“Is PCOS serious in kids?”
My daughter is only 15 years old and she was diagnosed with PCOS. I never knew that this was a disorder that kids can have, and thought it was mainly adults. Will this cause any serious complications?
5 Answers
Yes, multiple ovary cysts, infértil, obesity.
Yes, it is important to take care of the PCOS. The patient will need an OBG and endocrine doctor to treat, along with the PCP.
Yes, worse case scenario may cause infertility
Poly Cystic Ovarian Syndrome (PCOS) is a common disorder in women of child bearing age. About 7% of women in their reproductive age have PCOS (over 5 million American women). In adolescent girls prevalence of PCOS is unknown but it may be about 3% or more. So PCOS is common in adolescent girls.
Women with PCOS (irregular menses and hperandrognism (high male hormones)) are at a higher risk for insulin resistance, metabolic syndrome, cardiovascular disease, type II diabetes, obesity, endometrial cancer, infertility, social and psychological disorders. PCOS impacts their quality of life significantly.
There are more than three guideline to diagnose PCOS in adults.
1) National institute of health criteria: based on 2 criteria menstrual irregularity and hyperandrogenism
2 )PCOS society: Is based on any 2 of the following:
a) hyperandrogenism b) Irregular menses c) poly cystic Ovaries on ultrasound
3) Rotterdam criteria: Based on two out of three:
a) hyperandrogenism b) Irregular menses c) poly cystic Ovaries on ultrasound
The most commonly used criteria for diagnosing PCOS is the Rotterdam criteria.
Hyperandrogenism is defined as the physical manifestation of excess androgens ( mainly high testosterone and androstendione) such as hirsutism, acne androgenic alopecia (male type hair loss), and Acanthosis Nigricans (skin darkening due to insulin resistance).
Menstrual Irregularity is defined as Amenorrhea (no period for three or more months in a row) or Oligomenorrhea ( les than 8 periods a year) in the face of high levels of luteinizing hormone (LH).
Poly Cystic Ovaries are defined as presence of greater than 12 follicles in each ovaries at least each 2-9 mm in size giving rise to an ovarian volume greater than 10 ml as measured by ultrasound.
There are at least 4 phenotypes of PCOS in the Rotterdam criteria;
1) classic PCOS: is composed of chronic anovulation (menstrual irregularity), hyperandrogenism, and polycystic ovaries
2) Classic PCOS with chronic anovulation, hyperandrogenism, but no ovarian cysts.
3) Non-classic PCOS composed of, hyperandrogenism, polycystic ovaries but regular menstrual cycles.
4) Non-classic mild PCOS consists of chronic anovulation, polycystic ovaries), but normal androgens,
PCOS has therefore a wide spectrum of manifestation having a combination of two to having all of the conditions. Women who have the classic PCOS have worse metabolic and cardiovascular risk, such as, abnormal lipid levels, insulin resistance, metabolic syndrome, type 2 diabetes, hirsutism and androgenic and alopecia.
In adolescent girls with PCOS the criteria is not well defined. In routine practice, the adult criteria's are used for adolescents ( the Rotterdam criteria). However, the adult PCOS criteria have challenges in diagnosing adolescents girls. In many adolescents menstrual irregularity is common in the first 2 years after menarche ( physiologic menstrual irregularity or physiologic Anovulation). Many adolescents also have acne though they typically do not have excess androgens. A significant portion of normal adolescent girls have ovarian cysts similar to women with PCOS. Normal testosterone reference range are not well defined in adolescent girls.
Experts recognize that there is a dilemma in distinguishing physiological anovulation’ from true ovulatory dysfunction in adolescents but they noted that most adolescent menstrual cycles are with in certain range and recommend the follow definitions to be used in evaluating adolescent girls for ovulatory dysfunction.
I) Amenorrhea more than 3 consecutive months even in the first year after menarche.
2) Menstrual cycle less than 21 days or greater than 45 days, 2 years after menarche.
3) Lack of menses by 15 years of age or 2–3 years after breast development.
PCOS in adolescents can therefore be defined as:
1) irregular menses as defined above.
2) Persistently elevated testosterone and/or free testosterone and manifestations of hyperandrogenism such as moderate to severe hirsutism and persistent acne unresponsive to topical therapy.
Polycystic Ovaries were deferred for evaluation of adolescent PCOS until high quality data is available.
Also the expert panel included that:
1) Treatment of PCOS can be initiated in order to treat the symptoms and minimize the comorbidities of PCOS with out the establishing the diagnosis of PCOS.
2) The diagnosis of PCOS can be deferred, while symptomatic treatment and follow-up of the symptoms is an alternative option;
3) Obesity, hyperinsulinemia, and insulin resistance are common in adolescents with PCOS, but these features should not be used for diagnostic purposes;
4) PCOS is a diagnosis of exclusion. Other causes of abnormal period (menses) and hyperandrogenemia should be ruled out before establishing the diagnosis of PCOS.
The hallmark of PCOS both in adults and adolescents is anovulation and hyperandrogenism/hyperandrogenemia. These features stem from progesterone deficiency due to the absence of ovulation. During and after ovulation the corpus luteum produces a lot of progesterone that stabilizes the endometrial lining. When there is no implantation (fertilization) the corpus luteum dies and the progesterone production stops and the progesterone withdrawal causes uterine bleeding.
Menstrual cycle is controlled by the hypothalamus pituitary ovarian axis. The hypothalamus is the pulse generator and produces a generator called GnRH (gonadotropin releasing hormone). The GnRH stimulates pituitary hormones called LH/FSH (luteinizing and follicular stimulating hormone). These hormones stimulate some ovarian follicles to mature and produce hormones. The FSH recruits one of the follicular cells to mature into a graafian follicle for ovulation.
The LH stimulates the theca cells to make androgens which are converted by the granulose cells into estrogen. Estrogen stimulates the growth of endometrial lining and progesterone stabilizes the endometrial lining.
There are two phases in the menstrual cycle. They both take place in the ovaries and the uterus. In the ovaries they are called follicular and luteal phase while in the uterus they are mainly termed proliferative and secretory phase. The first menstrual bleeding is the beginning of the follicular phase. The proliferative (follicular) phase is driven by FSH in the ovaries and estrogen in the uterus. While the luteal phase is driven by LH in the ovaries and Progesterone in the uterus. The follicular (proliferative) phase is the most variable in duration it can last between 7 to 21 days (average 14 days). It is dominated by estrogen production and endometrial proliferation of up to 10 millimeter thickness of the endometrial layer called functionalis layer. While the luteal (secretory) phase is constant and lasts exactly 14 days. women with higher FSH will have shorter follicular phase and women with low FSH will have longer follicular phase. The variation in the length of follicular or proliferative phase in women is determined by the amount of FSH available. This variability is not only among women but also in the same women at different times of her life, she will have fluctuation in the level of FSH. When levels of FSH fluctuate in the same woman she will have shorter or longer duration of her cycle.
The luteal phase is driven by the corpus luteum after ovulation and produces a lot of progesterone up to 40 mg per day to support the endometrial lining. During the luteal phase an LH surge takes place that heralds ovulatory event within 2 days of the surge. Once the egg ovulates it is picked up by fimbria and travels to the uterus via the fallopian tube for implantation. The remaining tissue becomes corpus luteum and is the main source of progesterone. A woman is fertile when the egg is ready for implantation. A woman is most fertile bout 6 days after ovulation during days 20-24 days of the menstrual cycle. The uterine environment is conducive for implantation during these days though fertilization is possible any time after ovulation until day 24 of the menstrual cycle.
In the absence of implantation the corpus luteum only lives up 10 days and start to die around day 24 of the menstrual cycle. It takes 4 days for the corpus luteum to involute completely.
