Introduction

Polycystic ovary syndrome (PCOS) is the most common

endocrine disturbances of reproductive age females and
the most common cause of infertility, it’s a collection of
specific signs and symptoms rather than a well-defined
disorder (the Boston iv handbook of infertility ) .
Polycystic ovary syndrome is accompanied by a lot of
conditions as well as economic burden [The effects of
probiotic and selenium co-supplementation on parameters
of mental health, hormonal profiles, and biomarkers of
inflammation and oxidative stress in women with polycystic
ovary syndrome]
The term polycystic ovaries describes ovaries that contain
many small cysts (about twice as many as in normal
ovaries), usually no bigger than 8 millimeters each, located
just below the surface of the ovaries, these cysts are egg-
containing follicles that have not developed properly due to
a number of hormonal abnormalities(Polycystic ovaries
and Polycystic Ovary Syndrome) .
It involves defects in the hypothalamic‐pituitary axis
(Figure 1) . Increased ovarian androgen biosynthesis in
the polycystic ovary syndrome results from abnormalities
at all levels of the hypothalamic–pituitary–ovarian axis. The
increased frequency of luteinizing hormone (LH) pulses in
the polycystic ovary syndrome appears to result from an
increased frequency of hypothalamic gonadotropin-
releasing hormone (GnRH) pulses. The latter can result
from an intrinsic abnormality in the hypothalamic GnRH
pulse generator, favoring the production of luteinizing
hormone over follicle-stimulating hormone (FSH) in
patients with the polycystic ovary syndrome, in whom the
administration of progesterone can restrain the rapid pulse
frequency. By whatever mechanism, the relative increase
in pituitary secretion of luteinizing hormone leads to an
increase in androgen production by ovarian theca cells.
Increased efficiency in the conversion of androgenic
precursors in theca cells leads to enhanced production of
androstenedione, which is then converted by 17b-
hydroxysteroid dehydrogenase (17b) to form testosterone
or aromatized by the aromatase enzyme to form estrone.
Within the granulosa cell, estrone is then converted into
estradiol by 17b. Numerous autocrine, paracrine, and
endocrine factors modulate the effects of both luteinizing
hormone and insulin on the androgen production of theca
cells; insulin acts synergistically with luteinizing hormone
to enhance androgen production. Insulin also inhibits
hepatic synthesis of sex hormone–binding globulin, the key
circulating protein that binds to testosterone and thus
increases the proportion of testosterone that circulates in
the unbound, biologically available, or “free,” state.
Testosterone inhibits and estrogen stimulates hepatic
synthesis of sex hormone–binding globulin. The
abbreviation scc denotes side-chain cleavage enzyme,
StAR steroidogenic acute regulatory protein, and 3b-HSD
3b-hydroxysteroid dehydrogenase. Solid arrows denote a
higher degree of stimulation than dashed arrows.

Figure 1. The Hypothalamic–Pituitary–Ovarian Axis and the Role of Insulin.

Females with PCOS present with signs of amenorrhea or

oligomenorrhea and polycystic ovaries (2, 3). They are
potentially at elevated risk of multiple diseases and
disorders, including infertility (4), insulin resistance (5),
obesity (6), premature carotid arteriosclerosis (7), type 2
diabetes mellitus (8), and mood disorders,(Variant Alleles
of the ESR1, PPARG, HMGA2, and MTHFR Genes Are
Associated With Polycystic Ovary Syndrome Risk in a
Chinese Population: A Case-Control Study) chronic
inovulation, hyperandrogenism (pcos syndrom subblaxami
) * which is a hormone made in males but women produce
androgen too because women need to produce androgen
hormone since there is only one enzyme step from
separating androgen from production of estrogen
hormones* (obggyn.net)
The condition was first described in 1935 by American
gynecologists Irving F. Stein, Sr. and Michael L.
Leventhal ,( from whom its original name of Stein–
Leventhal syndrome is taken. [52][53](wikipedia ) ) as the
prescense of bilaterally enlarged ovaries with multiple
cysts in 7 women with infertility menstrual irregularly and
hyper androgen (pcos fahimeh )
In 1990 national institute of health introduced National
Institutes of Health Criteria (NIH) in PCOS which is clinical
or biochemical evidence of hyperandrogenemia (in the
absence of adrenal hyperplasia , hyperprolactinemia and
thyroid dysfunction ) in combination of oligomenorrhea or
amenorrhea ((pcos fahimeh )
In 2003 Diagnostic criteria for Rotterdam includes Two of
the following three criteria are required:
 oligo/anovulation
 hyperandrogenism :
-clinical (hirsutism or less commonly male pattern
alopecia)
or
-biochemical (raised FAI or free testosterone)
 polycystic ovaries on ultrasound ( Figure 1 )

