Gonadotropin-Resistant Ovary Syndrome Presented with Secondary Amenorrhea and Infertility: A Case Report.

Resistant ovary syndrome (ROS) is a presentation of hypergonadotrophic hypogonadism condition with very low incidence. Infertility is one of the most common complaintsof women with this syndrome. We herein present a case of a 27-year-old woman with all features of secondary amenorrhea and secondary sexual characteristics. In 2018,the patient was referred to the Hazret-e-Zeinab Infertility Center affiliated to Shiraz University of Medical Sciences, Shiraz, Iran. She was diagnosed with secondaryamenorrhea and increased gonadotropin secretion after menopause. However, the patient had a normal antral follicle count, anti-Müllerian hormone level, 46, XX karyotype,and thyroid function. After taking oral contraceptives her menstruation started, but she showed no response to high doses of exogenous gonadotropins. She was advised tohave an embryo derived from in vitro maturation. By using patients’ own oocyte maturation, this technique could be a better treatment for infertile women with ROS.This case report is particularly interesting due to the rarity of its prevalence and similarity with primary ovarian insufficiency.

BackgroundResistant ovary syndrome (ROS) is a rare endocrine disorder characterized with hypergonadotrophic hypogonadism. Infertility is a common complaint of woman presenting with ROS, and little progress has been made in term of reproduction with the patient’s own gamete. So far only one case report of live birth has been reported after in vitro maturation (IVM) of oocytes in a patient suffering from ROS in 2013.Case presentationA secondary infertile woman of 33 years-old was manifested with oligomenorrhea and markedly increased gonadotropin levels around postmenopausal range, but had normal antral follicle count, normal serum inhibin B and anti-Müllerian hormone levels. She had normal karyotype of 46,XX and normal thyroid function. There were no abnormal findings in some autoantibody assays and FSH receptor sequencing. After oral contraceptive pills combined with triptorelin depot were administered, her gonadotropin levels reduced but it showed no response to high doses of exogenous gonadotropins (hp-HMG 300IU/d for 15 days). Then endometrium was prepared with estradiol valerate and IVM from small antral follicles were performed. Five immature oocytes were retrieved. Twenty-four hours after IVM culture, 3 oocytes matured to metaphase II stage and were inseminated by intracytoplasmic sperm injection using her husband’s sperm. Two top-quality embryos were transferred and one embryo was cryopreserved. The patient got pregnant and delivered a healthy boy at term.ConclusionIVM using their own oocytes could be an available treatment for infertile women with ROS.

BackgroundResistant ovary syndrome (ROS) is a rare endocrine disorder and there have been few reports of live births by affected patients. As gonadotropin resistance leads immature oocytes, some researchers reported few live births with in vitro maturation (IVM) of oocytes, but IVM is not always successful in ROS patients. Here, we report an original case of ROS, associated with Ig-FSHR in the serum, who achieved a live birth following ovarian stimulation combined with dexamethasone treatment.Case presentationThe 30-year-old woman presented with secondary amenorrhea and infertility. Her serum FSH levels were found to be higher than normal, but in discordance with a normal anti-Müllerian hormone (AMH) level and antral follicle count. Genetic investigation found no mutations potentially affecting FSHR. With reference of previous ROS studies, the patient’s serum was analyzed for antibodies directed against FSHR and dot blot analysis showed strong reactivity with FSHR. Then, dexamethasone was proposed to the patient, and she successfully became pregnant, finally delivering a healthy girl by caesarean section.ConclusionTo our best knowledge, this is the first report of the successful treatment of ROS using ovarian stimulation combined with dexamethasone. In some cases of ROS, high doses of exogenous gonadotropins in combination with immunosuppressive therapy could be an effective approach.