Once the corpus luteum is dead Progesterone production ceases. The withdrawal of progesterone from stabilizing the endometrium causes constrictions of arterial blood supply of the endometrial lining. The endometrial lining ( the functionalis layer becomes necrotic and releases prostaglandins and other inflammatory agents to expedite the sloughing of the >10 millimeter functionalis layer. This also causes contractions of the uterine muscles to expel the sloughed endometrial tissue. This is also the cause of menstrual cramps.
The average woman will bleed for 2-6 days ( average 4 days plus or minus 2 days). The average blood flow is a bout 50 ml per menses. About 5 tampon.
High adsorbent tampon will hold about 10ml. Less than 20 ml or greater than 80 ml per period is abnormal.
In PCOS the GnRH pulse generator is abnormal. The frequency is more rapid the usual. LH release is more dominant than FSH. The LH to FSH ratio is >2 in over 60% of women. Since LH is in excess, the theca cells make a lot of androgens and the granulosa cell convert some of it to estrogen. There are plenty of androgens and estrogen in PCOS women. The excess androgens mainly testosterone and it free form free testosterone and Androstendione cause, acne, hirsutism male type baldness, voice change etcetera. While the estrogen increases endometrial lining. Some of the androgens and estrogens are also converter to estrone that causes endometrial hyperplasia and endometrial cancer. Women with PCOS also have low sex hormone biding globulin (SHBG). SHBG binds to androgens and lower their androgenic effect. When SHBG is low, even if androgens are normal the free hormone will be in excess to cause the skin manifestations oh hyperandrgenemia.
In PCOS Ovarian follicles develop but do not mature to ovulate but plenty of the follicles will be recruited and get suspended but do not ovulate. They become cysts and produce a lot of androgens and estrogen but not progesterone. Since these follicles do not ovulate to become corpus luteum there is progesterone deficiency. In the absence of Progesterone withdrawal there will not be a menstrual bleeding.
In PCOS Most women will have amenorrhea or Oligomenoria. They are producing excess androgens (also Estrogen). Excess androgens will also lead to excess weight gain and insulin resistance. More weight gain will lead to more insulin resistance. Excess insulin will lead to more stimulation of the ovaries to make more androgens making the condition worse.
Obesity also leads to more estrone formation leading to more endometrial hyperplasia or neoplasia.
Insulin resistance leads to prediabetes, type 2 diabetes, dyslipidemia, fatty liver, metabolic syndrome and cardiovascular disease. Insulin resistance also leads to Leptin resistance ( a hormone to controls appetite). During leptin resistance there is a persistent hunger that causes more food consumption and more weight gain.
In PCOS a hormone called Adiponectin is low. This hormone helps us burn fat and carbohydrates, But when this hormone is low we store more fat and gain more weight.
The treatment of PCOS is targeted in lowering the androgen levels and improving of the symptoms.
The corner stone of the treatment is the use of low androgenic Combined oral contraceptive. The Progestin component should be low androgenic. It is mainly done in two steps:
1) The endometrial layer should be cleaned with progesterone. Since they are not producing progesterone they do not go through the progesterone withdrawal to slough off the endometrial lining of the functionalis layer ( the basalis layer which is usually 2 mm usually stays). Due to lack of corpus luteum i.e. lack of progesterone the endometrial layer is thicker than usual and, it needs to be cleaned. Progesterone is used initially to cleaned it.
A) Provera 10 mg daily for 10 days or 10 mg twice a day for 5 days.
B) Micronized Progesterone 200 mg daily for 10 days
Once good sloughing takes place then Combined Oral Contraceptives (COC) should be used.
2) Combined Oral Contraceptives:
Drespirenone/ethinylEstradiol; yasmin/angeliq
Norgestimate/EthinylEstradiol: Orthotricyclen
Dosegestrel/EthinylEstradiol: Mircette/Cerazette
3) Cyclic Progestins: If the combined oral contraceptives are not optional cyclic predestines can be used for 10 days of each month. They will protect endometrial hyperplasia but will not suppress the ovarian hyperandrogenism (hirsulism, acne, balding etc.)
