**3. Polycystic ovary syndrome (PCOS)**

The most frequent hormonal disorder in reproductive age's women with oligo or anovulation and hyperandrogenemia is associated with PCOS in the majority of cases. Many factors such as psychological, social, and economic could play role in the disorder of the syndrome. Moreover, the association of PCOS with metabolic syndrome and its effects represent a new challenge of interest of the syndromes in the general population. The major symptoms are:


In PCOS, many symptoms included hirsutism, acne, alopecia, acanthosis nigricans, and obesity that are also linked to hyperinsulinemia [18–20]. One of seven teenagers (13%) has a major health problem because of obesity. Obesity is a major health problem affecting approximately 13% of teenagers. Normal body mass index (BMI) values range from 19 to 24.9 kg/m2 . Body mass index <19 kg/m2 characterizes underweight individuals. Body mass index ranging from 25 to 29.9 kg/m2 characterizes overweight people, 30–40 kg/m2 characterizes obese people, and >40 kg/m2 characterizes severely obese individuals. Menstrual cycle disorders are related to obesity in childhood and in young women. As the abdominal adipose tissue increases, increment of androgens aromatization is observed and subsequent endocrine abnormalities are appeared. Obesity is an independent factor aggravating PCOS endocrine abnormalities as subcutaneous abdominal tissue and liver contributes to extragonadal aromatization [21]. Obese women with PCOS have two types of insulin resistance, one related to the syndrome and the other related to obesity. The pancreas is involved in the mechanism of insulin resistance by increasing the release of insulin, which leads to stabilization of the glucose level in the early stage of the disease [21]. During pregnancy, the morbitity is increased with an increase in labor induction, urgent cesarean section, dystocia and abnormal presentation. The neonates are generally overweight and the risk for fetal death is increased. Moreover, diabetes during pregnancy is increased and needs follow-up. Recent data show an increased rate of overweight and obese women, specifically in the United States of the female population (64.1%) and obese women remain high (35.5%). In Europe, there is a diversity depending of the countries: low rate (6.2%) in Western and Northern Europe, high rate in Central, East and South Europe (36.5%). Oral contraceptives are the major treatment of PCOS decreasing all the clinical symptoms and the level of androgens. In obese adolescence, the oral contraceptive pills have a different pharmacokinetic profile with a decrease of the estrogens and progestogen clearance, but in contrary an increased SHBG was observed [22–26].

Contraceptive pills constitute the cornerstone of hormone therapy, as they promote reduction of hyperandrogenemia, hirsutism, and acne [27].

Therefore, there is a typical decreased effectiveness of contraceptive pills in obese adolescents, despite there are superior to the contraception with condoms.

#### **3.1. Therapeutical strategy**

The clinical examination always evaluates BMI, height, any hyperandrogenic, or galactorrhea signs. Laboratory investigations include estradiol, hCG, FSH as well as testosterone, and

Early diagnosis of genetic causes of hypogonadotropic hypogonadism occurs at <40%. The identification of new genes may improve the scientific knowledge in the function of hypotha-

In the case of hypogonadism, long-term hormone replacement therapy is recommended and

The most frequent hormonal disorder in reproductive age's women with oligo or anovulation and hyperandrogenemia is associated with PCOS in the majority of cases. Many factors such as psychological, social, and economic could play role in the disorder of the syndrome. Moreover, the association of PCOS with metabolic syndrome and its effects represent a new challenge of interest of the syndromes in the general population. The major symptoms are:

In PCOS, many symptoms included hirsutism, acne, alopecia, acanthosis nigricans, and obesity that are also linked to hyperinsulinemia [18–20]. One of seven teenagers (13%) has a major health problem because of obesity. Obesity is a major health problem affecting approximately 13% of teenagers. Normal body mass index (BMI) values range from 19 to 24.9 kg/m2

to obesity in childhood and in young women. As the abdominal adipose tissue increases, increment of androgens aromatization is observed and subsequent endocrine abnormalities are appeared. Obesity is an independent factor aggravating PCOS endocrine abnormalities as subcutaneous abdominal tissue and liver contributes to extragonadal aromatization [21]. Obese women with PCOS have two types of insulin resistance, one related to the syndrome and the other related to obesity. The pancreas is involved in the mechanism of insulin resistance by increasing the release of insulin, which leads to stabilization of the glucose level in the early stage of the disease [21]. During pregnancy, the morbitity is increased with an increase in labor induction, urgent cesarean section, dystocia and abnormal presentation. The neonates are generally overweight and the risk for fetal death is increased. Moreover, diabetes during pregnancy is increased and needs follow-up. Recent data show an increased rate of overweight and obese women, specifically in the United States of the female population (64.1%) and obese women remain high (35.5%). In Europe, there is a diversity depending of the countries: low rate (6.2%) in Western and Northern Europe, high rate in Central, East and South Europe (36.5%). Oral contraceptives are the major treatment of PCOS decreasing all the

characterizes overweight people, 30–40 kg/m2

characterizes underweight individuals. Body mass index ranging from

characterizes severely obese individuals. Menstrual cycle disorders are related

. Body

characterizes obese people,

17-OH progesterone levels.

190 Family Planning

lamic-pituitary-ovarian axis during puberty.

sometimes psychological support is also required.

**3. Polycystic ovary syndrome (PCOS)**

**a.** Hyperandrogenemia or hyperandrogenism

**c.** Polycystic appearance of the ovaries during sonography [18, 19].

**b.** Oligo or anovulation

mass index <19 kg/m2

25 to 29.9 kg/m2

and >40 kg/m2

Any other known disorders, that they are possible to cause hyperandrogenemia and oligo or amenorrhea have to be excluded. These are often associated with: nutrition, exercise, menstrual disorder treatment, metabolic syndrome and diabetes drug treatment and can be treated by contraceptive pills having progestagen with antiandrogenic action, as cyproterone acetate, dienogest, drospirenone [28, 29].

