[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"health-studies-list:{\"conditionNormalized\":\"primary-ovarian-insufficiency\",\"overallStatus\":[\"RECRUITING\",\"AVAILABLE\",\"NOT_YET_RECRUITING\"],\"orderBy\":\"LastUpdateSubmitDate:desc\",\"size\":25,\"offset\":0}":3,"health-study-condition:primary-ovarian-insufficiency":25},{"pageToken":4,"total":5,"offset":6,"count":5,"results":7},null,5,0,[8,50,88,118,149],{"id":9,"slug":10,"hasResults":11,"nctId":12,"briefTitle":13,"officialTitle":14,"acronym":4,"eligibilityCriteria":15,"healthyVolunteers":11,"sex":16,"minAge":17,"maxAge":18,"enrollmentInfo":19,"targetDuration":4,"studyType":22,"phases":4,"briefSummary":23,"conditions":24,"keywords":28,"overallStatus":37,"whyStopped":4,"lastUpdateSubmitDate":38,"lastUpdatePostDateStruct":39,"startDateStruct":42,"completionDateStruct":44,"leadSponsor":46,"locationsCount":49},"100620444","identifying-genome-variants-in-non-obstructive-azoospermia-noa-or-primary-ovarian-insufficiency-poi-100620444",false,"NCT07357701","Identifying Genome Variants in Non-Obstructive Azoospermia (NOA) or Primary Ovarian Insufficiency (POI)","Identifying Genome Variants and Evaluating PRDM9 and piRNA Clusters as Candidates for Infertility in a Cohort of Individuals With Non-Obstructive Azoospermia (NOA) or Primary Ovarian Insufficiency (POI)","* INCLUSION CRITERIA:\n\nIn order to be eligible to participate in this study, an individual must meet all of the following criteria:\n\n1. Provision of signed and dated informed consent form\n2. Stated willingness to comply with all study procedures and availability for the duration of the study\n3. Adult male or female, of reproductive age\n4. Clinical diagnosis of NOA, oligospermia, or POI.\n5. In good general health with no medical history suspected as the cause of infertility.\n\nEXCLUSION CRITERIA:\n\nAn individual who meets any of the following criteria will be excluded from participation in this study:\n\n1. Current use of medications that may cause infertility (chemotherapy, etc.)\n2. Pregnant or lactating\n3. Medical history indicating known common cause of infertility such as karyotype anomalies, Y-chromosome microdeletions, known monogenic causes, or other medical history affecting gamete production (i.e. injuries, surgical operations, infections, radiation, or chemotherapy).","ALL","18 Years","100 Years",{"count":20,"type":21},500,"ESTIMATED","OBSERVATIONAL","Background:\n\nInfertility affects 1 in 6 people. Often, the causes of infertility are unknown. Treatments are successful in only about 50% of cases. Infertility caused by non obstructive azoospermia in males and primary ovarian insufficiency in females can have genetic causes. Researchers want to learn more about these genes.\n\nObjective:\n\nTo identify genes that may cause infertility.\n\nEligibility:\n\nAdult men and women with non-obstructive azoospermia (NOA) or primary ovarian insufficiency (POI) of unknown cause.\n\nDesign:\n\nParticipants will provide a saliva sample. A kit will be sent to their home. The kit will contain a collection tube and a cotton swab. They will swirl the swab inside their mouth and then seal it in the tube. They will mail the tube back to the researchers.\n\nMale participants who are having a procedure done to collect tissue from their testes may opt to have leftover tissue provided to study researchers. This tissue would otherwise have been discarded. No new procedures will be performed just for this study.\n\nData may be collected from participants medical records.",[25,26,27],"Primary Ovarian Insufficiency","Azoospermia","Oligospermia",[29,30,31,32,33,34,35,25,36],"NOA","POI","Premature Ovarian Insufficiency","oligospermia","azoospermia","diminished ovarian reserve","nonobstructive azoospermia","Infertility","RECRUITING","2026-03-13",{"date":40,"type":41},"2026-03-16","ACTUAL",{"date":43,"type":41},"2026-03-11",{"date":45,"type":21},"2031-01-01",{"name":47,"class":48},"Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD)","NIH",2,{"id":51,"slug":52,"hasResults":11,"nctId":53,"briefTitle":54,"officialTitle":55,"acronym":56,"eligibilityCriteria":57,"healthyVolunteers":58,"sex":59,"minAge":60,"maxAge":61,"enrollmentInfo":62,"targetDuration":4,"studyType":22,"phases":4,"briefSummary":64,"conditions":65,"keywords":70,"overallStatus":76,"whyStopped":4,"lastUpdateSubmitDate":77,"lastUpdatePostDateStruct":78,"startDateStruct":80,"completionDateStruct":82,"leadSponsor":84,"locationsCount":87},"100582654","effects-of-estrogen-on-heart-health-in-women-with-primary-ovarian-insufficiency-100582654","NCT06866119","Effects