Hirsutism can be managed with medications if the Combined Oral contraceptives (COC)are not improving the symptoms. The following medications can be added:
1) Eflorenthin hydrochloride 13.9%.(topical) It kills androgenic hair 60-80%
2) Spironolactone 25 mg 100mg twice a day. It is androgen blocked. Should be used with COC since it is erotogenic.
3) Laser therapy
Acne can be managed as follows:
1) Topical benzoyl peroxide 5% gel
2) clindamycin 1% or erythromycin gel topical
3) retinoid oral isotretinion.
4) Minocycline 5-100 mg doxycycline oral daily.
GnRH agonists such as leuprolide ( Lupron) can be used to suppress GnRH. This can lowered androgens by suppressing ovarian function. Intermittent leuprolide acetate can also be give to initiate ovulation.
Insulin resistance can be managed with metformin. Some women can resume regular ovulatory menses by taking metformin. Metformin and pioglitazones (actos) may increase insulin sensitivity that may help the ovaries produce less androgens.
If there is dyslipidemia statins and fibrates should be used liberally in PCOS patients. There is an increased risk of cardiovascular disease in PCOS patients. Metabolic syndrome is also common in these patients.
There are many comorbidities with PCOS:
Nutritional and psychological interventions with life style modification are very important component of the management of PCOS. Weight loss and regular daily structured physical activity should be encouraged consistently.
Comorbidities of PCOS should be addressed.
1) Dyslipidemias; About 70% Women with PCOS have abnormal lipid profile.
2) Cardiovascular disease is more common with women with PCOS
3) Endometrial neoplasia
4) Obstructive sleep apnea; Even normal weight women with PCOS have 40% risk of developing sleep apnea.
5) Infertility. This is very common in women with PCOs
6) Early miscourage is 3 times more in PCOS
7) Gestational Hypertension and Gestational diabetes is 3 times common in PCOS
8) Preterm labor is also 3 fold more in PCOS
9) Perinatal mortality is very common.
10) Obesity; 80% of women with PCOS have obesity or are overweight.
11) type 2 diabetes or prediabetes: Over 50% of women with PCOS will develop diabetes or prediabetes by the age of 40 years.
12) Metabolic syndrome. PCOS can lead to metabolic syndrome.
13) Insulin resistance: insulin resistance is common in women with PCOS.
14) Hypertension; HTN is common in women with PCOS.
Since PCOS is a diagnoses by exclusion. The following diagnosis should be excluded:
1) hypothyroid or hyperthyroid.
2) Cushing disease and other adrenal anomalies
3) Pituitary abnormalities; pituitary tumors, hyperprolactinemia or hypo gonadotropic hypogonadism.
4) Ovarian failure.
5) Late onset Congenital adrenal hyperplasia.
6) Ovarian or Adrenal androgen producing tumors.
Going Back to your Daughter: Your daughter have PCOS. This condition is very common in women of childbearing age (mostly 15-45years). About 3% to as high as 20% adolescent girls may have PCOS. Most of these conditions may have their roots in childhood, but the symptoms and comorbidities start to show up in adult hood. PCOS in adolescents should be managed properly. The symptoms of PCOS should be treated regardless of the diagnosis of PCOS. Weight management should be a priority. Maintaining a reasonable weight will help in the management of PCOS. A healthy balanced diet and daily structured physical activity is very important to lessen the symptoms of PCOS. Untreated PCOS will have various comorbidities. They include: obesity, insulin resistance, dyslipidemias, fatty liver disease, cardiovascular disease, endometrial neoplasia, prediabetes, diabetes, gestational diabetes, hypertension, metabolic syndrome, sleep apnea. infertility, miscourage etc. Theses are serious issues to consider. Therefore PCOS needs to be managed early and should be taken seriously to avoid the above serious complications. You should work with your daughter's doctor closely, and let her get proper treatment. With early intervention the out come will be much better.
