Effects of Growth Hormone on the Nitric Oxide Pathway
The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details. |
ClinicalTrials.gov Identifier: NCT00470002 |
Recruitment Status :
Completed
First Posted : May 7, 2007
Last Update Posted : May 7, 2007
|
Tracking Information | ||||
---|---|---|---|---|
First Submitted Date ICMJE | May 4, 2007 | |||
First Posted Date ICMJE | May 7, 2007 | |||
Last Update Posted Date | May 7, 2007 | |||
Study Start Date ICMJE | May 2004 | |||
Primary Completion Date | Not Provided | |||
Current Primary Outcome Measures ICMJE |
Urinary nitrate excretion [ Time Frame: 10 days ] | |||
Original Primary Outcome Measures ICMJE | Same as current | |||
Change History | No Changes Posted | |||
Current Secondary Outcome Measures ICMJE |
Insulin-like growth factor-1 in serum [ Time Frame: 10 days ] | |||
Original Secondary Outcome Measures ICMJE | Same as current | |||
Current Other Pre-specified Outcome Measures | Not Provided | |||
Original Other Pre-specified Outcome Measures | Not Provided | |||
Descriptive Information | ||||
Brief Title ICMJE | Effects of Growth Hormone on the Nitric Oxide Pathway | |||
Official Title ICMJE | Effects of Growth Hormone (GH) on Parameters of the Nitric Oxide (NO) Pathway | |||
Brief Summary | The purpose of the study is to determine whether the treatment with growth hormone has an influence on the nitric oxide pathway in healthy males. | |||
Detailed Description | Nitric oxide (NO) is a potent endogenous vasodilator and has shown to inhibit key processes of atherosclerosis like monocyte adhesion, platelet aggregation, and vascular smooth muscle cell proliferation. Impaired endothelial NO production is a main feature of endothelial dysfunction, which by itself is an early step in the course of atherosclerotic vascular disease. Recent studies could confirm this close association between parameters of the NO pathway and cardiovascular disease and could further enhance the knowledge on the pathophysiological mechanisms. There is a significant relationship between insulin resistance and the endogenous NO synthase inhibitor asymmetric dimethylarginine (ADMA). Moreover, evidence could be provided that plasma levels of ADMA are a strong and independent predictor of mortality and cardiovascular outcome in haemodialysis patients. Patients with growth hormone deficiency are characterized by a 1.9 fold higher risk of death from cardiovascular disease. Again, there is good evidence, that alterations of the NO-pathway are involved in this increase of cardiovascular risk. A reduced endogenous systemic production of NO was found in patients with growth hormone deficiency, treatment with recombinant growth hormone normalized NO production. The effects of growth hormone on NO are possibly mediated by insulin-like growth factor-I (IGF-I), which stimulates NO synthesis in vitro. The onset of IGF-I increase in healthy volunteers treated with GH is evident after 12 h, the maximum effect takes place between 5 to 8 days. Also in adults with growth hormone deficiency, the major effects of growth hormone treatment on IGF-I levels are observed within 2 weeks. After discontinuation of growth hormone therapy, IGF-1 levels return to base line within 2-3 days. The aim of the present study is to further elucidate the in vivo effects of GH on the NO pathway and NO mediated cardiovascular functions. |
|||
Study Type ICMJE | Interventional | |||
Study Phase ICMJE | Phase 1 | |||
Study Design ICMJE | Allocation: Non-Randomized Intervention Model: Single Group Assignment Masking: None (Open Label) Primary Purpose: Basic Science |
|||
Condition ICMJE | Cardiovascular Disease | |||
Intervention ICMJE | Drug: Somatropin | |||
Study Arms ICMJE | Not Provided | |||
Publications * |
|
|||
* Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline. |
||||
Recruitment Information | ||||
Recruitment Status ICMJE | Completed | |||
Actual Enrollment ICMJE |
16 | |||
Original Actual Enrollment ICMJE | Same as current | |||
Actual Study Completion Date ICMJE | January 2005 | |||
Primary Completion Date | Not Provided | |||
Eligibility Criteria ICMJE | Inclusion Criteria:
Exclusion Criteria:
|
|||
Sex/Gender ICMJE |
|
|||
Ages ICMJE | 50 Years and older (Adult, Older Adult) | |||
Accepts Healthy Volunteers ICMJE | Yes | |||
Contacts ICMJE | Contact information is only displayed when the study is recruiting subjects | |||
Listed Location Countries ICMJE | Germany | |||
Removed Location Countries | ||||
Administrative Information | ||||
NCT Number ICMJE | NCT00470002 | |||
Other Study ID Numbers ICMJE | MES 03069 VP2-3900-4021576 IRB#3444 |
|||
Has Data Monitoring Committee | No | |||
U.S. FDA-regulated Product | Not Provided | |||
IPD Sharing Statement ICMJE | Not Provided | |||
Current Responsible Party | Not Provided | |||
Original Responsible Party | Same as current | |||
Current Study Sponsor ICMJE | Hannover Medical School | |||
Original Study Sponsor ICMJE | Same as current | |||
Collaborators ICMJE | Pharmacia | |||
Investigators ICMJE |
|
|||
PRS Account | Hannover Medical School | |||
Verification Date | May 2007 | |||
ICMJE Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP |