Ignite Creation Date:
2025-12-24 @ 11:34 PM
Ignite Modification Date:
2025-12-25 @ 9:23 PM
Study NCT ID:
NCT00392756
Status:
COMPLETED
Last Update Posted:
2022-07-11
First Post:
2006-10-25
Is NOT Gene Therapy:
False
Has Adverse Events:
False
Brief Title:
Examination of Idiopathic Hypogonadotropic Hypogonadism (IHH)and Kallmann Syndrome (KS)
Sponsor:
Organization:
Raw JSON
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Hypophysial responses to continuous and intermittent delivery of hypopthalamic gonadotropin-releasing hormone. Science. 1978 Nov 10;202(4368):631-3. doi: 10.1126/science.100883.'}, {'pmid': '9793755', 'type': 'BACKGROUND', 'citation': "Seminara SB, Hayes FJ, Crowley WF Jr. Gonadotropin-releasing hormone deficiency in the human (idiopathic hypogonadotropic hypogonadism and Kallmann's syndrome): pathophysiological and genetic considerations. Endocr Rev. 1998 Oct;19(5):521-39. doi: 10.1210/edrv.19.5.0344. No abstract available."}, {'pmid': '4609640', 'type': 'BACKGROUND', 'citation': 'Arimura A, Kastin AJ, Gonzalez-Barcena D, Siller J, Weaver RE, Schally AV. Disappearance of LH-releasing hormone in man as determined by radioimmunoassay. Clin Endocrinol (Oxf). 1974 Oct;3(4):421-5. doi: 10.1111/j.1365-2265.1974.tb02812.x. No abstract available.'}, {'pmid': '320223', 'type': 'BACKGROUND', 'citation': 'Pimstone B, Epstein S, Hamilton SM, LeRoith D, Hendricks S. Metabolic clearance and plasma half disappearance time of exogenous gonadotropin releasing hormone in normal subjects and in patients with liver disease and chronic renal failure. J Clin Endocrinol Metab. 1977 Feb;44(2):356-60. doi: 10.1210/jcem-44-2-356.'}, {'pmid': '6751801', 'type': 'BACKGROUND', 'citation': 'Clarke IJ, Cummins JT. The temporal relationship between gonadotropin releasing hormone (GnRH) and luteinizing hormone (LH) secretion in ovariectomized ewes. Endocrinology. 1982 Nov;111(5):1737-9. doi: 10.1210/endo-111-5-1737. No abstract available.'}, {'pmid': '9116125', 'type': 'BACKGROUND', 'citation': 'Karsch FJ, Bowen JM, Caraty A, Evans NP, Moenter SM. Gonadotropin-releasing hormone requirements for ovulation. Biol Reprod. 1997 Feb;56(2):303-9. doi: 10.1095/biolreprod56.2.303.'}, {'pmid': '3129947', 'type': 'BACKGROUND', 'citation': "Spratt DI, O'Dea LS, Schoenfeld D, Butler J, Rao PN, Crowley WF Jr. Neuroendocrine-gonadal axis in men: frequent sampling of LH, FSH, and testosterone. Am J Physiol. 1988 May;254(5 Pt 1):E658-66. doi: 10.1152/ajpendo.1988.254.5.E658."}, {'pmid': '10084591', 'type': 'BACKGROUND', 'citation': 'Hayes FJ, McNicholl DJ, Schoenfeld D, Marsh EE, Hall JE. Free alpha-subunit is superior to luteinizing hormone as a marker of gonadotropin-releasing hormone despite desensitization at fast pulse frequencies. J Clin Endocrinol Metab. 1999 Mar;84(3):1028-36. doi: 10.1210/jcem.84.3.5579.'}, {'pmid': '2403572', 'type': 'BACKGROUND', 'citation': 'Whitcomb RW, Crowley WF Jr. Clinical review 4: Diagnosis and treatment of isolated gonadotropin-releasing hormone deficiency in men. J Clin Endocrinol Metab. 1990 Jan;70(1):3-7. doi: 10.1210/jcem-70-1-3. No abstract available.'