Good Luck
Women with PCOS (irregular menses and hperandrognism (high male hormones)) are at a higher risk for insulin resistance, metabolic syndrome, cardiovascular disease, type II diabetes, obesity, endometrial cancer, infertility, social and psychological disorders. PCOS impacts their quality of life significantly.
There are more than three guideline to diagnose PCOS in adults.
1) National institute of health criteria: based on 2 criteria menstrual irregularity and hyperandrogenism
2 )PCOS society: Is based on any 2 of the following:
a) hyperandrogenism b) Irregular menses c) poly cystic Ovaries on ultrasound
3) Rotterdam criteria: Based on two out of three:
a) hyperandrogenism b) Irregular menses c) poly cystic Ovaries on ultrasound
The most commonly used criteria for diagnosing PCOS is the Rotterdam criteria.
Hyperandrogenism is defined as the physical manifestation of excess androgens ( mainly high testosterone and androstendione) such as hirsutism, acne androgenic alopecia (male type hair loss), and Acanthosis Nigricans (skin darkening due to insulin resistance).
Menstrual Irregularity is defined as Amenorrhea (no period for three or more months in a row) or Oligomenorrhea ( les than 8 periods a year) in the face of high levels of luteinizing hormone (LH).
Poly Cystic Ovaries are defined as presence of greater than 12 follicles in each ovaries at least each 2-9 mm in size giving rise to an ovarian volume greater than 10 ml as measured by ultrasound.
There are at least 4 phenotypes of PCOS in the Rotterdam criteria;
1) classic PCOS: is composed of chronic anovulation (menstrual irregularity), hyperandrogenism, and polycystic ovaries
2) Classic PCOS with chronic anovulation, hyperandrogenism, but no ovarian cysts.
3) Non-classic PCOS composed of, hyperandrogenism, polycystic ovaries but regular menstrual cycles.
4) Non-classic mild PCOS consists of chronic anovulation, polycystic ovaries), but normal androgens,
PCOS has therefore a wide spectrum of manifestation having a combination of two to having all of the conditions. Women who have the classic PCOS have worse metabolic and cardiovascular risk, such as, abnormal lipid levels, insulin resistance, metabolic syndrome, type 2 diabetes, hirsutism and androgenic and alopecia.
In adolescent girls with PCOS the criteria is not well defined. In routine practice, the adult criteria's are used for adolescents ( the Rotterdam criteria). However, the adult PCOS criteria have challenges in diagnosing adolescents girls. In many adolescents menstrual irregularity is common in the first 2 years after menarche ( physiologic menstrual irregularity or physiologic Anovulation). Many adolescents also have acne though they typically do not have excess androgens. A significant portion of normal adolescent girls have ovarian cysts similar to women with PCOS. Normal testosterone reference range are not well defined in adolescent girls.
Experts recognize that there is a dilemma in distinguishing physiological anovulation’ from true ovulatory dysfunction in adolescents but they noted that most adolescent menstrual cycles are with in certain range and recommend the follow definitions to be used in evaluating adolescent girls for ovulatory dysfunction.
I) Amenorrhea more than 3 consecutive months even in the first year after menarche.
2) Menstrual cycle less than 21 days or greater than 45 days, 2 years after menarche.
3) Lack of menses by 15 years of age or 2–3 years after breast development.
PCOS in adolescents can therefore be defined as:
1) irregular menses as defined above.
2) Persistently elevated testosterone and/or free testosterone and manifestations of hyperandrogenism such as moderate to severe hirsutism and persistent acne unresponsive to topical therapy.
Polycystic Ovaries were deferred for evaluation of adolescent PCOS until high quality data is available.
