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| Sponsored by: |
Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) |
|---|---|
| Information provided by: | Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) |
| ClinicalTrials.gov Identifier: | NCT00064987 |
Purpose
Men with idiopathic hypogonadotropic hypogonadism (IHH, Kallmann Syndrome) may have small testicular size, low testosterone levels, no history of puberty, and infertility. These men lack a hormone called gonadotropin releasing hormone (GnRH) that stimulates the development and maturation of the testes. This study will investigate the impact of hormonal treatments on men with IHH. The goal of hormonal therapy is to maximize the potential fertility in these individuals.
| Condition | Intervention | Phase |
|---|---|---|
|
Hypogonadism Kallmann Syndrome |
Procedure: Testicular biopsy Drug: gonadotropin releasing hormone (GnRH) Drug: follicle stimulating hormone (FSH) |
Phase II |
| Study Type: | Interventional |
| Study Design: | Treatment, Randomized, Open Label, Active Control, Parallel Assignment, Efficacy Study |
| Official Title: | Role of FSH in Human Gonadal Development |
| Estimated Enrollment: | 40 |
| Study Start Date: | April 2001 |
| Estimated Study Completion Date: | July 2011 |
| Estimated Primary Completion Date: | July 2010 (Final data collection date for primary outcome measure) |
Though steroid output of the testes is minimal during childhood, important changes take place that impact spermatogenic potential. Specifically, the number of Sertoli cells increases until testosterone secretion rises during puberty. In animal models, the proliferation of Sertoli cells appears to be regulated by follicle stimulating hormone (FSH) even though FSH levels in childhood are relatively low. At puberty, the number of Sertoli cells becomes fixed; however, the existing cell population then undergoes functional maturation. This switch from proliferation to maturation of Sertoli cells appears to result from rising levels of intratesticular testosterone.
FSH deficiency during testicular development results in decreased numbers of Sertoli cells, even if physiologic hormonal replacement therapy is introduced in adolescence or adulthood. The number of mature Sertoli cells appears to correlate with testicular size, sperm count, and future fertility. An improved understanding of the specific roles of FSH, luteinizing hormone (LH), and testosterone in testicular development may have direct clinical applications in the treatment of male infertility. This study will define the role of FSH in stimulating Sertoli cell proliferation in the human male.
Patients in this study will be randomized to receive either FSH and GnRH (Group 1) or GnRH alone (Group 2). Patients in Group 1 will receive subcutaneous FSH injections daily, titrated to achieve a FSH level of > 8.4 IU/L, for 4 months. Patients will then receive GnRH therapy for 18 months. GnRH will be administered via a portable infusion pump at 2-hour intervals to stimulate endogenous LH secretion. Patients in Group 2 will receive the same regimen of exogenous GnRH for 18 months without prior FSH administration.
All patients will undergo an initial assessment that includes an overnight 12-hour frequent blood sampling study, testicular ultrasound, and testicular biopsy. Patients will be followed through monthly study visits with blood tests and seminal fluid analysis. Patients will also have serial testicular ultrasounds to measure testicular growth. Patients in Group 1 will also have a second frequent blood sampling to measure LH, FSH, and testosterone and to confirm the absence of LH pulses.
Eligibility| Ages Eligible for Study: | 18 Years and older |
| Genders Eligible for Study: | Male |
| Accepts Healthy Volunteers: | No |
Inclusion Criteria
Exclusion Criteria
Contacts and Locations| Contact: Nelly Pitteloud, MD | 617-724-1830 | Npitteloud@partners.org |
| Contact: Andrew Dwyer, RN, NP | 617-726-8622 | Adwyer@partners.org |
| United States, Massachusetts | |
| Massachusetts General Hospital | Recruiting |
| Boston, Massachusetts, United States, 02114 | |
| Contact: Nelly Pitteloud, MD 617-724-1830 Npitteloud@partners.org | |
| Contact: Andrew Dwyer, RN, NP 617-726-8622 Adwyer@partners.org | |
| Principal Investigator: William F Crowley, Jr., MD | |
| Sub-Investigator: Frances J Hayes, MD | |
| Sub-Investigator: Nelly Pitteloud, MD | |
| Sub-Investigator: Andrew A Dwyer, RN, NP | |
| Principal Investigator: | William F Crowley, Jr., MD | Massachusetts General Hospital/Harvard Medical School |
More Information
| Responsible Party: | MGH ( William F. Crowley Jr., MD ) |
| Study ID Numbers: | U54HD028138-457 |
| Study First Received: | July 16, 2003 |
| Last Updated: | December 4, 2008 |
| ClinicalTrials.gov Identifier: | NCT00064987 |
| Health Authority: | United States: Food and Drug Administration |
|
Male reproduction hormones Hypogonadotropic hypogonadism FSH LH GnRH |
|
Gonadal Disorders Nervous System Malformations Endocrine System Diseases Kallmann Syndrome Septo-optic dysplasia Methyltestosterone Sex Differentiation Disorders Follicle Stimulating Hormone |
Testosterone 17 beta-cypionate Testosterone Hypogonadism Urogenital Abnormalities Genetic Diseases, Inborn Endocrinopathy Congenital Abnormalities Septo-Optic Dysplasia |
|
Pathologic Processes Disease Syndrome Physiological Effects of Drugs |
Nervous System Diseases Hormones, Hormone Substitutes, and Hormone Antagonists Hormones Pharmacologic Actions |