}, {'pmid': '1547923', 'type': 'BACKGROUND', 'citation': 'Simon D, Preziosi P, Barrett-Connor E, Roger M, Saint-Paul M, Nahoul K, Papoz L. Interrelation between plasma testosterone and plasma insulin in healthy adult men: the Telecom Study. Diabetologia. 1992 Feb;35(2):173-7. doi: 10.1007/BF00402551.'}, {'pmid': '3307391', 'type': 'BACKGROUND', 'citation': 'Lichtenstein MJ, Yarnell JW, Elwood PC, Beswick AD, Sweetnam PM, Marks V, Teale D, Riad-Fahmy D. Sex hormones, insulin, lipids, and prevalent ischemic heart disease. Am J Epidemiol. 1987 Oct;126(4):647-57. doi: 10.1093/oxfordjournals.aje.a114704.'}, {'pmid': '2202881', 'type': 'BACKGROUND', 'citation': 'Seidell JC, Bjorntorp P, Sjostrom L, Kvist H, Sannerstedt R. Visceral fat accumulation in men is positively associated with insulin, glucose, and C-peptide levels, but negatively with testosterone levels. Metabolism. 1990 Sep;39(9):897-901. doi: 10.1016/0026-0495(90)90297-p.'}, {'pmid': '1984562', 'type': 'BACKGROUND', 'citation': 'Pasquali R, Casimirri F, Cantobelli S, Melchionda N, Morselli Labate AM, Fabbri R, Capelli M, Bortoluzzi L. Effect of obesity and body fat distribution on sex hormones and insulin in men. Metabolism. 1991 Jan;40(1):101-4. doi: 10.1016/0026-0495(91)90199-7.'}, {'pmid': '1416554', 'type': 'BACKGROUND', 'citation': 'Barrett-Connor E. Lower endogenous androgen levels and dyslipidemia in men with non-insulin-dependent diabetes mellitus. Ann Intern Med. 1992 Nov 15;117(10):807-11. doi: 10.7326/0003-4819-117-10-807.'}, {'pmid': '8062607', 'type': 'BACKGROUND', 'citation': 'Andersson B, Marin P, Lissner L, Vermeulen A, Bjorntorp P. Testosterone concentrations in women and men with NIDDM. Diabetes Care. 1994 May;17(5):405-11. doi: 10.2337/diacare.17.5.405.'}, {'pmid': '6997122', 'type': 'BACKGROUND', 'citation': 'Ducimetiere P, Eschwege E, Papoz L, Richard JL, Claude JR, Rosselin G. Relationship of plasma insulin levels to the incidence of myocardial infarction and coronary heart disease mortality in a middle-aged population. Diabetologia. 1980 Sep;19(3):205-10. doi: 10.1007/BF00275270.'}, {'pmid': '3791676', 'type': 'BACKGROUND', 'citation': "Filippi G. Klinefelter's syndrome in Sardinia. Clinical report of 265 hypogonadic males detected at the time of military check-up. Clin Genet. 1986 Oct;30(4):276-84."}, {'pmid': '4147392', 'type': 'BACKGROUND', 'citation': 'Fromantin M, Gineste J, Didier A, Rouvier J. [Impuberism and hypogonadism at induction into military service. Statistical study]. Probl Actuels Endocrinol Nutr. 1973 May 3;16:179-99. No abstract available. French.'}, {'pmid': '6427277', 'type': 'BACKGROUND', 'citation': 'Filicori M, Butler JP, Crowley WF Jr. Neuroendocrine regulation of the corpus luteum in the human. Evidence for pulsatile progesterone secretion. J Clin Invest. 1984 Jun;73(6):1638-47. doi: 10.1172/JCI111370.'}, {'pmid': '960143', 'type': 'BACKGROUND', 'citation': 'Narasimha Rao P, Moore PH Jr. Synthesis of new steroid haptens for radioimmunoassay. Part I. 15beta-Carboxyethylmercaptotestosterone-bovine serum albumin conjugate. Measurement of testosterone in male plasma without chromatography. Steroids. 1976 Jul;28(1):101-9. doi: 10.1016/0039-128x(76)90129-x.'