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BMJ (Clinical Research Ed.) Sep 2003
Review
Topics: Anovulation; Body Weight; Electrocoagulation; Female; Hormones; Humans; Hyperprolactinemia; Hypogonadism; Hypothyroidism; Infertility, Female; Menopause, Premature; Ovulation Induction; Polycystic Ovary Syndrome
PubMed: 12958117
DOI: 10.1136/bmj.327.7414.546 -
Gynecological Endocrinology : the... Aug 2022
Topics: Androgens; Anovulation; Brain; Female; Humans; Hyperandrogenism; Phenotype; Polycystic Ovary Syndrome
PubMed: 35971943
DOI: 10.1080/09513590.2022.2106475 -
Human Reproduction (Oxford, England) May 1988Anovulatory disorders are physiological during puberty, postpartum period and just before the menopause. In pathology, they are one of the earliest symptoms of different... (Review)
Review
Anovulatory disorders are physiological during puberty, postpartum period and just before the menopause. In pathology, they are one of the earliest symptoms of different diseases: functional or organic hypothalamic diseases, pituitary destruction or inappropriate feedback by the peripheral hormones and, obviously, primary ovarian insufficiency. Their real interest lies in their pathophysiology. Functional hypothalamic disorders are defined as the inability to liberate GnRH in a physiological way. The role of endogenous opioids, as essential factors of gonadotrophin regulation will be discussed. Hyperprolactinaemias, which represent 20% of the anovulations, have an antigonadotrophic effect at the hypothalamic level, but the very mechanism of the inhibitory effect of prolactin on GnRH is still open to discussion. Although polycystic ovarian disease is one of the most common endocrine abnormalities in women, its pathophysiology remains far from fully understood. The relative parts played by hypothalamic disturbances and by abnormal feedback of gonadal steroids will be discussed.
Topics: Anovulation; Female; Humans; Hyperprolactinemia; Hypothalamic Diseases; Physical Exertion; Polycystic Ovary Syndrome
PubMed: 3292572
DOI: 10.1093/oxfordjournals.humrep.a136738 -
Annals of the New York Academy of... Jun 1997Normal pubertal development is often considered complete when the adolescent experiences her first menstrual period. However, sexual maturity is not attained until the... (Review)
Review
Normal pubertal development is often considered complete when the adolescent experiences her first menstrual period. However, sexual maturity is not attained until the onset of regular ovulatory cycles, which may take a number of months to years to accomplish. This maturation process is orchestrated by a neuroendocrine cascade and modified by autocrine and paracrine events in the ovary. The control of these complex relationships takes time and could not be expected to be fully functional with menarche. During the first menstrual months, the hypothalamic-pituitary-ovarian axis is immature, resulting in the secretion of only estrogens from the developing follicles; positive feedback to trigger ovulation develops later. Consequently, estrogen secretion is variable and unopposed by progesterone, which would normally be produced in ovulatory cycles. Estrogen-only primed endometrium often leads to irregular menstrual cycles with variable flow. Surprisingly, most adolescents do well and have few complaints in spite of these anovulatory cycles. If an abnormality is experienced with the menstrual cycle, once understood physiologically, it can be managed simply, by watchful expectancy or intermittent progestin therapy. Occasionally, sever menstrual bleeding is encountered, and in a proportion of these patients a thorough assessment will delineate an underlying medical problem that needs to be addressed. The management of these patients requires ingenuity from the pediatric reproductive endocrinologist and aggressive hormonal manipulation. Most patients do well, but some require long-term continuing care.
Topics: Adolescent; Anovulation; Child; Female; Humans; Menstrual Cycle
PubMed: 9238267
DOI: 10.1111/j.1749-6632.1997.tb52141.x -
Ryoikibetsu Shokogun Shirizu 1993
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Acta Bio-medica : Atenei Parmensis Aug 2022Obesity has been associated with reduced fertility, although the dynamics and mechanisms which link excess weight to reduced fertility are not yet fully clarified. Obese...
Obesity has been associated with reduced fertility, although the dynamics and mechanisms which link excess weight to reduced fertility are not yet fully clarified. Obese women, especially those with central obesity, are less likely to conceive per cycle. Obese women suffer from perturbations of the hypothalamus-pituitary-ovary axis, disturbances of the menstrual cycle and are up to three times more likely to suffer from oligo/anovulation. A delicate hormonal balance regulates follicular development and the maturation of oocytes and it has been observed that obesity can alter the hormonal environment: adipocytes, in fact, are responsible for the production of a hormone called leptin (present in high quantities in obese women) which has been associated with reduced fecundity. In addition to compromising ovulation, obesity negatively affects the development and implantation of the endometrium. The expression of polycystic ovary syndrome (PCOS) is regulated, in part, by weight, so obese women with PCOS often have a more severe phenotype and higher subfertility rates. Furthermore, obesity impairs women's response to medically assisted procreation (MAP) treatments. The authors have set out to delineate a broad-ranging overview of obesity's impact on female fertility, by drawing upon sources spanning the 1994-2022 period. Assisted reproductive technology (ART) procedures are also discussed as they relate to obese patients. In addition the dynamics by which maternal obesity reportedly affects fetal, neonatal and child development have also been briefly enunciated.
Topics: Anovulation; Female; Fertility; Humans; Infertility, Female; Obesity; Polycystic Ovary Syndrome; Pregnancy
PubMed: 36043953
DOI: 10.23750/abm.v93i4.13466 -
Indian Journal of Pediatrics Oct 2023Hyperandrogenism is a common condition encountered by pediatric and adolescent physicians. Most girls with hyperandrogenism represent physiological pubertal variation;... (Review)
Review
Hyperandrogenism is a common condition encountered by pediatric and adolescent physicians. Most girls with hyperandrogenism represent physiological pubertal variation; pathology may be present in a substantial minority. Systematic evaluation is essential to avoid unnecessary work-up in physiological causes while not missing pathological causes. Polycystic ovarian syndrome (PCOS), unexplained, persistent hyperandrogenism of ovarian origin, is the most common form in adolescent girls. The high prevalence of physiological peripubertal hirsutism, anovulation, and polycystic ovarian morphology results in mislabeling many girls as having the polycystic ovarian syndrome, a disorder with lifelong implications. The use of strict criteria of age-specific anovulation, hyperandrogenism, and duration is essential to reduce their stigmatization. The exclusion of secondary causes by screening tests (cortisol, thyroid profile, prolactin, and 17OHP) is essential before undertaking treatment for PCOS. Lifestyle measures, estrogen-progesterone preparations, antiandrogens, and metformin are the cornerstone of managing the disorder.
Topics: Female; Adolescent; Humans; Child; Hyperandrogenism; Polycystic Ovary Syndrome; Anovulation; Hirsutism
PubMed: 37402107
DOI: 10.1007/s12098-023-04678-7 -
The Journal of Clinical Endocrinology... Sep 2013Adolescents are at high risk for menstrual dysfunction. The diagnosis of anovulatory disorders that may have long-term health consequences is too often delayed. (Review)
Review
CONTEXT
Adolescents are at high risk for menstrual dysfunction. The diagnosis of anovulatory disorders that may have long-term health consequences is too often delayed.
EVIDENCE ACQUISITION
A review of the literature in English was conducted, and data were summarized and integrated from the author's perspective.
MAIN FINDINGS
Normal adolescent anovulation causes only minor menstrual cycle irregularity: most cycles range from 21-45 days, even in the first postmenarcheal year, 90% by the fourth year. Approximately half of symptomatic menstrual irregularity is due to neuroendocrine immaturity, and half is associated with increased androgen levels. The former is manifest as aluteal or short/deficient luteal phase cycles and usually resolves spontaneously. The latter seems related to polycystic ovary syndrome because adolescent androgen levels are associated with adult androgens and ovulatory dysfunction, but data are sparse. Obesity causes hyperandrogenemia and, via unclear mechanisms, seems to suppress LH; it may mimic polycystic ovary syndrome. The role of pubertal insulin resistance in physiological adolescent anovulation is unclear. High-sensitivity gonadotropin and steroid assays, the latter by specialty laboratories, are necessary for accurate diagnosis of pubertal disorders. Polycystic ovaries are a normal ultrasonographic finding in young women and are associated with nearly 2-fold increased anti-Müllerian hormone levels. Oral contraceptives are generally the first-line treatment for ongoing menstrual dysfunction, and the effects of treatment are similar among preparations.
CONCLUSIONS
Menstrual cycle duration persistently outside 21-45 days in adolescents is unusual, and persistence ≥ 1 year suggests that disordered hypothalamic-pituitary-gonadal function be considered. Research is needed on the mechanisms and prognosis of adolescent anovulation.