of Estrogen on Heart Health in Women With Primary Ovarian Insufficiency","Effects of Estrogen Replacement on Cardiometabolic Endpoints in Women With Primary Ovarian Insufficiency","ENCODE","Inclusion criteria (I):\n\n* female sex\n* age 30-40\n* CASE PARTICIPANTS ONLY: clinically documented POI diagnosis within 6 months\n* CASE PARTICIPANTS ONLY: planning to clinically initiate 100mcg transdermal 17beta-estradiol twice weekly and micro-ionized progesterone (either 100mg daily or 200mg cyclically)\n* CONTROL PARTICIPANTS ONLY: regular menstrual cycles every 21-35 days\n\nExclusion criteria (E):\n\n* CASE PARTICIPANTS ONLY: genetic POI etiology\n* CASE PARTICIPANTS ONLY: any prior initiation of ERT\n* systemic estrogen, progesterone or testosterone therapy within the past 6 months (including contraception, except for locally acting intrauterine devices - IUDs)\n* lipid lowering therapy within the past 6 months\n* use of antihypertensive medication within the past 6 months\n* current treatment with prescription, systemic (oral, IV, or IM) steroids or anti-inflammatory\u002Fimmune suppressant medical therapies (excluding topical therapies, UV therapy, ASA-derivative therapies, or NSAIDS) for autoimmune\u002Finflammatory diseases (psoriasis, RA, IBD, lupus), post-transplant care, asthma, or pain syndromes\n* use of oral steroids or prescription oral anti-inflammatory\u002Fimmune suppressant medication for \\>7 days within the past 1 month\n* use of IV or IM steroids or IV or IM anti-inflammatory\u002Fimmune suppressant medication within the past 3 months\n* self-reported history of breast and\u002For estrogen dependent malignancy\n* self-reported history of deep vein thromboembolism, pulmonary embolism or stroke\n* self-reported severe liver disease such as cirrhosis\n* self-reported hypercoagulable disorder\n* uncontrolled hypertension at baseline Visit #1- systolic blood pressure (SBP) ≥180 and\u002For diastolic blood pressure (DBP) ≥110\n* tobacco use within 6 months\n* self-reported history of myocardial infarction, stroke, coronary revascularization or diabetes as a CVD risk equivalent\n* stable or unstable angina\n* self-reported history of heart failure\n* pregnancy or breastfeeding\n* concurrent enrollment in conflicting research study",true,"FEMALE","30 Years","40 Years",{"count":63,"type":21},45,"The goal of this observational study is to study the effects of treating women with Primary Ovarian Insufficiency (POI) with estrogen replacement therapy to bolster the evidence backing cardiometabolic preventive care in women with POI. The main question it aims to answer is:\n\nDoes 6 months of estrogen replacement therapy for women with POI improved markers of heart health?\n\nWomen newly diagnosed with POI (within 6 months) who are planning to start estrogen replacement therapy from their clinical provider will undergo assessment of markers of heart health before and after 6 months of treatment. These markers will also be compared to those obtained from healthy women without POI.",[25,66,67,68,69],"Premature Menopause","Metabolic Complications","Endothelial Function (FMD)","Estrogen Replacement Therapy",[71,72,73,74,30,75],"primary ovarian insufficiency","premature menopause","estrogen replacement therapy","cardiovascular disease prevention","ERT","NOT_YET_RECRUITING","2026-01-05",{"date":79,"type":41},"2026-01-07",{"date":81,"type":21},"2026-03-01",{"date":83,"type":21},"2026-06",{"name":85,"class":86},"Massachusetts General Hospital","OTHER",1,{"id":89,"slug":90,"hasResults":11,"nctId":91,"briefTitle":92,"officialTitle":93,"acronym":4,"eligibilityCriteria":94,"healthyVolunteers":11,"sex":59,"minAge":95,"maxAge":96,"enrollmentInfo":97,"targetDuration":99,"studyType":22,"phases":4,"briefSummary":100,"conditions":101,"keywords":104,"overallStatus":37,"whyStopped":4,"lastUpdateSubmitDate":109,"lastUpdatePostDateStruct":110,"startDateStruct":112,"completionDateStruct":114,"leadSponsor":116,"locationsCount":87},"100543559","assessment-of-endometrial-thickness-among-adolescent-and-young-adult-patients-on-estrogen-replacement-therapy-using-daily-oral-micronized-progesterone-versus-the-etonogestrel-implant-100543559","NCT06357442","Assessment