}, {'pmid': '8636341', 'type': 'BACKGROUND', 'citation': "Groome NP, Illingworth PJ, O'Brien M, Pai R, Rodger FE, Mather JP, McNeilly AS. Measurement of dimeric inhibin B throughout the human menstrual cycle. J Clin Endocrinol Metab. 1996 Apr;81(4):1401-5. doi: 10.1210/jcem.81.4.8636341."}, {'pmid': '2105862', 'type': 'BACKGROUND', 'citation': 'Landy H, Schneyer AL, Whitcomb RW, Crowley WF Jr. Validation of highly specific and sensitive radioimmunoassays for lutropin, follitropin, and free alpha subunit in unextracted urine. Clin Chem. 1990 Feb;36(2):340-4.'}, {'pmid': '9203460', 'type': 'BACKGROUND', 'citation': 'Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care. 1997 Jul;20(7):1183-97. doi: 10.2337/diacare.20.7.1183. No abstract available.'}, {'pmid': '12213860', 'type': 'RESULT', 'citation': 'Pitteloud N, Hayes FJ, Dwyer A, Boepple PA, Lee H, Crowley WF Jr. Predictors of outcome of long-term GnRH therapy in men with idiopathic hypogonadotropic hypogonadism. J Clin Endocrinol Metab. 2002 Sep;87(9):4128-36. doi: 10.1210/jc.2002-020518.'}, {'pmid': '9922906', 'type': 'RESULT', 'citation': 'Hayes FJ, Seminara SB, Crowley WF Jr. Hypogonadotropic hypogonadism. Endocrinol Metab Clin North Am. 1998 Dec;27(4):739-63, vii. doi: 10.1016/s0889-8529(05)70039-6.'}, {'pmid': '9010147', 'type': 'RESULT', 'citation': 'Nachtigall LB, Boepple PA, Pralong FP, Crowley WF Jr. Adult-onset idiopathic hypogonadotropic hypogonadism--a treatable form of male infertility. N Engl J Med. 1997 Feb 6;336(6):410-5. doi: 10.1056/NEJM199702063360604.'}, {'pmid': '9174769', 'type': 'RESULT', 'citation': 'Whitcomb RW, Crowley WF Jr. Hypogonadotropic hypogonadism: gonadotropin-releasing hormone therapy. Curr Ther Endocrinol Metab. 1997;6:353-5. No abstract available.'}, {'pmid': '2122732', 'type': 'RESULT', 'citation': 'Crowley WF, Whitcomb RW. Gonadotropin-releasing hormone deficiency in men: diagnosis and treatment with exogenous gonadotropin-releasing hormone. Am J Obstet Gynecol. 1990 Nov;163(5 Pt 2):1752-8. doi: 10.1016/0002-9378(90)91440-n.'}, {'pmid': '2502554', 'type': 'RESULT', 'citation': "Finkelstein JS, Spratt DI, O'Dea LS, Whitcomb RW, Klibanski A, Schoenfeld DA, Crowley WF Jr. Pulsatile gonadotropin secretion after discontinuation of long term gonadotropin-releasing hormone (GnRH) administration in a subset of GnRH-deficient men. J Clin Endocrinol Metab. 1989 Aug;69(2):377-85. doi: 10.1210/jcem-69-2-377."}, {'pmid': '3098771', 'type': 'RESULT', 'citation': 'Spratt DI, Carr DB, Merriam GR, Scully RE, Rao PN, Crowley WF Jr. The spectrum of abnormal patterns of gonadotropin-releasing hormone secretion in men with idiopathic hypogonadotropic hypogonadism: clinical and laboratory correlations. J Clin Endocrinol Metab. 1987 Feb;64(2):283-91. doi: 10.1210/jcem-64-2-283.'}, {'pmid': '3096182', 'type': 'RESULT', 'citation': "Spratt DI, Finkelstein JS, O'Dea LS, Badger TM, Rao PN, Campbell JD, Crowley WF Jr. Long-term administration of gonadotropin-releasing hormone in men with idiopathic hypogonadotropic hypogonadism. A model for studies of the hormone's physiologic effects. Ann Intern Med. 1986 Dec;105(6):848-55. doi: 10.7326/0003-4819-105-6-848."