Figure 1. Ultrasonography
The criteria for a diagnosis of polycystic ovaries based on ultrasonographic
data include bilateral ovarian enlargement ( 9 cm in maximal diameter), 10 or more follicles 2 to 10 mm in diameter
per ovary, and increased density and area of stroma.
(MEDICAL PROGRESS REVIEW ARTICLE POLYCYSTIC OVARY SYNDROME S TEPHEN F RANKS ,
M.D.)
Other etiologies must be excluded such as congenital
adrenal hyperplasia, androgen secreting (Reproductive
health Polycystic ovary syndrome An update Volume 41,
No.10, October 2012
(http://www.racgp.org.au/afp/2012/october/) Pages 752-
756 Jacqueline Boyle Helena J Teede)
In 2009 the androgen excess and PCOS society
introduced criteria for PCOS based on them should be
defined by the presence of hyper androgen (clinical and or
biochemical ) ovarian dysfunction (ovulation disturbance
and or PCOS morphology ) and the exclusion of other
androgen excess or related disorders ( ((pcos fahimeh )
Table 1 shows summary of these diagnostic criteria

Table 1.Diagnostic Criteria for polycystic ovary syndrome

National Institutes of
Health criteria (1990)
• Must meet both criteria
Clinical and/or biochemical
evidence of
hyperandrogenism
Menstrual dysfunction
Exclusion of other known
disorders is required as
well.
European Society for
Human
Reproduction and
Embryology
and American Society for
Reproductive Medicine
Rotterdam
criteria (2003)
• Must meet two of three
criteria
Clinical and/or biochemical
evidence of
hyperandrogenism
Oligoovulation or
anovulation
Polycystic ovaries
Exclusion of other known
disorders
is required as well.
Androgen Excess Society
criteria (2006)
• Must meet both criteria
Clinical and/or biochemical
evidence of
hyperandrogenism
Clinical and/or biochemical
evidence of
hyperandrogenism
Exclusion of other known
disorders is required as
well.

Jon Havelock, MD, FRCSC

(Polycystic ovary syndrome)

treatment of polycystic ovary focuses on managing your
individual concerns, such as infertility, hirsutism, acne or
obesity. Specific treatment might involve lifestyle changes
or medication. Your doctor may recommend weight loss
through a low-calorie diet combined with moderate
exercise activities. Even a modest reduction in your weight
— for example, losing 5 percent of your body weight —
might improve your condition. Losing weight may also
increase the effectiveness of medications your doctor
recommends for PCOS, and can help with infertility.

Table 1 shows the drugs used in PCOS , indications ,

dosages and the adverse effects of each drugs
Methods:
This is an analytic study / observational cross sectional
performed on 180 females from Baghdad medical city
2015-2017 with age range 15-30 .
PCOS was diagnosed according to the revised Rotterdam
2003 criteria [5]. Accordingly two of the three following
criteria should be present: 1- oligo- or anovulation, 2-
clinical and/ or biochemical signs of hyperandrogenism
and 3- polycystic ovaries on ultrasound scan[5].

(Taiwanese Journal of Obstetrics & Gynecology)

The participants with hyperprolactinemia, thyroid
disorders, congenital adrenal hyperplasia, Cushing
disease, steroids , confirmed malignancy, heart failure and
renal failure were excluded (Table 1) .
(The new england journal of medicine 1223 review article medical progress)

The body mass index (BMI) or Quetelet index is a value

derived from the mass (weight) and height of an individual.
The BMI is defined as the body mass divided by
the square of the body height, and is universally expressed
in units of kg/m2, resulting from mass in kilograms and
height in metres.
It is an attempt to quantify the amount of tissue mass
(muscle, fat, and bone) in an individual, and then
categorize that person as underweight, normal
weight, overweight, or obese based on that value.
Commonly accepted BMI ranges are underweight: under
18.5 kg/m2, normal weight: 18.5 to 25, overweight: 25 to
30, obese: over 30.

Ethical approval :
Verbal informed consent were obtained from all participant
and the study was approved by Baghdad university college
of medicine.

Statistical analysis :
Data were analyzed by statistical package for social
sciences for windows software (SPSS Version
24).Differences between groups were analyzed by one-
way ANOVA . All P-values less than 0.05 were statistically
significant.
Result :
Our study was conducted on 180 women from 15-30 years
old all of the participants were classified to BMI >25 or BMI
25 diagnosed with PCOS according to Rotterdam criteria
and statistical analysis was performed.

Discussion :
Acknowledgements :
We are grateful to Baghdad medical city for technical
support and sample collection we especially thank all
women participated in this study
References: