Ataxia TelangiectasiaPhase 4GHATNCT01052623
Status of Growth Hormone/ Insulin-like Growth Factor-1 (GH/IGF-1) Axis and Growth Failure in Ataxia Telangiectasia (AT)
A Phase 4 study testing Somatropin, Clonidine, L-Arginin-Hydrochloride, Estradiol valerate in people with Ataxia Telangiectasia and Growth Failure, run by Johann Wolfgang Goethe University Hospital at 1 site in Germany.
Trial summary
This study will evaluate the status of the growth hormone/ insulin-like growth factor-1 (GH/IGF-1) axis in relation to growth failure, body weight and composition and neuroprotection in children with Ataxia telangiectasia (AT). Read more about this study
- Who is it for?
- Ages 3 to 18 years
- Conditions the study is for
- Ataxia Telangiectasia, Growth Failure
- What is being tested?
- Somatropin, Clonidine, L-Arginin-Hydrochloride, Estradiol valerate
- Type of treatment
- Pill or oral medicine, Injection or infusion
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 24 participants
- Where
- 1 siteGermany
- Study dates
- Jan 2010to Sep 2012
- Phase
- Phase 4
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 3 to 18 years
- All sexes
- No healthy volunteers
- Child, Adult
Who may be able to join
- Have a diagnosis of AT
- Have no fusion of epiphyses/closed growth plates as determined by X-ray of left wrist and hand (special skeletal age film)
- Be between 3 years to 18 years old and have not completed puberty
- Consent to permit blood and/or tissue samples for storage
- Demonstrate growth failure: height below the 10th percentile for chronological age
- Have a primary care physician at home
Show all 9Show fewer
- Demonstrate growth failure, defined as growth velocity (measured as linear growth) that is less than 5% to 10% of that expected for children of the same age group, over the past 12 months
- Willingness to remain hospitalized for several days
- Provide evidence of serum IGF-1 level performed within the preceding 6 months and the results fall below 25% range of normal limits for age
Who cannot join
- Have fusion of epiphyseal plates
- Be under the age of 3 years or have reached completion of puberty
- Have a serum IGF-1 level that is above the 25% range of normal limits for age
- Be above the 10th percentile height for chronological age
- Demonstrate any history of anaphylactic reaction or hypersensitivity to one of the GH formulation
- Have any active or suspected neoplasia
Show all 15Show fewer
- Demonstrate signs of intracranial hypertension as evidenced by papilledema upon examination by fundoscopy
- Have any condition that, in the investigator's opinion, places the patient at undue risk by participating in the study
- Be unwilling to undergo testing or procedures associated with this protocol
- Have acute or chronic infections
- Have a hypersensitivity to one of the drugs: Clonidine hydrochlorid, Arginine hydrochlorid, Estradiol valerate, Somatropin
- Have a presence of bradycardia, cardiac arrhythmia, have symptoms of a sick sinus syndrome
- Suffer from depression
- Have acute or recurrent thrombosis
- Have acute liver diseases
Trial locations and contacts
1 site in 1 country.
Germany1 site, 1 recruiting
- Recruiting
Children's Hospital, Goethe-University
Frankfurt am Main, 60590
Stefan Zielen, Prof. Dr., 0049-69-6301-83063, Stefan.Zielen@kgu.de
Ralf Schubert, Dr., 0049-69-6301-83611, Ralf.Schubert@kgu.de
About this study
Official title: Status of the Growth Hormone/ Insulin-like Growth Factor-1 (GH/IGF-1) Axis in Relation to Growth Failure, Body Weight and Neuroprotection in Children With Ataxia Telangiectasia
This study will evaluate the status of the growth hormone/ insulin-like growth factor-1 (GH/IGF-1) axis in relation to growth failure, body weight and composition and neuroprotection in children with Ataxia telangiectasia (AT).