}, {'pmid': '3900124', 'type': 'RESULT', 'citation': 'Spratt DI, Crowley WF Jr, Butler JP, Hoffman AR, Conn PM, Badger TM. Pituitary luteinizing hormone responses to intravenous and subcutaneous administration of gonadotropin-releasing hormone in men. J Clin Endocrinol Metab. 1985 Nov;61(5):890-5. doi: 10.1210/jcem-61-5-890.'}, {'pmid': '6813732', 'type': 'RESULT', 'citation': 'Hoffman AR, Crowley WF Jr. Induction of puberty in men by long-term pulsatile administration of low-dose gonadotropin-releasing hormone. N Engl J Med. 1982 Nov 11;307(20):1237-41. doi: 10.1056/NEJM198211113072003.'}, {'pmid': '6767977', 'type': 'RESULT', 'citation': 'Crowley WF Jr, Beitins IZ, Vale W, Kliman B, Rivier J, Rivier C, McArthur JW. The biologic activity of a potent analogue of gonadotropin-releasing hormone in normal and hypogonadotropic men. N Engl J Med. 1980 May 8;302(19):1052-7. doi: 10.1056/NEJM198005083021903.'}, {'pmid': '17761590', 'type': 'RESULT', 'citation': 'Raivio T, Falardeau J, Dwyer A, Quinton R, Hayes FJ, Hughes VA, Cole LW, Pearce SH, Lee H, Boepple P, Crowley WF Jr, Pitteloud N. Reversal of idiopathic hypogonadotropic hypogonadism. N Engl J Med. 2007 Aug 30;357(9):863-73. doi: 10.1056/NEJMoa066494.'}, {'pmid': '11788640', 'type': 'RESULT', 'citation': 'Pitteloud N, Hayes FJ, Boepple PA, DeCruz S, Seminara SB, MacLaughlin DT, Crowley WF Jr. The role of prior pubertal development, biochemical markers of testicular maturation, and genetics in elucidating the phenotypic heterogeneity of idiopathic hypogonadotropic hypogonadism. J Clin Endocrinol Metab. 2002 Jan;87(1):152-60. doi: 10.1210/jcem.87.1.8131.'}, {'pmid': '21209029', 'type': 'RESULT', 'citation': 'Shaw ND, Seminara SB, Welt CK, Au MG, Plummer L, Hughes VA, Dwyer AA, Martin KA, Quinton R, Mericq V, Merino PM, Gusella JF, Crowley WF Jr, Pitteloud N, Hall JE. Expanding the phenotype and genotype of female GnRH deficiency. J Clin Endocrinol Metab. 2011 Mar;96(3):E566-76. doi: 10.1210/jc.2010-2292. Epub 2011 Jan 5.'}, {'pmid': '32034419', 'type': 'DERIVED', 'citation': 'Delaney A, Volochayev R, Meader B, Lee J, Almpani K, Noukelak GY, Henkind J, Chalmers L, Law JR, Williamson KA, Jacobsen CM, Buitrago TP, Perez O, Cho CH, Kaindl A, Rauch A, Steindl K, Garcia JE, Russell BE, Prasad R, Mondal UK, Reigstad HM, Clements S, Kim S, Inoue K, Arora G, Salnikov KB, DiOrio NP, Prada R, Capri Y, Morioka K, Mizota M, Zechi-Ceide RM, Kokitsu-Nakata NM, Tonello C, Vendramini-Pittoli S, da Silva Dalben G, Balasubramanian R, Dwyer AA, Seminara SB, Crowley WF, Plummer L, Hall JE, Graham JM, Lin AE, Shaw ND. Insight Into the Ontogeny of GnRH Neurons From Patients Born Without a Nose. J Clin Endocrinol Metab. 2020 May 1;105(5):1538-51. doi: 10.1210/clinem/dgaa065.'}]}, 'descriptionModule': {'briefSummary': 'The purpose of the study is to examine how Kallmann syndrome (KS) and idiopathic hypogonadotropic hypogonadism (IHH) affect reproductive hormones. These disorders are caused by a defect in Gonadotropin Releasing Hormone (GnRH) secretion. GnRH is a hormone released by a small gland in the brain called the hypothalamus. When GnRH is released, it signals another gland in the brain, the pituitary, to secrete the reproductive hormones that influence sex hormone (testosterone, estrogen) levels and gamete (sperm, egg cell) production.