#### **3.2. Functional uterine bleeding in adolescence**

In adolescence, it is quite possible a disorder of negative regression of gonadotropins by gonadal steroids to be happened. The average age of menarche, based on recent data, has been reduced in developed as well as in developing countries over the last few decades and is attributed to various conditions, such as metabolic syndrome, eating disorders, gynecological cancer, and heart stroke diseases [30–33].

Dysfunctional bleeding is characterized by abnormal bleeding without functional impairment. It is caused by ovarian dysfunction in 10% of the cases in women of reproductive. The incidence is 10–17% among adolescents and is mainly dependent on the immaturity of the hypothalamic-pituitary-ovarian axis. They are not attributable to structural damage of the genital tract. In addition, they are observed during all the years of reproductive age.

It constitutes an exclusionary diagnosis at the onset of reproductive age and it is anovulatory almost in all cases (80–90%). The reason of the bleeding concludes the lack of cyclic secretion of progesterone resulting in continuous stimulation and endometrial hyperplasia of endogenous estradiol. Throughout of this progress the endometrium is overpowered, its perfusion capacities die resulting in necrosis, while in other places it continues to be repaired [34].

They are usually characterized as anovulatory cycles, even they can also be appeared in normal cycles as well as they are almost the half of the total metrorrhagia cases.

In some cases, asymptomatic structural abnormalities also coexist, such as polyps and subserous or intramural fibroids. They usually do not affect the whole of the endometrium and are often of high intensity without excluding the possibility of remaining drooping for several days. They are generally irregular with fluctuations in their intensity. It is quite often the first clinical manifestation of systemic hematological diseases especially in adolescents. The disorders are limited just to one of the three phases of the hemostatic procedure. In thrombocytopenia and von Willebrand's disease, there is insufficient platelet clot formation (1st phase of hemostasis) resulting in metrorrhagia [9]. Menorrhagia may occur in the rare case of VIII, XIII, and fibrinogen deficiency (2nd phase of hemostasis), mutation of the M.T.H.F.R. (C677T) gene (LAME). In these cases, there is a lack of primary platelet clot and fibrin production. Finally, fibrinolysis (3rd phase of hemostasis) in endometrium can be also observed, especially in cases of unexplained or intense menorrhagia [9].

surface of the endometrium. In contrast, in cases of interruption of the E2/P relationship, they are diffuse. The exact mechanism of tissue apoptosis in hyperestrogenic endometrium is unclear. The abnormal development of the endometrium includes additional qualitative and quantitative changes in microvascularization such as spiral arterial compression and venous growth, which are often stretched, thus forming abnormal venous networks. Of particular interest is the fact that the process of neovascularization is inadequate in or near the hemorrhage focal area while adjacent intact endometrium does not show an increase in microvascularization. The abnormal morphology of microvascularization accompanies or is the cause of endometrial hemostasis disorders. Because of the lack of the arachidonic acid precursor, prostaglandin production is inadequate. Prostaglandins cause more dilation than contraction, and angiotensin-2 production is reduced. All of the above leads to the conclusion that bleeding, in these cases, is caused by vascular density disorders accompanied by structural abnormalities leading to rupture or degradation of the microvascular system. This process is followed by the release of lysosomal proteolytic enzymes from the epithelial and stromal cells and from endometrial migrating leukocytes and macrophages, while granulocytes and activated NK cells secrete perforins. In addition, the ability of contraction of basal and myometrial vessels is inadequate or absent. All of the above changes contribute to the inadequate structure and layout and ultimately to the degradation of the capillary network and constitute the major agents of extensive hemorrhage. Based on the above, the best therapeutic results are obtained when the bleeding hypertrophic-hyperplastic endometrium is excluded by performing suction biopsy or scraping. In these cases, an extensive stripping of the base layer is created followed by vasoconstriction of the arteries and arterioles as well as by tissue reconstruction. Functional hemorrhage due to progesteronism manifests as escape bleeding in women taking progestogens or using contraceptive tablets. The intensity, duration, and other features of these cases' bleeding depend on: type, dose and duration of progestogen administration, the estrogen-progestogen relationship, endogenous estradiol levels and the particular endometrial response to hormonal administration [7, 9]. Endometrial histology in these cases is predominantly influenced by progesterone and ranges between atrophy with or without cortical conversion of the layer and mixed appearance of productive and secretory elements. The greater the dose and the duration of administration, the more pronounced is the secretory type atrophy with a pronounced pro-stratum gland-layer relationship. In this case there is a corrugated endometrial layer especially in the initial periods of use containing migratory lymphocytes and macrophages as well as granular endometrial cells. All of the above lesions are associated with abnormalities of endometrial angiogenesis. These changes are accompanied by structural lesions and vasodilation leading to bleeding during the first months of use. The increased concentration of migratory leukocytes and other cells associated with immunity and the imbalance between metalloproteinases (proteolytic MMP enzymes that cause an intrauterine extracellular matrix) and their inhibitors against them, cause even greater vasodilation [7, 9]. In conclusion, the development of an abnormal and fragile network of microvascular surfaces in combination with the release of proteolytic enzymes and poor vasoconstriction due to reduced production of vasoconstrictors as a result of increased degradation by endopeptidase is the key factor in the manifestation of the above functional bleeding. Fortunately, the continuation of contraceptives decreases the frequency with the end result being usually observed only during the

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first 6–12 months of use.