Read the detailed description
Growth failure and GH/IgF-1 deficiency has been described in patients diagnosed with Ataxia telangiectasia (AT) [Boder et al.,1958]. This condition is a fatal inherited disease caused by a mutation of the ATM gene on chromosome 11 leading to chromosomal instability, immunodeficiency, cancer susceptibility and and endocrinological abnormalities. In this regard, several groups demonstrated a cross-linking of ATM with growth factor pathways. Participation of the ATM protein in insulin signaling through phosphorylation of eIF-4E-binding protein 1 has been postulated [Yang et al.,2000]. Peretz et al.[2001] described that expression of the insulin-like growth factor-I receptor is (IGF-I R) ATM dependent in a pathway regulating radiation response. In addition, Shahrabani-Gargir et al.[2004] found that the ATM gene controls IGF-I R gene expression in a DNA damage response pathway. Suzuki et al.[2004] described that IGF-I phosphorylates AMPK-alpha, a key regulator of cholesterol and fatty acid synthesis, acts in an ATM-dependent manner . We have recently demonstrated reduced levels of circulating Insulin-like growth factor-I (IGF-I) and its main binding protein 3 (IGFBP-3) in AT patients accompanied with decreased body mass index [Schubert et al.,2005]. Furthermore, apart from regulating somatic growth and metabolism, evidence suggests that the GH/IGF-I axis is involved in the regulation of brain growth, development and myelination. Moreover, GH and particularly IGF-1 have potential neuroprotective effects in different in vitro and in vivo experimental models. In addition we have recently shown that extracerebellar MRI-lesions in AT go along with deficiency of the GH/IGF-1 Axis, markedly reduced body weight, high ataxia scores and advanced age [Kieslich et al.,2009]. Supplementation with these growth hormones might overcome the progressive dystrophy and may have clinical benefits against the progression of neurodegeneration and immunodeficiency.
We found that supplementation with GH significantly increased longevity of Atm-deficient mice and improve T-cell immunity and locomotor behaviour [Schubert et al.,2009]. Surprisingly IGF-1 was not generated in the ATM deficient mice, indicating that the GH/IGF-1 signalling is impaired. Taken this into account a accurate diagnostic approach of the GH/IGF-1 axis is mandatory including a IGF-1 generation test before long term treatment either with GH or IGF-1 is justified in humans.
- Conditions
- Ataxia Telangiectasia, Growth Failure
- Being tested
- Somatropin, Clonidine, L-Arginin-Hydrochloride, Estradiol valerate
- Keywords
- GH/IGF-1, Ataxia telangiectasia (AT), IGF-1 Generation Test, Growth hormone
- Medical subject headings
- Ataxia Telangiectasia, Failure to Thrive
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Somatropin, Clonidine, L-Arginin-Hydrochloride, Estradiol valerateDrug
Also called Catapressan, Growth hormone, NutropinAq, Progynova 21 mite
1 mg Estradiol valerate with for two days before GH-testing pre pubertal girls older than 8 years and pre pubertal boys older than 10 years. L-Arginin-Hydrochloride in the vein (0.5 g/kg KG maximum dose 30g) over 30 minutes. Clonidine orally (0,075 mg/m2 BSA). Somatropin-NutropinAq subcutaneum,a single one shot (dose 0.03 mg/KG, daily, over five days).
| Study group | Role | What they receive |
|---|---|---|
| Growth hormone-testing (GH/IGF-1-testing) | Experimental | Patients (girls over 8 years and boys over 10 years) are primed with estradiol 1 mg orally for 2 days, to help avoid false results of growth hormone (GH) levels in blood samples. Then provocation testing is done, with two tests back to back. It determines blood levels of GH and the body's response to testing with drugs called arginine and clonidine. Patients are admitted to the pediatric inpatient unit and will have an intravenous (IV) line placed in the arm. Arginine is given by IV over 30 minutes, and blood samples are taken as indicated.