of Endometrial Thickness Among Adolescent and Young Adult Patients on Estrogen Replacement Therapy Using Daily Oral Micronized Progesterone Versus the Etonogestrel Implant.","Assessment of Endometrial Thickness Among Adolescent and Young Adult Patients on Estrogen Replacement Therapy Using Continuous Oral Micronized Progesterone Versus the Etonogestrel Implant: a Prospective Pilot Study","Inclusion Criteria:\n\n* Age 12-25 years at baseline\n* Female assigned at birth, with uterus\n* Diagnosis of primary ovarian insufficiency or hypogonadotropic hypogonadism, requiring estrogen replacement therapy\n* Receiving estradiol therapy-oral (1-2mg) or transdermal (0.05-0.1mg)-for at least 3 months\n* Never used progesterone therapy or discontinued progesterone therapy at least 90-days prior to enrollment\n* Consents to initiating progesterone therapy\n\nExclusion Criteria:\n\n* Uterine abnormality (e.g., Müllerian Anomaly, uterine fibroids)\n* Inability to characterize the endometrial lining on ultrasound\n* History of chemotherapy or radiation therapy\n* Inability to complete study questionnaire","12 Years","25 Years",{"count":98,"type":21},34,"6 Months","The goal of this observational study is to compare endometrial stripe thickness in adolescent and young adult (AYA) patients with a uterus on estrogen replacement therapy using oral progesterone versus the etonogstrel implant for endometrial protection.\n\nThe main questions it aims to answer are:\n\nAim 1: Characterize the mean endometrial thickness in AYA on estrogen hormone replacement therapy before initiation of progesterone therapy\n\nAim 2: Characterize the mean changes and variability in endometrial thickness in AYA treated for 6 months with either the etonogestrel implant or continuous oral progesterone\n\nAim 3: Assess satisfaction, side effects, bleeding patterns, any progesterone modifications, and adherence in AYA treated for 6 months with either etonogestrel implant or continuous progesterone\n\nParticipants will be asked to:\n\n* Get two pelvic ultrasounds\n* Fill out two surveys\n* Continue their current hormone replacement therapy\n* Initiate one of two progesterone therapies (prometrium 100mg daily or Nexplanon)\n\nResearchers will compare the change in endometrial thickness after 6 months of progesterone use to see if there is a significant difference in the mean change between the prometrium and Nexplanon groups.",[25,102,103],"Hypogonadotropic Hypogonadism","Hormone Replacement Therapy",[105,106,71,107,108],"hormone replacement therapy","hypogonadism","endometrial protection","progesterone replacement therapy","2024-12-03",{"date":111,"type":41},"2024-12-06",{"date":113,"type":41},"2024-07-01",{"date":115,"type":21},"2026-07-01",{"name":117,"class":86},"University of Colorado, Denver",{"id":119,"slug":120,"hasResults":11,"nctId":121,"briefTitle":122,"officialTitle":123,"acronym":124,"eligibilityCriteria":125,"healthyVolunteers":58,"sex":59,"minAge":126,"maxAge":127,"enrollmentInfo":128,"targetDuration":95,"studyType":22,"phases":4,"briefSummary":130,"conditions":131,"keywords":137,"overallStatus":37,"whyStopped":4,"lastUpdateSubmitDate":140,"lastUpdatePostDateStruct":141,"startDateStruct":143,"completionDateStruct":145,"leadSponsor":147,"locationsCount":87},"100528927","polycystic-ovary-syndrome-mitochondrial-dysfunction-obesity-insulin-resistance-infertility-pomodori-cohort-100528927","NCT06167135","Polycystic Ovary Syndrome, Mitochondrial Dysfunction, Obesity, Insulin Resistance Infertility (POMODORI) Cohort","Polycystic Ovary Syndrome, Insulin Resistance, Infertility, Obesity, and the Associated Mitochondrial Dysfunction With These Disorders in Hungarian Patients","POMODORI","Inclusion Criteria:\n\n* Presence of polycystic ovary syndrome (PCOS) or insulin resistance (IR) associated with other multisystemic phenotypes, mitochondrial dysfunction\n* history of infertility associated with other multisystemic phenotypes, mitochondrial dysfunction\n* a known history of mitochondrial dysfunction and PCOS and\u002For IR\n* general health is good and there is no serious general medical condition that would prevent participation would make participation highly risky\n\nExclusion Criteria:\n\n* poor cooperation\n* refusal to participate in the study","20 Years","45 Years",{"count":129,"type":21},150,"Enrolling of 150 female patients of fertile age diagnosed with PCOS, insulin resistance, infertility, or mitochondrial disease, and the same number of age- and sex-matched controls are planned.