011 Feb 16
  • Conway G1, Dewailly D1, Diamanti-Kandarakis E1, Escobar-Morreale HF1, Franks S1, Gambineri A1, Kelestimur F1, Macut D1, Micic D1, Pasquali R2, Pfeifer M1, Pignatelli D1, Pugeat M1, Yildiz BO1; ESE PCOS Special Interest Group.The polycystic ovary syndrome: a position statement from the European Society of Endocrinology. Eur J Endocrinol. 2014 Oct;171(4):P1-29

Deja un comentario