\n\nThis study involves a detailed evaluation and 24-48 hours stay at the hospital.\n\nIn this study, males and females ages 16 and older with IHH have a detailed evaluation which involves an overnight study at the hospital. Some men (18 years and older) may continue on to receive treatment with pulsatile GnRH. This treatment replaces the hormone which is absent in IHH and results in normalized testosterone and typically is effective in developing fertility.', 'detailedDescription': 'The specific aims of this study are:\n\n* To identify men and women with hypogonadotropic hypogonadism and to define the spectrum of abnormalities in GnRH secretion in these patients.\n* To study the physiology and control of the reproductive system in the human male and female.\n* To determine the relationship between glucose metabolism and testosterone levels in men with hypogonadotropic hypogonadism.\n* To characterize the neuroendocrine and metabolic phenotype of participants with IHH and use this information to make genotype-phenotype correlations.\n\nDespite variability in the triggers, timing, and pace of sexual maturity between species, all species utilize the final pathway of hypothalamic secretion of GnRH to initiate and maintain the reproductive axis. Thus, GnRH is required for reproductive competence in the human. The classic studies of Knobil and his colleagues in the 1970s clearly demonstrated that pulsatile release of GnRH from the hypothalamus is a prerequisite for physiologic gonadotrope function, with continuous stimulation resulting in a paradoxical decrease in gonadotrope responsiveness.\n\nAbsence, decreased frequency or decreased amplitude of pulsatile GnRH release results in the clinical syndrome of hypogonadotropic hypogonadism (HH). Deficient GnRH secretion may occur in isolation (idiopathic hypogonadotropic hypogonadism \\[IHH\\]), in association with anosmia (Kallmann syndrome \\[KS\\]) or as a result of a variety of structural and functional lesions of the hypothalamic-pituitary axis. The phenotypic expression of GnRH deficiency in the human demonstrates considerable heterogeneity, suggesting that patients with IHH and KS may represent part of a spectrum of isolated GnRH deficiency as opposed to representing discrete diagnostic subsets.\n\nDefining the physiology of GnRH is critical to understanding the clinical heterogeneity of isolated GnRH deficiency. This protocol will utilize the disease model of HH to increase our understanding of the physiology of GnRH secretion. Examining the baseline characteristics of patients with isolated GnRH deficiency allows the determination of the normal requirements for endogenous GnRH secretion in the human.\n\nRecent studies have revealed an association between hyperinsulinemia and low testosterone levels in men. This finding has been demonstrated in normal physiological conditions as well as in insulin resistant states. However, the causal nature and directionality of this relationship is not yet understood. Specifically, do lower testosterone levels cause insulin resistance resulting in hyperinsulinemia or vice versa? Because insulin resistance is an important risk factor for cardiovascular disease as well as type 2 diabetes, it is important to investigate this relationship for the implications it may have for prevention of and therapeutic interventions for these disorders.'