Polycystic ovary syndrome ( PCOS ) is a series of symptoms due to increased androgens (male hormones) in women. Signs and symptoms of PCOS include irregular or no menstrual periods, heavy menstruation, excess body and facial hair, acne, pelvic pain, difficulty conceiving, and thick spots, darker velvet skin. Related conditions include type 2 diabetes, obesity, obstructive sleep apnea, heart disease, mood disorders, and endometrial cancer.
PCOS is due to a combination of genetic and environmental factors. Risk factors include obesity, insufficient physical exercise, and a family history of a person with the condition. The diagnosis is based on two of the following three findings: no ovulation, high androgen levels, and ovarian cysts. Cysts can be detected with ultrasound. Other conditions that produce similar symptoms include adrenal hyperplasia, hypothyroidism, and hyperprolactinemia.
PCOS does not have a cure. Treatment may involve lifestyle changes such as weight loss and exercise. Birth control pills can help improve the regularity of menstruation, excessive hair growth, and acne. Metformin and anti-androgen can also help. Acne treatment and other hair removal techniques can be used. Efforts to increase fertility include weight loss, clomiphene, or metformin. In-vitro fertilization is used by some people whose other measures are ineffective.
PCOS is the most common endocrine disorder among women between the ages of 18 and 44. It affects about 2% to 20% of this age group depending on how it is defined. This is one of the main causes of poor fertility. The earliest known explanation of what is now known as PCOS dates from 1721 in Italy.
Video Polycystic ovary syndrome
Signs and symptoms
Common PCOS signs and symptoms include the following:
- Menstrual disorders: PCOS produces mostly oligomenorrhea (less than nine menstrual periods in a year) or amenorrhea (no menstrual period for three months or more), but other types of menstrual disorders may also occur.
- Infertility: This is generally a direct result of chronic anovulation (lack of ovulation).
- High levels of masculinizing hormones: Known as hyperandrogenism, the most common signs are acne and hirsutism (male hair growth patterns, such as chin or chest), but may produce hyperorrhea (severe and prolonged menstrual periods), androgenic alopecia (increased hair thinning or diffuse hair loss), or other symptoms. About three-quarters of women with PCOS (by NIH/NICHD diagnostic criteria 1990) have evidence of hyperandrogenemia.
- Metabolic syndrome: This appears as a predisposition to central obesity and other symptoms associated with insulin resistance. Insulin serum, insulin resistance, and homocysteine ​​levels are higher in women with PCOS.
Asians affected by PCOS tend not to develop hirsutism compared to other ethnic backgrounds.
Maps Polycystic ovary syndrome
Cause
PCOS is an uncertain heterogeneous cause disorder. There is some evidence that it is a genetic disease. Such evidence includes grouping of family cases, larger concordances in monozygotes compared with dizygotic twins and the heritability of endocrine and metabolic features of PCOS. There is some evidence that higher exposure than typical androgen levels in utero increases the risk of developing PCOS later in life.
Genetic components seem to be inherited autosomally dominantly with high genetic penetration but variable expressiveness in women; this means that each child has a 50% chance of inheriting a predisposing genetic variant from the parent, and, if a girl receives a variant (s), the girl will have the disease to some extent. Genetic variants can be inherited from the father or mother, and can be passed on to two boys (who may be asymptomatic carriers or may have symptoms such as premature baldness and/or excessive hair) and girls, who will show signs of PCOS. The phenotype appears to manifest itself at least partially through high levels of androgens secreted by ovarian follicle ovarian cells from women with alleles. The exact genes affected have not been identified. In rare cases, a single gene mutation can lead to a syndrome phenotype. The current understanding of the pathogenesis of the syndrome suggests, however, that it is a complex multigenic disorder.
The severity of symptoms of PCOS seems to be largely determined by factors such as obesity.
PCOS has several aspects of metabolic disorders, because the symptoms are reversible. Although considered a gynecological problem, PCOS consists of 28 clinical symptoms.
Although the name suggests that the ovaries are central to disease pathology, cysts are a symptom not a cause of disease. Some symptoms of PCOS will persist even if both ovaries are removed; the disease can appear even if the cyst does not exist. Since the first description by Stein and Leventhal in 1935, the diagnostic, symptom, and causal criteria are debatable. Gynecologists often see it as a gynecological problem, with the ovaries being the primary organ affected. However, recent insights suggest a multisystem disorder, with the main problem lies in the regulation of hormones in the hypothalamus, with the involvement of many organs. The name PCOD is used when there is evidence of ultrasound. The term PCOS is used because there is a broad spectrum of symptoms, and ovarian cysts are seen in only 15% of people.