Topics: Adolescent; Anovulation; Female; Humans; Menstrual Cycle; Menstruation Disturbances; Ovary; Pituitary Gland; Polycystic Ovary Syndrome
PubMed: 23913942
DOI: 10.1210/jc.2013-1770 -
BMJ (Clinical Research Ed.) Jan 2017To compare the effectiveness of alternative first line treatment options for women with WHO group II anovulation wishing to conceive. (Review)
Review
OBJECTIVE
To compare the effectiveness of alternative first line treatment options for women with WHO group II anovulation wishing to conceive.
DESIGN
Systematic review and network meta-analysis.
DATA SOURCES
Cochrane Central Register of Controlled Trials, Medline, and Embase, up to 11 April 2016.
STUDY SELECTION
Randomised controlled trials comparing eight ovulation induction treatments in women with WHO group II anovulation: clomiphene, letrozole, metformin, clomiphene and metformin combined, tamoxifen, gonadotropins, laparoscopic ovarian drilling, and placebo or no treatment. Study quality was measured on the basis of the methodology and categories described in the Cochrane Collaboration Handbook. Pregnancy, defined preferably as clinical pregnancy, was the primary outcome; live birth, ovulation, miscarriage, and multiple pregnancy were secondary outcomes.
RESULTS
Of 2631 titles and abstracts initially identified, 54 trials reporting on 7173 women were included. All pharmacological treatments were superior to placebo or no intervention in terms of pregnancy and ovulation. Compared with clomiphene alone, both letrozole and the combination of clomiphene and metformin showed higher pregnancy rates (odds ratio 1.69, 95% confidence interval 1.33 to 2.14; 1.71, 1.28 to 2.27; respectively). Letrozole led to higher live birth rates when compared with clomiphene alone (1.67, 1.11 to 2.49). Metformin led to lower multiple pregnancy rates compared with clomiphene alone (0.22, 0.05 to 0.93).
CONCLUSIONS
In women with WHO group II anovulation, letrozole and the combination of clomiphene and metformin are superior to clomiphene alone in terms of pregnancy. Compared with clomiphene alone, letrozole is the only treatment showing a significantly higher rate of live birth.
SYSTEMATIC REVIEW REGISTRATION
PROSPERO CRD42015027579.
READERS' NOTE
This is the second version of this paper. The original version was corrected following the retraction of two studies and removal of another which were ineligible (references 40, 41, and 75 of the original paper). These studies are not shown in this version. A tracked changes version of the original version is attached as a supplementary file to the correction notice, which explains the issue further.
Topics: Anovulation; Clomiphene; Drug Therapy, Combination; Female; Humans; Infertility, Female; Letrozole; Metformin; Network Meta-Analysis; Nitriles; Ovulation Induction; Pregnancy; Pregnancy Rate; Treatment Outcome; Triazoles
PubMed: 28143834
DOI: 10.1136/bmj.j138 -
Endocrinology and Metabolism (Seoul,... Apr 2021Polycystic ovary syndrome (PCOS) is a common endocrine disorder in reproductive-aged women, characterized by hyperandrogenism, oligo/anovulation, and polycystic ovarian...
Polycystic ovary syndrome (PCOS) is a common endocrine disorder in reproductive-aged women, characterized by hyperandrogenism, oligo/anovulation, and polycystic ovarian morphology. Combined oral contraceptives (COCs), along with lifestyle modifications, represent the first-line medical treatment for the long-term management of PCOS. Containing low doses of estrogen and different types of progestin, COCs restore menstrual cyclicity, improve hyperandrogenism, and provide additional benefits such as reducing the risk of endometrial cancer. However, potential cardiometabolic risk associated with these agents has been a concern. COCs increase the risk of venous thromboembolism (VTE), related both to the dose of estrogen and the type of progestin involved. Arterial thrombotic events related to COC use occur much less frequently, and usually not a concern for young patients. All patients diagnosed with PCOS should be carefully evaluated for cardiometabolic risk factors at baseline, before initiating a COC. Age, smoking, obesity, glucose intolerance or diabetes, hypertension, dyslipidemia, thrombophilia, and family history of VTE should be recorded. Patients should be re-assessed at consecutive visits, more closely if any baseline cardiometabolic risk factor is present. Individual risk assessment is the key in order to avoid unfavorable outcomes related to COC use in women with PCOS.
Topics: Adult; Anovulation; Contraception; Contraceptives, Oral, Combined; Female; Humans; Hyperandrogenism; Polycystic Ovary Syndrome
PubMed: 33853290
DOI: 10.3803/EnM.2021.958