The next day, the clonidine test is performed according to current guidelines. Then the IGF-1 generation test is done to see if the patient has the ability to generate IGF-1 in response to injections of GH for 5 consecutive days. Receives: Drug: Somatropin, Clonidine, L-Arginin-Hydrochloride, Estradiol valerate |
What is being measured
The primary outcome is the main question the study is designed to answer.
To evaluate the GH increase after Arginine Provocation Test
Measured: at minute 0, 30, 60, 90 und 120 after infusion
Secondary outcomes (1)
The GH increase after Clonidine Provocation Test. To evaluate the safety and efficacy of the IGF-1 generation test. To correlate GH/IgF-1 deficiency to BMI To correlate GH/IgF-1 deficiency to MRI findings
Measured: at minute 0, 30, 60, 90 und 120 after dosing of Clonidin. IgF-1 generation test after 5 days.
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted20 Jan 2010 (estimated)
- Study startJan 2010
- Primary completionDec 2011 (estimated)
- Study completionSep 2012 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (10)Papers the sponsor has linked to this study.
- Other trials for Ataxia TelangiectasiaStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 4
- Primary purpose
- Diagnosis
- Allocation
- Non-randomised
- Intervention model
- Single group
- Masking
- None (open label)
- Enrolment
- 24 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Johann Wolfgang Goethe University Hospital
- Sponsor type
- University, hospital or other
- Investigators
- Stefan Zielen, Prof. Dr., Principal investigator, Children´s Hospital, Goethe-University
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT01052623
- Sponsor's protocol ID
- FRA.GHAT.2009
- Acronym
- GHAT
- Status last verified
- Jul 2010
- First submitted
- 19 Jan 2010
- Last updated
- 5 Jul 2010
- Results posted
- No
- Data monitoring committee
- No
Publications
BODER E, SEDGWICK RP. Ataxia-telangiectasia; a familial syndrome of progressive cerebellar ataxia, oculocutaneous telangiectasia and frequent pulmonary infection. Pediatrics. 1958 Apr;21(4):526-54. No abstract available.
PubMed 13542097Lavin MF. Ataxia-telangiectasia: from a rare disorder to a paradigm for cell signalling and cancer. Nat Rev Mol Cell Biol. 2008 Oct;9(10):759-69. doi: 10.1038/nrm2514.
PubMed 18813293Schubert R, Reichenbach J, Zielen S. Growth factor deficiency in patients with ataxia telangiectasia. Clin Exp Immunol. 2005 Jun;140(3):517-9. doi: 10.1111/j.1365-2249.2005.02782.x.
PubMed 15932513Isgaard J, Aberg D, Nilsson M. Protective and regenerative effects of the GH/IGF-I axis on the brain. Minerva Endocrinol. 2007 Jun;32(2):103-13.
PubMed 17557036Yang DQ, Kastan MB. Participation of ATM in insulin signalling through phosphorylation of eIF-4E-binding protein 1. Nat Cell Biol. 2000 Dec;2(12):893-8. doi: 10.1038/35046542.
PubMed 11146653Peretz S, Jensen R, Baserga R, Glazer PM. ATM-dependent expression of the insulin-like growth factor-I receptor in a pathway regulating radiation response. Proc Natl Acad Sci U S A. 2001 Feb 13;98(4):1676-81. doi: 10.1073/pnas.98.4.1676. Epub 2001 Feb 6.
PubMed 11172010Shahrabani-Gargir L, Pandita TK, Werner H. Ataxia-telangiectasia mutated gene controls insulin-like growth factor I receptor gene expression in a deoxyribonucleic acid damage response pathway via mechanisms involving zinc-finger transcription factors Sp1 and WT1. Endocrinology. 2004 Dec;145(12):5679-87. doi: 10.1210/en.2004-0613. Epub 2004 Sep 2.
PubMed 15345673Suzuki A, Kusakai G, Kishimoto A, Shimojo Y, Ogura T, Lavin MF, Esumi H. IGF-1 phosphorylates AMPK-alpha subunit in ATM-dependent and LKB1-independent manner. Biochem Biophys Res Commun. 2004 Nov 19;324(3):986-92. doi: 10.1016/j.bbrc.2004.09.145.
PubMed 15485651Kieslich M, Hoche F, Reichenbach J, Weidauer S, Porto L, Vlaho S, Schubert R, Zielen S. Extracerebellar MRI-lesions in ataxia telangiectasia go along with deficiency of the GH/IGF-1 axis, markedly reduced body weight, high ataxia scores and advanced age. Cerebellum. 2010 Jun;9(2):190-7. doi: 10.1007/s12311-009-0138-0.
PubMed 19898915Schubert R, Schmitz N, Pietzner J, Tandi C, Theisen A, Dresel R, Christmann M, Zielen S. Growth hormone supplementation increased latency to tumourigenesis in Atm-deficient mice. Growth Factors. 2009 Oct;27(5):265-73. doi: 10.1080/08977190903112663.
PubMed 19626507
Study at a glance
From the registry record, last updated by the sponsor on 5 Jul 2010. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Status of the Growth Hormone/ Insulin-like Growth Factor-1 (GH/IGF-1) Axis in Relation to Growth Failure, Body Weight and Neuroprotection in Children With Ataxia Telangiectasia
- ClinicalTrials.gov ID
- NCT01052623
- Acronym / sponsor ID
- GHAT / FRA.GHAT.2009
- Conditions
- Ataxia Telangiectasia, Growth Failure
- Keywords
- GH/IGF-1, Ataxia telangiectasia (AT), IGF-1 Generation Test, Growth hormone
- Phase
- Phase 4
- Study type
- Interventional
- Recruitment status
- Unknown status
- Enrolment
- 24 participants (estimated)
- Lead sponsor
- Johann Wolfgang Goethe University HospitalUniversity, hospital or other
- Study start
- Jan 2010
- Primary completion
- Dec 2011 (estimated)
- Study completion
- Sep 2012 (estimated)
- First posted
- 20 Jan 2010 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
This study will evaluate the status of the growth hormone/ insulin-like growth factor-1 (GH/IGF-1) axis in relation to growth failure, body weight and composition and neuroprotection in children with Ataxia telangiectasia (AT).
Detailed description
Growth failure and GH/IgF-1 deficiency has been described in patients diagnosed with Ataxia telangiectasia (AT) [Boder et al.,1958]. This condition is a fatal inherited disease caused by a mutation of the ATM gene on chromosome 11 leading to chromosomal instability, immunodeficiency, cancer susceptibility and and endocrinological abnormalities. In this regard, several groups demonstrated a cross-linking of ATM with growth factor pathways. Participation of the ATM protein in insulin signaling through phosphorylation of eIF-4E-binding protein 1 has been postulated [Yang et al.,2000]. Peretz et al.[2001] described that expression of the insulin-like growth factor-I receptor is (IGF-I R) ATM dependent in a pathway regulating radiation response. In addition, Shahrabani-Gargir et al.[2004] found that the ATM gene controls IGF-I R gene expression in a DNA damage response pathway. Suzuki et al.[2004] described that IGF-I phosphorylates AMPK-alpha, a key regulator of cholesterol and fatty acid synthesis, acts in an ATM-dependent manner . We have recently demonstrated reduced levels of circulating Insulin-like growth factor-I (IGF-I) and its main binding protein 3 (IGFBP-3) in AT patients accompanied with decreased body mass index [Schubert et al.,2005]. Furthermore, apart from regulating somatic growth and metabolism, evidence suggests that the GH/IGF-I axis is involved in the regulation of brain growth, development and myelination. Moreover, GH and particularly IGF-1 have potential neuroprotective effects in different in vitro and in vivo experimental models. In addition we have recently shown that extracerebellar MRI-lesions in AT go along with deficiency of the GH/IGF-1 Axis, markedly reduced body weight, high ataxia scores and advanced age [Kieslich et al.,2009]. Supplementation with these growth hormones might overcome the progressive dystrophy and may have clinical benefits against the progression of neurodegeneration and immunodeficiency.