Objectives After completing this article, readers should be able to: Development and maturation of the reproductive system begins in fetal life and is a surprisingly active process throughout the first postnatal months. The reproductive system becomes quiescent during childhood until its reactivation triggers pubertal development. Puberty begins with increased pulsatile secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus, increased pituitary responsiveness to GnRH, increased secretion of gonadotropins,gonadal maturation, and increasing production of sex steroids. Increased concentrations of sex steroids induce the development of secondary sexual characteristics, acceleration of growth, and ultimate fertility. Factors that determine the timing of pubertal onset remain poorly understood and the subject of intense investigation, but general health, nutrition, and genetic factors all are known to contribute.The diagnostic criteria for pubertal delay are based roughly on statistical norms (ie, delay of more than 2 to 3 standard deviations from the mean age of pubertal onset), but in fact they are somewhat arbitrary. Puberty is considered to be clinically delayed if sexual maturation has not become apparent by age 14 years in boys or age 13 years in girls. This clinical diagnosis also is made in the absence of menarche by age 16 years or in the absence of menarche within 5 years of pubertal onset. Using these criteria, approximately 2.5% of healthy adolescents will be identified as having pubertal delay. Most are boys. After evaluation, the majority of these adolescents will be found to have no pathology; rather, onset of their otherwise normal puberty simply is sufficiently late or slow relative to that of their peers to have triggered concern and evaluation. When puberty does begin, it is entirely normal. Some adolescents have a variety of other causes to explain pubertal delay(TableT1), and with careful evaluation, most are diagnosed accurately. In constitutional delay of puberty, the normal prepubertal growth nadir is protracted. Presumably, the pubertal increase of pulsatile GnRH secretion is slow to develop, which delays pubertal levels of sex steroid secretion and their developmental effects on secondary sexual characteristics and growth hormone production. The prototypic patient who has constitutional delay of puberty is a 14- or 15-year-old boy who presents after most of his peers have begun puberty. Boys present far more often than girls because short stature and sexual immaturity extract a higher psychosocial price in males than in females. In many cases, delay of puberty is superimposed on constitutional short stature, exaggerating the effects of the delay. History may reveal similarly delayed puberty in the patient's parents or siblings. Findings on physical examination are unremarkable except possibly for early signs of puberty unnoticed by the patient. Laboratory evaluation results are normal, although bone age is delayed and consistent with the extent of pubertal maturation.The outcome of isolated constitutional delay of puberty is excellent;neither sexual maturity nor final adult height is affected by the timing of pubertal onset. However, when constitutional delay of puberty is superimposed on constitutional short stature, final height will be short. Resolving the relative effects of these factors in final height has been difficult in the studies performed to date.Chronic illness may affect pubertal onset, tempo, and potential. The pathophysiology of pubertal delay in chronic illness is variable,frequently multifactorial, and in some cases, not well-established. Chronic illness may affect underlying genetic potential, disturb physiologic function, or limit adequate nutrition. Chronic use of glucocorticoids, cancer chemotherapy, other medications, or radiation therapy may have short- or long-term consequences for growth or sexual maturation.Adolescents who have chronic conditions, about which they already are acutely self-conscious, deserve particularly close monitoring of their pubertal course to allow early detection of pubertal difficulties. Often, only reassurance that puberty ultimately will proceed and eventual development will be normal is all that is required. However,when more pathologic pubertal derangements are detected, they should be treated early to maximize the potential for catch-up. Nutrition should be a priority, especially in those conditions where it frequently is compromised (eg, inflammatory bowel disease, cystic fibrosis), with supplementation used where appropriate. The risks and benefits of proposed medications and therapies, especially their effects on growth and maturation, always should be considered. Other explanations for pubertal delay should be investigated when the disease process does not explain maturational insufficiency or delay adequately. Finally,hormone replacement or augmentation with exogenous sex steroids is appropriate in some settings, but it is not a substitute for aggressive management of the underlying condition.Delayed puberty is not a common presentation of panhypopituitarism;affected children typically present with short stature earlier in childhood. Panhypopituitarism presenting in adolescence is usually due to idiopathic hypothalamic failure. However, other unusual central nervous system etiologies (eg, tumor, Langerhans cell histiocytosis)should be ruled out.The syndromes of isolated gonadotropin deficiency (IGD) are heterogeneous in clinical presentation. They occur more frequently in boys than in girls and often are difficult to distinguish from constitutional delay. IGD in association with hyposmia or anosmia is known as Kallman syndrome. The KAL-1 gene encodes a protein that allows fetal GnRH neurons to migrate from the olfactory placode through the cribiform plate and into the hypothalmus. Deletion of the KAL-1 gene is associated with sensorineural deafness, kidney malformations, and pes cavus. Boys who have GnRH deficiency often have a small phallus and testes, but findings on history and physical examination may be entirely normal except for sexual immaturity. Delayed bone age is the only consistent laboratory finding.Thyroid hormone is required for normal puberty. Its absence may delay the onset or retard the progress of pubertal maturation by interfering with gonadotropin secretion. Thyroid replacement therapy usually normalizes gonadotropin secretion and allows puberty to proceed normally.Hyperprolactinemia may cause primary or secondary amenorrhea, but it is an otherwise rare cause of delayed puberty. Elevated prolactin levels interfere with gonadotropin production and may be due to a functioning pituitary adenoma (prolactinoma) or related to use of prescribed or illicit drugs (eg, phenothiazines, cocaine). Measurement of serum prolactin is a useful part of the evaluation for amenorrhea or delayed puberty, even in the absence of galactorrhea, and always should be obtained in the presence of galactorrhea. Prolactinomas may not be visible on imaging studies of the brain,making diagnosis more difficult.Bilateral gonadal failure is uncommon and is characterized by markedly elevated concentrations of serum gonadotropins. The most common causes of gonadal failure are congenital: Turner syndrome(gonadal dysgenesis) and Klinefelter syndrome. Other congenital causes of gonadal failure and acquired bilateral gonadal failure are rare.Girls who have Turner syndrome have short stature, variable but incomplete puberty, primary amenorrhea, and characteristic congenital anomalies. Growth retardation is the most consistent characteristic and begins in utero. Rarely is a pubertal growth spurt seen. For some girls, the diagnosis will not be made until they present with pubertal insufficiency. Most girls who have Turner syndrome have primary ovarian failure that gives rise to markedly elevated levels of gonadotropins by adolescence, although variable sexual development still occurs. More than 50% of patients in one study had some breast development, and some pubic and axillary hair is typical for most patients. A minority of affected girls experience spontaneous menarche at an average age of 13.4 years, but most girls who have Turner syndrome require long-term estrogen replacement therapy.Klinefelter syndrome is relatively common. The genotype is typically 46,XXY, but genetic variability and mosaicism occur. Many affected boys are not identified until puberty or early adulthood. Often, some spontaneous pubertal development occurs, but testes become fibrotic and smaller as boys become older. Males who have Klinefelter syndrome present with small testicles and external genitalia and often have gynecomastia. Affected boys tend to be tall in childhood, and their tall stature sometimes delays diagnosis despite their pubertal immaturity. Borderline intellectual abilities or behavioral difficulties sometimes lead to diagnosis in childhood or may be appreciated in retrospect. In adolescence, young men who have Klinefelter syndrome present with small testicles and hypogonadism. Testosterone production is abnormally low, follicle-stimulating hormone values are high, and oligospermia or azospermia is seen.Iatrogenic gonadal failure may occur in the aftermath of chemotherapy,radiation therapy, or surgery. Acquired gonadal failure also may have traumatic, postinfectious, autoimmune, or metabolic causes. Mumps orchitis is the most common infectious cause of gonadal failure. Autoimmune oophritis, a rare cause of ovarian failure, often is associated with Addison disease and other autoimmune endocrinopathies. In galactosemia, the effects of galactose or its metabolites on the prenatal or neonatal ovary may cause delayed or deficient puberty in girls or may be a cause of menstrual dysfunction.Among patients who have complete androgen insensitivity, phenotypic females have the XY genotype and present with primary amenorrhea and sparse or absent pubic and axillary hair despite normal thelarche. Prader-Willi syndrome is associated with hypogonadism, short stature,and obesity in both males and females. Micropenis and bilateral cryptorchidism are characteristic of boys; hypoplasia of the labia majora and clitoris are seen in girls, who also frequently have delayed or absent menarche. Hypogonadotropic hypogonadism occurs in both the Laurence-Moon syndrome and the Bardet-Biedl syndrome. Boys who have Noonan syndrome have abnormal testes (cryptorchidism, atrophy,anorchia), and their sexual maturation is consistently delayed. Many have primary gonadal failure with no spontaneous puberty, and infertility is common.In the "vanishing testes syndrome," 46,XY karyotype and masculine-appearing genitalia are associated with absent testes and failure of puberty. Presumably, testicular atrophy or destruction occurred some time after fetal differentiation of the external genitalia. Patients who have "resistant ovaries syndrome" have a 46,XX karyotype and typically present with sexual immaturity and primary amenorrhea. Further evaluation reveals small ovaries with primordial follicles despite elevated gonadotropin concentrations. The pathophysiology is believed to be due to abnormalities in gonadotropin receptors or antibodies to these receptors.A long list of other congenital disorders and syndromes may be associated with pubertal delay or failure. These include Bloom syndrome, LEOPARD syndrome, ataxia telangectasia syndrome, and the cerebrohepatorenal syndrome. Enzyme defects in steroid synthesis(eg, cholesterol desmolase complex, 3-beta-hydroxysteroid dehydrogenase) also can lead to pubertal failure. Genetic males who have these disorders are born with ambiguous genitalia.Other conditions, including eating disorders, malnutrition, and excessive exercise, may cause hypogonadotropic hypogonadism that results in pubertal delay or insufficiency. Girls are affected more often than boys and typically present with primary or secondary amenorrhea. Girls who are competitive athletes have significantly later pubarche and menarche than their peers, with the delays proportional to the intensity of their training. Similarly, eating disorders can disrupt normal pubertal progress profoundly. Weight gain usually corrects these abnormalities, although women who have eating disorders are at higher risk for menstrual irregularity independent of weight.Congenital anomalies of the female reproductive tract usually present with delayed onset of menses despite normal development of