PCOS may be associated or aggravated by exposure during the prenatal period, epigenetic factors, environmental impacts (especially industrial endocrine disruptors such as bisphenol A and certain drugs) and increased rates of obesity.
Pathogenesis
Polycystic ovaries develop when the ovaries are stimulated to produce excess amounts of androgenic hormones, especially testosterone, by one or a combination of the following (almost certainly combined with genetic susceptibility):
- excessive luteinizing hormone release (LH) by the anterior pituitary gland
- through high levels of insulin in the blood (hyperinsulinemia) in women whose ovaries are sensitive to this stimulus
This syndrome derives its most widely used name because of its common mark on ultrasound examination of ovarian cyst (poly) ovaries. This "cyst" is actually an immature follicle instead of a cyst. The follicle has grown from the primordial follicle, but its development has stopped ("captured") in the early antral stage because of impaired ovarian function. Follicles may be oriented along the periphery of the ovary, appearing as 'pearl strands' on ultrasound examination.
Women with PCOS have an increased frequency of hypothalamus GnRH pulses, which in turn results in an increase in the LH/FSH ratio.
The majority of women with PCOS have insulin resistance and/or are obese. Their high insulin levels contribute to or cause abnormalities seen in the hypothalamus-pituitary-ovarian axis leading to PCOS. Hyperinsulinemia increases the frequency of GnRH, LH on the dominance of FSH, increased ovarian androgen production, decreased follicular maturation, and decreased SHBG bond. Furthermore, excessive insulin, acting through its cognitive receptors in the presence of cAMP component signaling, increases the activity of 17-hydroxylase through PI3K, a 17-hydroxylase activity responsible for synthesizing androgen precursors. The combined effect of hyperinsulinemia contributes to an increased risk of PCOS. Insulin resistance is a common finding among women of normal weight as well as overweight women.
Adipose tissue has aromatase, an enzyme that converts androstenedione into estrone and testosterone into estradiol. An excess of adipose tissue in obese women creates a paradox of androgen excess (which is responsible for hirsutism and virilization) and estrogen (which inhibits FSH through negative feedback).
PCOS can be associated with chronic inflammation, with some researchers linking inflammatory mediators with anovulation and other PCOS symptoms. Similarly, there appears to be a link between PCOS and an increase in oxidative stress levels.
It has been previously suggested that excessive androgen production in PCOS may be caused by a decrease in serum levels of IGFBP-1, which in turn increases the level of free IGF-I, which stimulates ovarian androgen production, but recent data suggests this mechanism is unlikely.
PCOS is also associated with a particular sub-genotype of FMR1. Research has shown that women with heterozygous-normal/low FMR1 have polycystic symptoms of excessive follicle activity and hyperactive ovarian function.
Transgender men may experience higher levels of PCOS than expected due to increased testosterone, if they choose to take hormone therapy as part of their gender presentation.
Diagnosis
Not everyone with PCOS has a polycystic ovary (PCO), nor does everyone with ovarian cysts have PCOS; although pelvic ultrasound is a major diagnostic tool, it is not the only one. Diagnosis directly uses Rotterdam criteria, even when this syndrome is associated with a variety of symptoms.
Definition
Two commonly used definitions:
NIH
- In 1990, a consensus workshop sponsored by NIH/NICHD suggested that someone has PCOS if they have all of the following:
- oligoovulation
- signs of androgen (clinical or biochemical) excess
- exceptions to other disturbances that can cause menstrual irregularities and hyperandrogenism
Rotterdam
- In 2003, a consensus workshop sponsored by ESHRE/ASRM in Rotterdam indicated that PCOS would be present if two of the 3 criteria were met, in the absence of another entity that might lead to this finding
- oligoovulation and/or anovulation
- excess androgen activity
- polycystic ovaries (by gynecological ultrasound)
Rotterdam's definition is broader, including more women, the most prominent being women without androgen overload. Critics say that the findings obtained from women's studies with androgen excess can not be extrapolated to women without androgen overload.