We found that supplementation with GH significantly increased longevity of Atm-deficient mice and improve T-cell immunity and locomotor behaviour [Schubert et al.,2009]. Surprisingly IGF-1 was not generated in the ATM deficient mice, indicating that the GH/IGF-1 signalling is impaired. Taken this into account a accurate diagnostic approach of the GH/IGF-1 axis is mandatory including a IGF-1 generation test before long term treatment either with GH or IGF-1 is justified in humans.
Study design
- Primary purpose
- Diagnosis
- Allocation
- Non-randomised
- Intervention model
- Single group
- Masking
- None (open label)
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| Growth hormone-testing (GH/IGF-1-testing) | Experimental | Drug: Somatropin, Clonidine, L-Arginin-Hydrochloride, Estradiol valeratePatients (girls over 8 years and boys over 10 years) are primed with estradiol 1 mg orally for 2 days, to help avoid false results of growth hormone (GH) levels in blood samples. Then provocation testing is done, with two tests back to back. It determines blood levels of GH and the body's response to testing with drugs called arginine and clonidine. Patients are admitted to the pediatric inpatient unit and will have an intravenous (IV) line placed in the arm. Arginine is given by IV over 30 minutes, and blood samples are taken as indicated. The next day, the clonidine test is performed according to current guidelines. Then the IGF-1 generation test is done to see if the patient has the ability to generate IGF-1 in response to injections of GH for 5 consecutive days. |
Who may qualify
- Ages
- 3 to 18 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Child, Adult
Key inclusion criteria (9 listed)
- Have a diagnosis of AT
- Have no fusion of epiphyses/closed growth plates as determined by X-ray of left wrist and hand (special skeletal age film)
- Be between 3 years to 18 years old and have not completed puberty
- Consent to permit blood and/or tissue samples for storage
- Demonstrate growth failure: height below the 10th percentile for chronological age
Key exclusion criteria (15 listed)
- Have fusion of epiphyseal plates
- Be under the age of 3 years or have reached completion of puberty
- Have a serum IGF-1 level that is above the 25% range of normal limits for age
- Be above the 10th percentile height for chronological age
- Demonstrate any history of anaphylactic reaction or hypersensitivity to one of the GH formulation
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Somatropin, Clonidine, L-Arginin-Hydrochloride, Estradiol valerateAlso: Catapressan, Growth hormone, NutropinAq, Progynova 21 mite1 mg Estradiol valerate with for two days before GH-testing pre pubertal girls older than 8 years and pre pubertal boys older than 10 years. L-Arginin-Hydrochloride in the vein (0.5 g/kg KG maximum dose 30g) over 30 minutes. Clonidine orally (0,075 mg/m2 BSA). Somatropin-NutropinAq subcutaneum,a single one shot (dose 0.03 mg/KG, daily, over five days). | Drug | Growth hormone-testing (GH/IGF-1-testing) |
Primary outcome
To evaluate the GH increase after Arginine Provocation Test
Time frame: at minute 0, 30, 60, 90 und 120 after infusion
1 secondary outcome
The GH increase after Clonidine Provocation Test. To evaluate the safety and efficacy of the IGF-1 generation test. To correlate GH/IgF-1 deficiency to BMI To correlate GH/IgF-1 deficiency to MRI findings
Time frame: at minute 0, 30, 60, 90 und 120 after dosing of Clonidin. IgF-1 generation test after 5 days.
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 5 Jul 2010.
- Background: PubMed 13542097BODER E, SEDGWICK RP. Ataxia-telangiectasia; a familial syndrome of progressive cerebellar ataxia, oculocutaneous telangiectasia and frequent pulmonary infection. Pediatrics. 1958 Apr;21(4):526-54. No abstract available.