secondary sexual characteristics. Congenital anomalies associated with the apparent absence of menses include imperforate hymen, vaginal atresia, or vaginal aplasia. Other girls present in the early teen years with cyclic abdominal pain as a result of a normally responsive endometrium and spillage of menstrual fluid into the pelvis("concealed menarche").The extensive differential diagnosis of delayed puberty requires a systematic and focused approach to evaluation. Anosmia, galactorrhea,or symptoms of hypothyroidism may suggest a specific diagnosis. A careful history can identify excessive exercise or symptoms of chronic illness or psychiatric disease. A positive family history for pubertal delay would support the diagnosis of constitutional delay of puberty. Careful measurement of growth and determination of sexual maturity are the initial steps in physical assessment. Early signs of sexual development, unnoticed by the patient, may eliminate the need for a costly evaluation. A careful physical examination can help to identify stigmata of unsuspected congenital syndromes.Determination of serum gondotropin levels will distinguish disorders of congenital or acquired gonadal failure from other causes of delayed puberty. By adolescence (bone age 10 to 12 y), gonadal failure consistently produces markedly elevated levels of serum gonadotropins. When these are present, findings from the history and physical examination will often point to the specific diagnosis. Chromosomal analysis is indicated to confirm clinical suspicion of gonadal dysgenesis or Klinefelter syndrome. On the other hand, when serum gonadotropins are normal or low, constitutional delay of puberty is the most frequent diagnosis. However, further laboratory evaluation may be required to exclude the possibility of occult chronic illness or endocrinopathy. Reasonable screening studies include a complete blood count, erythrocyte sedimentation rate, and measurement of serum prolactin and serum thyrotropin-stimulating hormone. Even when results of these studies are normal, IGD remains a possible diagnosis because no studies reliably distinguish IGD from constitutional delay(Figs. 1and 2). Measurement of first morning urinary testosterone or stimulation testing using a GnRH agonist eventually may help to differentiate these conditions, but neither study currently is in broad general use.Ideally, management of pubertal delay should address the underlying cause if one can be identified. For patients whose hypothalamic hypogonadism is related to exercise, eating disorder, or chronic illness, every effort should be made to effect changes in overall health and nutrition that will allow spontaneous puberty to proceed. Constitutional delay of puberty may be managed by reassurance alone, given our understanding that even striking delays will have no effect on final adult height or development (Fig. 1). Expectant management is more acceptable to families when clinicians can point out early signs of puberty that were not obvious to the patient. However,short-term hormonal therapy to "jump start" puberty may be appropriate when severe delay has led to psychosocial dysfunction.Testosterone injections (eg, testosterone enanthate 100 mg intramuscularly administered monthly for 6 mo) are used for boys whose pubertal development already has begun. For boys who have not yet begun puberty, oral oxandrolone can be used at a starting dose of 1.25 mg daily. Such treatment should be monitored by specialists familiar with the potential side effects, including hepatic peliosis and premature epiphyseal closure. All boys treated with sex steroids should be monitored at 3- to 6-month intervals to assess response to treatment and skeletal maturation. Treatment is discontinued when it is expected that endogenous hormone production is established.Patients who have gonadotropin deficiency or hypogonadism require lifelong replacement with sex steroids and should be managed in consultation with a pediatric endocrinologist. Testosterone supplementation is begun in boys at approximately age 12 years. It may be administered by injection, transdermal patch, or topical gel. Doses initially are small and are increased based on careful follow-up of secondary sexual characteristics and growth to achieve a relatively normal puberty. Once puberty is complete, lifelong testosterone replacement is continued.For girls who have hypogonadism, replacement hormone therapy is begun to coincide with puberty in peers. Estrogen replacement may be started with a transdermal estradiol patch or small daily doses of conjugated estrogens or ethinyl estradiol that are increased gradually to adult replacement levels. As with boys, careful monitoring of secondary sexual characteristics and growth is required. Cyclic hormonal replacement, typically with low-dose oral contraceptives, should be instituted after 1 to 2 years of estrogen replacement or once breakthrough bleeding has occurred.Adolescents who have marked pubertal delay are at risk for psychosocial difficulties that should be sought actively in the initial evaluation. Delayed or absent puberty is more troublesome for boys than for girls. Significant delay may lead to poor body image, low self-esteem, teasing, bullying, parental overprotection, social withdrawal and isolation, declining academic performance, and school avoidance. Boys who look younger than their chronologic age have fewer opportunities for age-appropriate activities and social interaction,date less, and report feelings of unpopularity.Girls who have pubertal delay present with fewer psychosocial concerns. Indeed, some value their immature body habitus. For girls who have eating disorders, for example, early puberty consistently is associated with increasing dissatisfaction with weight or body image. The psychosocial burden imposed on the adolescent by delayed puberty should help to determine the extent of intervention. Simple reassurance may suffice when puberty is expected to proceed and psychosocial effects are few. Some form of hormonal therapy to accelerate puberty may be appropriate in cases of substantial psychosocial distress, even in cases of constitutional delay in which puberty is expected to progress spontaneously.