- Androgen Excess PCOS Society
- In 2006, Androgen Excess PCOS Society suggested tightening the diagnostic criteria for all of the following:
- excess androgen activity
- oligoovulation/anovulation and/or polycystic ovaries
- the exclusion of another entity that will cause excess androgen activity
Standard rating
- Taking history, especially for menstrual patterns, obesity, hirsutism and acne. The clinical prediction rule found that these four questions could diagnose PCOS with a sensitivity of 77.1% (95% confidence interval [CI] 62.7% -88.0%) and specificity 93.8% (95% CI 82.8% 98.7%)./li>
- Gynecological ultrasonography, specifically looking for small ovarian follicles. This is believed to be the result of a disturbed ovarian function with failed ovulation, reflected by rarer or nonexistent menstruations typical of the condition. In a normal menstrual cycle, one egg is released from the dominant follicle - in essence, a cyst that spurts to release the egg. After ovulation, the rest of the follicle turns into a corpus luteum that produces progesterone, which shrinks and disappears after about 12-14 days. In PCOS, there is a so-called "follicular arrest"; that is, some follicles develop into a size of 5-7 mm, but not farther. No single follicle reaches a preovulation measure (16 mm or more). According to the Rotterdam criteria, which are widely used for diagnosis, 12 or more small follicles should be seen in the ovaries on ultrasound examination. Recent research has shown that there must be at least 25 follicles in the ovary to establish it as having polycystic ovarian morphology (PCOM) in women aged 18-35 years. The follicle may be oriented at the periphery, giving the appearance of a 'string of pearls'. If high-resolution transvaginal ultrasonography machines are not available, a minimum of 10 ml ovarian volume is considered an acceptable definition to have polycystic ovarian morphology rather than the number of follicles.
- Laparoscopic examination can reveal the outer surface of the ovaries that are thickened, smooth, and pearl-white. (This is usually an incidental finding if laparoscopy is done for some other reason, since it will not routinely check the ovaries in this way to confirm the diagnosis of PCOS.) Serum (blood) androgen levels (hormones associated with male development), including androstenedione and testosterone may increase. Dehydroepiandrosterone sulfate levels above 700-800 Âμg/dL are highly suggestive of adrenal dysfunction because DHEA-S is made exclusively by the adrenal gland. Free testosterone levels are considered the best measure, with ~ 60% of PCOS patients showing a supranormal level. Free androgen index (FAI) from the ratio of testosterone to sex hormone-binding globulin (SHBG) is high and is intended to be a testosterone-free predictor, but is a poor parameter for this and is no better than testosterone itself as a marker for PCOS, possibly because FAI is correlated with level of obesity.
Some other blood tests are suggestive but not diagnostic. The Luteinizing hormone (LH) ratio to FSH (Follicle-stimulating hormone), when measured in an international unit, increases in women with PCOS. The general cuts for determining high abnormal LH/FSH ratios are 2: 1 or 3: 1 as tested on Day 3 of the menstrual cycle. The pattern is not very sensitive; a 2: 1 or higher ratio was present in fewer than 50% of women with PCOS in one study. There are often low levels of sex hormone-binding globulin, especially among obese or overweight women.
The Anti-MÃÆ'¼llerian (AMH) hormone is increased in PCOS, and can be part of its diagnostic criteria.
Related conditions
- Biochemical screen and fast fold profile
- A 2-hour oral glucose tolerance test (GTT) in women with risk factors (obesity, family history, history of gestational diabetes) may indicate impaired glucose tolerance (insulin resistance) in 15-33% of women with PCOS. Frank diabetes can be seen in 65-68% of women with this condition. Insulin resistance can be observed in people of normal weight and overweight people, although more commonly in the latter (and in those who meet the stricter NIH criteria for diagnosis); 50-80% of people with PCOS may have insulin resistance at some level.
- Fasting insulin level or GTT with insulin levels (also called IGTT). Increased insulin levels have helped to predict the response to drugs and may indicate women requiring higher metformin doses or second-drug use for significantly lower insulin levels. Increased blood sugar and insulin values ​​do not predict who responds to insulin-lowering drugs, low-glycemic diet, and exercise. Many women with normal levels may benefit from combination therapy. Hypoglycemic responses in which insulin levels are two hours higher and blood sugar is lower than fasting consistent with insulin resistance. A mathematical derivation known as HOMAI, calculated from fasting values ​​in glucose and insulin concentrations, allows direct and reasonably accurate measurement of insulin sensitivity (insulin-level x/glucose levels of 22.5).
- The testing of glucose tolerance (GTT) rather than fasting glucose may improve the diagnosis of impaired glucose tolerance and diabetes frankly among people with PCOS according to prospective controlled trials. While fasting glucose levels may remain within normal limits, oral glucose testing revealed that up to 38% of asymptomatic women with PCOS (compared to 8.5% in the general population) actually had impaired glucose tolerance, 7.5% of those with diabetes were honest â € < â €
Differential diagnosis
Other causes of irregular or absent menstruation and hirsutism, such as hypothyroidism, congenital adrenal hyperplasia (21-hydroxylase deficiency), Cushing's syndrome, hyperprolactinemia, androgen secreting neoplasms, and other pituitary or adrenal disorders, should be investigated.