Also the expert panel included that:
1) Treatment of PCOS can be initiated in order to treat the symptoms and minimize the comorbidities of PCOS with out the establishing the diagnosis of PCOS.
2) The diagnosis of PCOS can be deferred, while symptomatic treatment and follow-up of the symptoms is an alternative option;
3) Obesity, hyperinsulinemia, and insulin resistance are common in adolescents with PCOS, but these features should not be used for diagnostic purposes;
4) PCOS is a diagnosis of exclusion. Other causes of abnormal period (menses) and hyperandrogenemia should be ruled out before establishing the diagnosis of PCOS.
The hallmark of PCOS both in adults and adolescents is anovulation and hyperandrogenism/hyperandrogenemia. These features stem from progesterone deficiency due to the absence of ovulation. During and after ovulation the corpus luteum produces a lot of progesterone that stabilizes the endometrial lining. When there is no implantation (fertilization) the corpus luteum dies and the progesterone production stops and the progesterone withdrawal causes uterine bleeding.
Menstrual cycle is controlled by the hypothalamus pituitary ovarian axis. The hypothalamus is the pulse generator and produces a generator called GnRH (gonadotropin releasing hormone). The GnRH stimulates pituitary hormones called LH/FSH (luteinizing and follicular stimulating hormone). These hormones stimulate some ovarian follicles to mature and produce hormones. The FSH recruits one of the follicular cells to mature into a graafian follicle for ovulation.
The LH stimulates the theca cells to make androgens which are converted by the granulose cells into estrogen. Estrogen stimulates the growth of endometrial lining and progesterone stabilizes the endometrial lining.
There are two phases in the menstrual cycle. They both take place in the ovaries and the uterus. In the ovaries they are called follicular and luteal phase while in the uterus they are mainly termed proliferative and secretory phase. The first menstrual bleeding is the beginning of the follicular phase. The proliferative (follicular) phase is driven by FSH in the ovaries and estrogen in the uterus. While the luteal phase is driven by LH in the ovaries and Progesterone in the uterus. The follicular (proliferative) phase is the most variable in duration it can last between 7 to 21 days (average 14 days). It is dominated by estrogen production and endometrial proliferation of up to 10 millimeter thickness of the endometrial layer called functionalis layer. While the luteal (secretory) phase is constant and lasts exactly 14 days. women with higher FSH will have shorter follicular phase and women with low FSH will have longer follicular phase. The variation in the length of follicular or proliferative phase in women is determined by the amount of FSH available. This variability is not only among women but also in the same women at different times of her life, she will have fluctuation in the level of FSH. When levels of FSH fluctuate in the same woman she will have shorter or longer duration of her cycle.
The luteal phase is driven by the corpus luteum after ovulation and produces a lot of progesterone up to 40 mg per day to support the endometrial lining. During the luteal phase an LH surge takes place that heralds ovulatory event within 2 days of the surge. Once the egg ovulates it is picked up by fimbria and travels to the uterus via the fallopian tube for implantation. The remaining tissue becomes corpus luteum and is the main source of progesterone. A woman is fertile when the egg is ready for implantation. A woman is most fertile bout 6 days after ovulation during days 20-24 days of the menstrual cycle. The uterine environment is conducive for implantation during these days though fertilization is possible any time after ovulation until day 24 of the menstrual cycle.
In the absence of implantation the corpus luteum only lives up 10 days and start to die around day 24 of the menstrual cycle. It takes 4 days for the corpus luteum to involute completely.
Once the corpus luteum is dead Progesterone production ceases. The withdrawal of progesterone from stabilizing the endometrium causes constrictions of arterial blood supply of the endometrial lining. The endometrial lining ( the functionalis layer becomes necrotic and releases prostaglandins and other inflammatory agents to expedite the sloughing of the >10 millimeter functionalis layer. This also causes contractions of the uterine muscles to expel the sloughed endometrial tissue. This is also the cause of menstrual cramps.