}, 'eligibilityModule': {'sex': 'ALL', 'stdAges': ['CHILD', 'ADULT', 'OLDER_ADULT'], 'minimumAge': '16 Years', 'healthyVolunteers': False, 'eligibilityCriteria': 'Eligibility\n\nAges Eligible for Study:\n\n* Adolescents (16-17yrs)\n* Adults (18 years and older)\n\n * Genders Eligible for Study:\n* Male and Female\n\n * Accepts Healthy Volunteers:\n* No\n\nCriteria\n\nInclusion Criteria:\n\n* adolescent boys (age 16-17 years) and adult male individuals (age 18 years and older) with a single serum sample demonstrating low testosterone in association with low or inappropriately normal gonadotropin levels\n* adolescent girls (age 16-17 years) and adult female individuals (age 18 years and older) with a single serum sample demonstrating low estradiol (estrogen) in association with low or inappropriately normal gonadotropin levels\n* suitable male and female hypogonadotropic hypogonadal subjects\n\nExclusion Criteria:\n\n* no specific exclusion criteria'}, 'identificationModule': {'nctId': 'NCT00392756', 'briefTitle': 'Examination of Idiopathic Hypogonadotropic Hypogonadism (IHH)and Kallmann Syndrome (KS)', 'organization': {'class': 'OTHER', 'fullName': 'Massachusetts General Hospital'}, 'officialTitle': 'Role of Gonadotropin Pulsations in the Reversal of Hypogonadotropic Hypogonadism', 'orgStudyIdInfo': {'id': 'U54HD028138-024'}, 'secondaryIdInfos': [{'id': '5U54HD028138', 'link': 'https://reporter.nih.gov/quickSearch/5U54HD028138', 'type': 'NIH'}]}, 'armsInterventionsModule': {'armGroups': [{'type': 'NO_INTERVENTION', 'label': 'off treatment', 'description': 'Subjects undergo the baseline evaluation off treatment'}, {'type': 'EXPERIMENTAL', 'label': 'GnRH Treatment', 'description': 'Subjects receive long term pulsatile GnRH therapy', 'interventionNames': ['Drug: gonadotropin releasing hormone (GnRH)']}], 'interventions': [{'name': 'gonadotropin releasing hormone (GnRH)', 'type': 'DRUG', 'description': 'pulsatile GnRH is delivered to adult men (18+ yrs) via portable microinfusion pump. A small dose (30 microliters) is delivered subcutaneously every 120 minutes. The initial dose is 25 ng/Kg which is increased until normal serum testosterone levels are achieved.', 'armGroupLabels': ['GnRH Treatment']}]}, 'contactsLocationsModule': {'locations': [{'zip': '02114-2696', 'city': 'Boston', 'state': 'Massachusetts', 'country': 'United States', 'facility': 'Massachusetts General Hospital', 'geoPoint': {'lat': 42.35843, 'lon': -71.05977}}], 'overallOfficials': [{'name': 'Stephanie B Seminara, MD', 'role': 'PRINCIPAL_INVESTIGATOR', 'affiliation': 'Massachusetts General Hospital'}]}, 'sponsorCollaboratorsModule': {'leadSponsor': {'name': 'Massachusetts General Hospital', 'class': 'OTHER'}, 'responsibleParty': {'type': 'PRINCIPAL_INVESTIGATOR', 'investigatorTitle': 'Chief, Reproductive Endocrine Unit; Professor of Medicine, Harvard Medical School; Director, Harvard Reproductive Endocrine Sciences Center', 'investigatorFullName': 'Stephanie B. Seminara, MD', 'investigatorAffiliation': 'Massachusetts General Hospital'}}}}