Management
The main treatments for PCOS include: lifestyle changes and medications.
Treatment goals can be considered under four categories:
- Decreases the level of insulin resistance
- Recovery of fertility
- Treatment of hirsutism or acne
- Regular menstrual restoration, and prevention of endometrial hyperplasia and endometrial cancer
In each of these areas, there is a great debate about optimal care. One of the main reasons for this is the lack of large-scale clinical trials comparing different treatments. Smaller experiments tend to be less reliable and therefore can produce conflicting results.
Common interventions that help reduce weight or insulin resistance can be beneficial for all of these goals, as they overcome what is believed to be the underlying cause.
When PCOS seems to cause significant emotional distress, proper support may be useful.
Diet
If PCOS is associated with overweight or obesity, successful weight loss is the most effective method to restore normal ovulation/menstruation, but many women find it very difficult to achieve and maintain significant weight loss. A scientific review in 2013 found similar weight loss and body composition and improvements in pregnancy rates, menstrual regularity, ovulation, hyperandrogenism, insulin resistance, lipids, and quality of life occurred with independent weight loss from dietary composition. However, a low GI diet, in which a significant portion of total carbohydrates obtained from fruits, vegetables, and grain sources, has resulted in greater menstrual regularity than a macronutrient-fit healthy diet.
Vitamin D deficiency can play some role in the development of metabolic syndrome, so treatment of such deficiencies is indicated. However, a systematic review of 2015 found no evidence that vitamin D supplementation reduced or decreased metabolism and hormonal dysregulation in PCOS. In 2012, interventions using dietary supplements to correct metabolic deficiencies in people with PCOS have been tested in small, uncontrolled and non-randomized clinical trials; the resulting data is not sufficient to recommend its use.
Drugs
Drugs for PCOS include oral contraceptives and metformin. Oral contraceptives increase the production of globulin-binding hormones, which increases the free binding of testosterone. It reduces the symptoms of hirsutism caused by high testosterone and regulates it back to a normal menstrual period. Metformin is a drug commonly used in type 2 diabetes mellitus to reduce insulin resistance, and used off label (in the UK, US, AU and EU) to treat insulin resistance seen in PCOS. In many cases, metformin also supports ovarian function and return to normal ovulation. Spironolactone can be used for its antiandrogenic effect, and topical eflornithine cream can be used to reduce facial hair. Newer classes of insulin resistance drugs, thiazolidinediones (glitazones), have shown equivalent efficacy for metformin, but metformin has a more favorable side-effect profile. The National Institute for Clinical Health and Clinical Excellence recommended in 2004 that women with PCOS and body mass index above 25 were given metformin when other therapies failed to produce results. Metformin may not be effective in any type of PCOS, and therefore there is some disagreement as to whether it should be used as a common first-line therapy. The use of statins in the underlying management of underlying metabolic syndrome remains unclear.
It is difficult to get pregnant with PCOS because it causes irregular ovulation. Drugs to induce fertility while trying to conceive include clomiphene ovulation inductor or pulsatile leuprolide. Metformin increases the effectiveness of fertility treatment when used in combination with clomiphene. Metformin is considered safe for use during pregnancy (pregnancy category B in the US). A review in 2014 concluded that the use of metformin did not increase the risk of major birth defects in women treated with metformin during the first trimester.
Infertility
Not all women with PCOS have difficulty getting pregnant. For those who do, anovulation or ovulation is rarely a common cause. Other factors include changes in gonadotropin levels, hyperandrogenemia, and hyperinsulinemia. Like women without PCOS, women with ovulating PCOS may be infertile due to other causes, such as tubal obstruction due to a history of sexually transmitted diseases.
For women with weight loss anovulation with PCOS, weight loss and diet adjustment, especially to reduce the intake of simple carbohydrates, associated with the return of natural ovulation.
For women who, after weight loss are still anovulable or for anovulously slender women, ovulation induction medications clomiphene citrate and FSH are the primary treatments used to promote ovulation. Previously, anti-diabetic drugs metformin recommended treatment for anovulation, but it seems less effective than clomiphene.
For women unresponsive to clomiphene and diet and lifestyle modification, there are options available including assisted reproductive technology procedures such as controlled ovarian hyperstimulation with follicular follicle injection (FSH) followed by in vitro fertilization (IVF).