The average woman will bleed for 2-6 days ( average 4 days plus or minus 2 days). The average blood flow is a bout 50 ml per menses. About 5 tampon.
High adsorbent tampon will hold about 10ml. Less than 20 ml or greater than 80 ml per period is abnormal.
In PCOS the GnRH pulse generator is abnormal. The frequency is more rapid the usual. LH release is more dominant than FSH. The LH to FSH ratio is >2 in over 60% of women. Since LH is in excess, the theca cells make a lot of androgens and the granulosa cell convert some of it to estrogen. There are plenty of androgens and estrogen in PCOS women. The excess androgens mainly testosterone and it free form free testosterone and Androstendione cause, acne, hirsutism male type baldness, voice change etcetera. While the estrogen increases endometrial lining. Some of the androgens and estrogens are also converter to estrone that causes endometrial hyperplasia and endometrial cancer. Women with PCOS also have low sex hormone biding globulin (SHBG). SHBG binds to androgens and lower their androgenic effect. When SHBG is low, even if androgens are normal the free hormone will be in excess to cause the skin manifestations oh hyperandrgenemia.
In PCOS Ovarian follicles develop but do not mature to ovulate but plenty of the follicles will be recruited and get suspended but do not ovulate. They become cysts and produce a lot of androgens and estrogen but not progesterone. Since these follicles do not ovulate to become corpus luteum there is progesterone deficiency. In the absence of Progesterone withdrawal there will not be a menstrual bleeding.
In PCOS Most women will have amenorrhea or Oligomenoria. They are producing excess androgens (also Estrogen). Excess androgens will also lead to excess weight gain and insulin resistance. More weight gain will lead to more insulin resistance. Excess insulin will lead to more stimulation of the ovaries to make more androgens making the condition worse.
Obesity also leads to more estrone formation leading to more endometrial hyperplasia or neoplasia.
Insulin resistance leads to prediabetes, type 2 diabetes, dyslipidemia, fatty liver, metabolic syndrome and cardiovascular disease. Insulin resistance also leads to Leptin resistance ( a hormone to controls appetite). During leptin resistance there is a persistent hunger that causes more food consumption and more weight gain.
In PCOS a hormone called Adiponectin is low. This hormone helps us burn fat and carbohydrates, But when this hormone is low we store more fat and gain more weight.
The treatment of PCOS is targeted in lowering the androgen levels and improving of the symptoms.
The corner stone of the treatment is the use of low androgenic Combined oral contraceptive. The Progestin component should be low androgenic. It is mainly done in two steps:
1) The endometrial layer should be cleaned with progesterone. Since they are not producing progesterone they do not go through the progesterone withdrawal to slough off the endometrial lining of the functionalis layer ( the basalis layer which is usually 2 mm usually stays). Due to lack of corpus luteum i.e. lack of progesterone the endometrial layer is thicker than usual and, it needs to be cleaned. Progesterone is used initially to cleaned it.
A) Provera 10 mg daily for 10 days or 10 mg twice a day for 5 days.
B) Micronized Progesterone 200 mg daily for 10 days
Once good sloughing takes place then Combined Oral Contraceptives (COC) should be used.
2) Combined Oral Contraceptives:
Drespirenone/ethinylEstradiol; yasmin/angeliq
Norgestimate/EthinylEstradiol: Orthotricyclen
Dosegestrel/EthinylEstradiol: Mircette/Cerazette
3) Cyclic Progestins: If the combined oral contraceptives are not optional cyclic predestines can be used for 10 days of each month. They will protect endometrial hyperplasia but will not suppress the ovarian hyperandrogenism (hirsulism, acne, balding etc.)
Hirsutism can be managed with medications if the Combined Oral contraceptives (COC)are not improving the symptoms. The following medications can be added:
1) Eflorenthin hydrochloride 13.9%.(topical) It kills androgenic hair 60-80%
2) Spironolactone 25 mg 100mg twice a day. It is androgen blocked. Should be used with COC since it is erotogenic.