In vitro maturation of oocytes: uncommon indications

A rare case of Mayer–Rokitansky–Küster–Hauser syndrome presenting with primary amenorrhea and chronic headaches: a case report

Laparoscopic ovarian surgery to induce follicular response in patients with premature ovarian insufficiency, diminished ovarian reserve, or resistant ovary syndrome

The average age of menopause, denoted by the last menstrual period, occurs at an average age of 50.7 years in the western world (1) and this age has been found to be constant across generations, although one group have reported a secular trend to advancing menopausal age (2). The age of menopause in an individual is determined by both genetic and environmental factors (1, 3). Menopause before the age of 40 is most commonly taken to be the definition of ‘premature ovarian failure’ and this coincides approximately with youngest one percent of the frequency distribution of the age of menopause (Fig. 8.1.5.1). For every decade before 40 the prevalence of POF is estimated to decrease by a factor of 10. Thus, in presence of normal karyotype, 1:1000 of women at 30 has POF, 1:10 000 at 20 and 1:100 000 of women will present with gonadal failure and primary amenorrhoea. In terms of the mode of presentation, premature ovarian failure (POF) is the aetiology of 20% of cases with primary amenorrhoea and 10% of those with secondary amenorrhoea. Premature ovarian failure (POF) refers to the cessation of ovarian function at an earlier than expected age due to ovarian pathology. Primary ovarian failure is used in two contexts—to describe very early onset ovarian failure presenting with primary amenorrhoea and also to differentiate ovarian pathology from secondary ovarian failure, which refers to lack of ovarian activity as a result of gonadotropin deficiency. Primary ovarian insufficiency is recently favoured as an all-encompassing term that accounts for the variable course and occasional remission (4). The term hypergonadotropic hypogonadism is also used to emphasize ovarian origin. Resistant ovary syndrome (ROS) is an obsolete term, used to describe the coexistence of hypergonadotropic hypogonadism with normal ovarian follicles on histology of the ovary. It was soon realized that women with ROS progressed to complete ovarian failure and that ovarian follicles on histology were commonly found in established ovarian failure, negating the usefulness of this diagnostic label. Very early onset ovarian failure with a known genetic cause is often labelled inaccurately as ‘gonadal dysgenesis’ as in most situations it is thought that early ovarian development is normal.

Perrault syndrome (PRLTS) is a rare autosomal recessive disorder characterized by sensorineural hearing loss in both sexes and ovarian dysfunction in females with a 46, XX karyotype. Due to its rarity and diagnostic challenges, herein we report on a 26-year-old woman who presented with secondary amenorrhea, congenital deafness in one ear, and progressive hearing loss in the other. Physical examination showed poorly developed breasts and normal external genitalia. Lab tests revealed high follicle-stimulating hormone (FSH) levels, indicating ovarian failure. Imaging revealed a small uterus and streak ovaries without follicular activity. Initially misdiagnosed with various overlapping syndromes such as Turner, Turner mosaic, and Swyer syndromes, she was started on oral contraceptive pills which induced menstruation and minimal breast development but caused mood swings and depression, leading to inconsistent use. Later, karyotyping revealed a normal 46,XX karyotype, shrouding the case in mystery. A few years later, after additional investigations, her hearing loss and reproductive disruptions were connected, and she was diagnosed with PRLTS. The absence of neurological symptoms suggests type I PRLTS. This case underscores the diagnostic challenges of PRLTS and highlights the importance of genetic testing for accurate diagnosis. It also emphasizes the need for a multidisciplinary approach and further research to improve understanding and management of this rare condition.

Infertility due to Gonadotropin-Resistant Ovary Syndrome (GROS) is a rare type of hypergonadotropic hypogonadism. Here, we report an original case of GROS, associated with compound heterozygous follicle-stimulating hormone receptor (FSHR) variants, in a woman who achieved a live birth by in vitro maturation (IVM) of her oocytes. This 31-year-old woman consulted our assisted reproduction center for a second opinion after having been advised, because of pervasive high serum follicle-stimulating hormone (FSH) levels, to pursue in vitro fertilization (IVF) with donor oocytes. She presented with primary infertility and progressively prolonged menstrual cycles. Her serum FSH levels were indeed found to be high, but in discordance with a normal anti-Müllerian hormone (AMH) level and antral follicle count. Genetic investigation found the patient to be compound heterozygous for two FSHR variants: I160T, a known pathologic variant, and N558H, which has never been previously reported. As there was no ovarian response to high daily doses of exogenous gonadotropins, IVM was proposed to the patient with success and she finally delivered at term a healthy boy. Effects of the receptor variants were analyzed in heterologous cells. Whereas the I160T mutation blocked FSHR membrane trafficking and FSH-stimulated cAMP-dependent signaling in transfected CHO cells, the novel variant, N558H, functioned equivalently to wild-type FSHR in the assays employed. In conclusion, IVM should always be offered as a first-line therapy to infertile women presenting with GROS. The N558H variant discovered in FSHR is novel, but its functional significance, if any, is unresolved and merits further investigation as it may be associated with a recessive FSHR-related disorder.

To determine whether mutations in the FSH receptor gene are associated with premature ovarian failure (POF) or resistant ovary syndrome (ROS) in women in the UK. To determine whether an allelic variant of the FSH receptor gene affects fertility parameters in women with polycystic ovary syndrome (PCOS). A mutation screen using DNA from women with POF and ROS. Restriction digest of amplified DNA from women with POF, ROS, PCOS and controls to determine allelic variant status. Fertility parameters were compared between allelic variant subgroups of women with PCOS. The study population comprised 49 women with POF, 5 with ROS, 93 with PCOS and 51 controls. In women with PCOS, fertility and menstrual status was recorded and serum FSH and ovarian volume were measured. No mutation of the FSH receptor gene was found in women with POF or ROS. The allelic variant Thr307/Ser680 was found to be similarly prevalent in all study groups. The Thr307/Ser680 variant was found to have no phenotype in terms of fertility parameters in women with PCOS. Mutations of the FSH receptor gene are rare in women with premature ovarian failure or resistant ovary syndrome in the UK. Polymorphisms of the FSH receptor gene do not appear to have pathophysiological significance with regard to ovarian function.