- Background: PubMed 18813293Lavin MF. Ataxia-telangiectasia: from a rare disorder to a paradigm for cell signalling and cancer. Nat Rev Mol Cell Biol. 2008 Oct;9(10):759-69. doi: 10.1038/nrm2514.
- Background: PubMed 15932513Schubert R, Reichenbach J, Zielen S. Growth factor deficiency in patients with ataxia telangiectasia. Clin Exp Immunol. 2005 Jun;140(3):517-9. doi: 10.1111/j.1365-2249.2005.02782.x.
- Background: PubMed 17557036Isgaard J, Aberg D, Nilsson M. Protective and regenerative effects of the GH/IGF-I axis on the brain. Minerva Endocrinol. 2007 Jun;32(2):103-13.
- Background: PubMed 11146653Yang DQ, Kastan MB. Participation of ATM in insulin signalling through phosphorylation of eIF-4E-binding protein 1. Nat Cell Biol. 2000 Dec;2(12):893-8. doi: 10.1038/35046542.
- Background: PubMed 11172010Peretz S, Jensen R, Baserga R, Glazer PM. ATM-dependent expression of the insulin-like growth factor-I receptor in a pathway regulating radiation response. Proc Natl Acad Sci U S A. 2001 Feb 13;98(4):1676-81. doi: 10.1073/pnas.98.4.1676. Epub 2001 Feb 6.
- Background: PubMed 15345673Shahrabani-Gargir L, Pandita TK, Werner H. Ataxia-telangiectasia mutated gene controls insulin-like growth factor I receptor gene expression in a deoxyribonucleic acid damage response pathway via mechanisms involving zinc-finger transcription factors Sp1 and WT1. Endocrinology. 2004 Dec;145(12):5679-87. doi: 10.1210/en.2004-0613. Epub 2004 Sep 2.
- Background: PubMed 15485651Suzuki A, Kusakai G, Kishimoto A, Shimojo Y, Ogura T, Lavin MF, Esumi H. IGF-1 phosphorylates AMPK-alpha subunit in ATM-dependent and LKB1-independent manner. Biochem Biophys Res Commun. 2004 Nov 19;324(3):986-92. doi: 10.1016/j.bbrc.2004.09.145.
- Background: PubMed 19898915Kieslich M, Hoche F, Reichenbach J, Weidauer S, Porto L, Vlaho S, Schubert R, Zielen S. Extracerebellar MRI-lesions in ataxia telangiectasia go along with deficiency of the GH/IGF-1 axis, markedly reduced body weight, high ataxia scores and advanced age. Cerebellum. 2010 Jun;9(2):190-7. doi: 10.1007/s12311-009-0138-0.
- Background: PubMed 19626507Schubert R, Schmitz N, Pietzner J, Tandi C, Theisen A, Dresel R, Christmann M, Zielen S. Growth hormone supplementation increased latency to tumourigenesis in Atm-deficient mice. Growth Factors. 2009 Oct;27(5):265-73. doi: 10.1080/08977190903112663.
- Related InfoLink provided by the sponsor.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Stefan Zielen, Prof. Dr. principal investigator
Children´s Hospital, Goethe-University
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 4 study testing Somatropin, Clonidine, L-Arginin-Hydrochloride, Estradiol valerate in people with Ataxia Telangiectasia and Growth Failure, run by Johann Wolfgang Goethe University Hospital at 1 site in Germany.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 9 inclusion and 15 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 5 Jul 2010. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Germany. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 4 studies take place after a treatment is approved, to learn more about its long-term benefits and risks in everyday use.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Contact Stefan Zielen, Prof. Dr. (0049-69-6301-83063, Stefan.Zielen@kgu.de), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
To evaluate the GH increase after Arginine Provocation Test (time frame: at minute 0, 30, 60, 90 und 120 after infusion). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT01052623, which also lists 10 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 5 Jul 2010.