3) Laser therapy
Acne can be managed as follows:
1) Topical benzoyl peroxide 5% gel
2) clindamycin 1% or erythromycin gel topical
3) retinoid oral isotretinion.
4) Minocycline 5-100 mg doxycycline oral daily.
GnRH agonists such as leuprolide ( Lupron) can be used to suppress GnRH. This can lowered androgens by suppressing ovarian function. Intermittent leuprolide acetate can also be give to initiate ovulation.
Insulin resistance can be managed with metformin. Some women can resume regular ovulatory menses by taking metformin. Metformin and pioglitazones (actos) may increase insulin sensitivity that may help the ovaries produce less androgens.
If there is dyslipidemia statins and fibrates should be used liberally in PCOS patients. There is an increased risk of cardiovascular disease in PCOS patients. Metabolic syndrome is also common in these patients.
There are many comorbidities with PCOS:
Nutritional and psychological interventions with life style modification are very important component of the management of PCOS. Weight loss and regular daily structured physical activity should be encouraged consistently.
Comorbidities of PCOS should be addressed.
1) Dyslipidemias; About 70% Women with PCOS have abnormal lipid profile.
2) Cardiovascular disease is more common with women with PCOS
3) Endometrial neoplasia
4) Obstructive sleep apnea; Even normal weight women with PCOS have 40% risk of developing sleep apnea.
5) Infertility. This is very common in women with PCOs
6) Early miscourage is 3 times more in PCOS
7) Gestational Hypertension and Gestational diabetes is 3 times common in PCOS
8) Preterm labor is also 3 fold more in PCOS
9) Perinatal mortality is very common.
10) Obesity; 80% of women with PCOS have obesity or are overweight.
11) type 2 diabetes or prediabetes: Over 50% of women with PCOS will develop diabetes or prediabetes by the age of 40 years.
12) Metabolic syndrome. PCOS can lead to metabolic syndrome.
13) Insulin resistance: insulin resistance is common in women with PCOS.
14) Hypertension; HTN is common in women with PCOS.
Since PCOS is a diagnoses by exclusion. The following diagnosis should be excluded:
1) hypothyroid or hyperthyroid.
2) Cushing disease and other adrenal anomalies
3) Pituitary abnormalities; pituitary tumors, hyperprolactinemia or hypo gonadotropic hypogonadism.
4) Ovarian failure.
5) Late onset Congenital adrenal hyperplasia.
6) Ovarian or Adrenal androgen producing tumors.
Going Back to your Daughter: Your daughter have PCOS. This condition is very common in women of childbearing age (mostly 15-45years). About 3% to as high as 20% adolescent girls may have PCOS. Most of these conditions may have their roots in childhood, but the symptoms and comorbidities start to show up in adult hood. PCOS in adolescents should be managed properly. The symptoms of PCOS should be treated regardless of the diagnosis of PCOS. Weight management should be a priority. Maintaining a reasonable weight will help in the management of PCOS. A healthy balanced diet and daily structured physical activity is very important to lessen the symptoms of PCOS. Untreated PCOS will have various comorbidities. They include: obesity, insulin resistance, dyslipidemias, fatty liver disease, cardiovascular disease, endometrial neoplasia, prediabetes, diabetes, gestational diabetes, hypertension, metabolic syndrome, sleep apnea. infertility, miscourage etc. Theses are serious issues to consider. Therefore PCOS needs to be managed early and should be taken seriously to avoid the above serious complications. You should work with your daughter's doctor closely, and let her get proper treatment. With early intervention the out come will be much better.
Good Luck
Younger girls are being diagnosed mainly due to weight issues being more common. The fat cells can produce extra cortisol which causes increase weight increase hair growth and irregular periods. Usually getting to a healthy weight can make some of the problems better.It can be difficult to get pregnant when she is ready to start a family.