Characterization of idiopathic premature ovarian failure

OBJECTIVE Premature ovarian insufficiency (POI) affects 1:100 women before the age of 40. The objectives include exploring correlations between body mass index, years since the onset of premature ovarian insufficiency, follicular stimulating hormone, and estradiol; and studying prevalence of five common serologic autoimmunologic para-meters during POI diagnosis.METHODS The records of idiopathic POI patients presenting with secondary amenorrhea who visited the Gynecologic Endocrinology Unit, Siriraj Hospital, between January 1, 2000 and December 31, 2016 were reviewed. Extracted data included body mass index, years since premature ovarian insufficiency onset, levels of follicular stimulating hormone and estradiol. Five common serologic autoimmunologic para-meters were also retrieved where available.RESULTS Among the 161 idiopathic POI patients analyzed, a signifi-cant reverse correlation was found between serum follicular stimulating hormone and estradiol (r=-0.209, p=0.008), while no correlations were identified between body mass index, years since the onset of pre-mature ovarian insufficiency, and serum estradiol (p=0.141, p=0.240, respectively). After excluding cases with abnormal karyotypes which can potentially cause POI, the remaining 146 cases was comprised of 72 cases with a normal 46,XX karyotype (the first group) and 74 cases who declined karyotype investigation (the second group). At least one of the serologic autoimmunologic parameters was investigated in 43 cases in the first group and in 20 cases in the second group. Anti-nuclear antibody was the most prevalent in the first group (25.0%) while anti-thyroglobulin was the most prevalent in the second group (30.7%).CONCLUSIONS Only serum follicular stimulating hormone and estra-diol exhibited significant reverse correlation in POI cases with secondary amenorrhea. Baseline serologic autoimmunologic parameters were positive but didn’t indicate autoimmune diseases during POI diagnosis.

Premature ovarian failure and dehydroepiandrosterone

Otolaryngology–Head and Neck SurgeryVolume 128, Issue 2 p. 296-297 Case Report Metastasis of Retinoblastoma to the Parotid Gland: Diagnosis by Fine Needle Aspiration Cytology B. Khademi MD, Corresponding Author B. Khademi MD [email protected] Department of Otolaryngology and Pathology, Shiraz Medical School, Shiraz University of Medical Sciences, Shiraz, IranB. Khademi, MD, Department of Otolaryngology, Khalili Hospital, Khalili Street, Shiraz, Iran; e-mail, [email protected]Search for more papers by this authorV. Derakhshandeh MD, V. Derakhshandeh MD Department of Otolaryngology and Pathology, Shiraz Medical School, Shiraz University of Medical Sciences, Shiraz, IranSearch for more papers by this authorM. Vasei MD, M. Vasei MD Department of Otolaryngology and Pathology, Shiraz Medical School, Shiraz University of Medical Sciences, Shiraz, IranSearch for more papers by this authorS. Torabi MD, S. Torabi MD Department of Otolaryngology and Pathology, Shiraz Medical School, Shiraz University of Medical Sciences, Shiraz, IranSearch for more papers by this author B. Khademi MD, Corresponding Author B. Khademi MD [email protected] Department of Otolaryngology and Pathology, Shiraz Medical School, Shiraz University of Medical Sciences, Shiraz, IranB. Khademi, MD, Department of Otolaryngology, Khalili Hospital, Khalili Street, Shiraz, Iran; e-mail, [email protected]Search for more papers by this authorV. Derakhshandeh MD, V. Derakhshandeh MD Department of Otolaryngology and Pathology, Shiraz Medical School, Shiraz University of Medical Sciences, Shiraz, IranSearch for more papers by this authorM. Vasei MD, M. Vasei MD Department of Otolaryngology and Pathology, Shiraz Medical School, Shiraz University of Medical Sciences, Shiraz, IranSearch for more papers by this authorS. Torabi MD, S. Torabi MD Department of Otolaryngology and Pathology, Shiraz Medical School, Shiraz University of Medical Sciences, Shiraz, IranSearch for more papers by this author First published: 01 September 2016 https://doi.org/10.1067/mhn.2003.62Read the full textAboutPDF ToolsExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. Volume128, Issue2February 2003Pages 296-297 RelatedInformation