\n\nDuring the research biomarkers already with mitochondrial dysfunction in the scientific literature and common mtDNA abnormalities (deletions, point mutations, copy number changes, etc.) are examined.",[132,133,134,25,135,136],"Infertility, Female","Polycystic Ovary Syndrome","Insulin Resistance","Mitochondrial Alteration","Obesity",[133,134,138,136,139,135,25],"Female Infertility","Mitochondrial Dysfunction","2023-12-12",{"date":142,"type":41},"2023-12-18",{"date":144,"type":41},"2021-09-10",{"date":146,"type":21},"2033-09-30",{"name":148,"class":86},"Semmelweis University",{"id":150,"slug":151,"hasResults":11,"nctId":152,"briefTitle":153,"officialTitle":154,"acronym":30,"eligibilityCriteria":155,"healthyVolunteers":11,"sex":59,"minAge":156,"maxAge":157,"enrollmentInfo":158,"targetDuration":4,"studyType":22,"phases":4,"briefSummary":160,"conditions":161,"keywords":162,"overallStatus":37,"whyStopped":4,"lastUpdateSubmitDate":166,"lastUpdatePostDateStruct":167,"startDateStruct":169,"completionDateStruct":171,"leadSponsor":173,"locationsCount":87},"100464406","investigation-of-copy-number-variations-and-genetic-variants-in-poi-100464406","NCT05327283","Investigation of Copy Number Variations and Genetic Variants in POI","Insight Into the Genomics of Idiopathic Premature Ovarian Insufficiency","Inclusion Criteria:\n\n* age at diagnosis \\\u003C38 years;\n* a normal 46,XX karyotype (no FRM1 premutation);\n* at least one marker of ovarian reserve not age-appropriate:\n\n  * baseline FSH levels \\> cut-off \\[1\\] and\u002For\n  * age-specific AMH \\\u003C cut-off \\[2\\] and\u002For\n  * AFC \\\u003C 5; and\u002For\n* cancellation of a PMA cycle because of poor response (\\\u003C3 follicles) to high-dose gonadotrophins (250 U\u002Fdie) and\u002For\n* retrieval of \\\u003C 4 oocytes in response to high-dose stimulation protocols (3000 U of gonadotrophins).\n\nExclusion Criteria:\n\n* patients with POI-related conditions, such as ovarian surgery or previous chemo- or radio-therapy; endometriosis or known autoimmune or metabolic diseases.","15 Years","38 Years",{"count":159,"type":21},100,"Primary ovarian insufficiency (POI), also known as premature ovarian failure, is an ovarian defect characterized by the premature (before the age of 40 years) depletion of ovarian follicles. POI affects about 1% of women, reaching 30% in some familial cases.\n\nThis heterogeneous disorder is characterized by progressive cessation of the ovarian function with temporary or intermittent amenorrhea associated with elevated serum FSH concentration and low AMH dosage. Low serum AMH dosage is able to detect a diminished ovarian pool occurring before the onset of FSH elevation and the ultimate deficiency leading to amenorrhea.\n\nPOI causes infertility and a poor ovarian response in IVF stimulations, and it has important health consequences for affected patients, including psychological distress, infertility, osteoporosis, autoimmune disorders, ischaemic heart disease.\n\nAlthough the cause of POI remains unknown in about 80% of the cases, several mechanisms have been proposed to explain ovarian dysfunction. Currently, a wide spectrum of causes has been linked to POI, including genetic, autoimmune, infectious, or iatrogenic ones.\n\nGenetic causes are highly heterogeneous and might explain at least some of the sporadic idiopathic cases, which comprise 50-90% of cases. Ten to fifteen percent of cases are X-linked abnormalities, mainly Turner Syndrome (45,X) or X structural abnormalities such as X deletions, X inversions, isochromosomes or X-autosome translocations. Also fragile X mental retardation 1 (FMR1) gene permutation (defined as having 55 to 200 CGG repeats in the 5' untranslated region of the gene) is another frequent genetic etiology.\n\nIrrespectively, the majority of cases remains idiopathic, and identifying precise causative genes for POI has been challenging.",[25],[163,164,165],"Premature ovarian failure","array-CGH","NGS","2022-04-22",{"date":168,"type":41},"2022-04-25",{"date":170,"type":4},"2012-01-31",{"date":172,"type":21},"2030-12-31",{"name":174,"class":86},"Ospedale Policlinico San Martino"]