Although surgery is not common, polycystic ovaries can be treated with laparoscopic procedures called "ovarian drilling" (small 4-10 follicles with electrocautery, laser, or biopsy needles), which often lead to a return of spontaneous ovulation or ovulation after adjuvant treatment with clomiphene or FSH. (Resection of ovarian slices is no longer used because of complications such as adhesion and the presence of drugs that are often effective.) However, there are concerns about the long-term effects of ovarian drilling on ovarian function.
Hirsutism and acne
When necessary (eg, in women of childbearing age who need contraception), standard contraceptive pills are often effective in reducing hirsutism. Progestogens such as norgestrel and levonorgestrel should be avoided because of their androgenic effects.
Other drugs with anti-androgen effects include flutamide, and spironolactone, which can provide some improvement in hirsutism. Metformin can reduce hirsutism, perhaps by reducing insulin resistance, and is often used if there are other features such as insulin resistance, diabetes, or obesity which should also benefit from metformin. Eflornithine (Vaniqa) is a drug applied to the skin in the form of cream, and acts directly on the hair follicles to inhibit hair growth. Usually applied to the face. 5-alpha reductase inhibitors (such as finasteride and dutasteride) can also be used; they work by blocking the conversion of testosterone into dihydrotestosterone (the latter responsible for most of the changes in hair growth and androgenic acne).
Although these agents have demonstrated significant efficacy in clinical trials (for oral contraceptives, in 60-100% of individuals), hair growth reduction may not be enough to eliminate social embarrassment of hirsutism, or discomfort with plucking or shaving. Individuals vary in their response to different therapies. Usually worth another drug if it does not work, but drugs do not work well for all individuals.
Menstrual irregularity
If fertility is not the main purpose, then menstruation can usually be regulated with the contraceptive pill. The purpose of regulating menstruation, in essence, is for the comfort of women, and perhaps their sense of well-being; there is no medical requirement for the regular period, as long as it happens quite often.
If regular menstrual cycles are undesirable, then therapy for irregular cycles is not necessarily required. Most experts say that, if menstrual bleeding occurs at least every three months, the endometrium (lining of the uterus) is being shed frequently enough to prevent an increased risk of endometrial or cancer abnormalities. If menstruation is less frequent or absent, some form of progestogen replacement is recommended. Another alternative is oral progestogens taken at intervals (eg, every three months) to induce predictable menstrual bleeding.
Alternative medicine
2017's review concludes that although myo-inositol and D-chiro-inositols can regulate the menstrual cycle and increase ovulation, there is a lack of evidence about the effect on the likelihood of pregnancy. A review of 2012 and 2017 have found myo-inositol supplementation seems to be effective in improving some of the hormonal disorders of PCOS. The 2011 review found insufficient evidence to conclude any beneficial effect of D-chiro-inositol. There is not enough evidence to support the use of acupuncture.
Prognosis
The diagnosis of PCOS shows the following risks: Endometrial hyperplasia and endometrial cancer (uterine lining cancer) are possible, due to overaccumulation of the uterine lining, and also the lack of progesterone resulting in prolonged uterine uterine cell stimulation. It is unclear whether this risk is directly caused by syndrome or from associated obesity, hyperinsulinemia, and hyperandrogenism.
The risk of ovarian cancer and breast cancer did not increase significantly overall.
Epidemiology
The prevalence of PCOS depends on the choice of diagnostic criteria. The World Health Organization estimates that it affects 116 million women worldwide in 2010 (3.4% of women). One community-based prevalence study using the Rotterdam criteria found that about 18% of women had PCOS, and that 70% of them were previously undiagnosed.
Polycystic ovary ultrasound findings are present in 8-25% of normal women. 14% of women on oral contraceptives were found to have polycystic ovaries. Ovarian cysts are also a common side effect of intrauterine devices that release levonorgestrel (IUD).
History
This condition was first described in 1935 by the American gynecologist Irving F. Stein, Sr. and Michael L. Leventhal, whose real name is from Stein-Leventhal syndrome was taken.
The earliest published description of a person with what is now known as PCOS in 1721 in Italy. Changes in ovarian cysts are described in 1844.
Name
Other names for this syndrome include polycystic ovary syndrome, polycystic ovary disease, functional ovarian hyperandrogenism, ovarian hypertension, sclerosistic ovarian syndrome, and Stein-Leventhal syndrome. The last eponymous option is the real name; now used, if at all, only for a subset of women with all the symptoms of amenorrhea with infertility, hirsutism, and polycystic ovaries enlarged.
The most common name for this disease comes from typical findings in medical images, called polycystic ovaries. A polycystic ovary has a large number of growing eggs that are visible near its surface, looking like many small cysts.
See also
- Androgen-dependent syndromes
- PCOS Challenge (reality television series)
References
External links
Source of the article : Wikipedia
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