Severe Adult Growth Hormone DeficiencyNCT00468624
Effect of Pegvisomant on GH/IGF-I Relationship in GHD
A study testing arginine stimulation test after each limb in people with Severe Adult Growth Hormone Deficiency, run by The Christie NHS Foundation Trust at 1 site in United Kingdom.
Trial summary
Approximately 50% of middle-aged patients with severe AGHD have a normal age-related serum IGF-I. It remains unclear if in these individuals serum IGF-I is GH dependent or independent. Read more about this study
- Who is it for?
- Ages 18 to 70 yearsHealthy volunteers can take part
- Conditions the study is for
- Severe Adult Growth Hormone Deficiency
- What is being tested?
- arginine stimulation test after each limb
- Type of treatment
- Surgery or procedure
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- Not given
- Where
- 1 siteUnited Kingdom
- Study dates
- Dec 2004to Jul 2005
- Phase
- Interventional
- 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 18 to 70 years
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Who may be able to join
- Over 18 years of age
- Confirmed severe AGHD
- GH response <9 mU/l (preferably <4) to insulin-induced hypoglycaemia or glucagon stimulation test plus (These tests will have taken place as part of routine management).
- Full, stable pituitary replacement therapy
- Willing to provide informed consent
Who cannot join
- Unwilling to provide written consent
- Current GH therapy
- Pharmacological doses of glucocorticoids
- Any acute illness
Trial locations and contacts
1 site in 1 country.
About this study
Official title: A Study of the Relationship Between Serum Growth Hormone (GH) and Insulin-Like Growth Factor One (IGF-I) in Patients With Severe Adult Growth Hormone Deficiency (AGHD)
Approximately 50% of middle-aged patients with severe AGHD have a normal age-related serum IGF-I. It remains unclear if in these individuals serum IGF-I is GH dependent or independent. This study compared the relationship between GH and serum IGF-I in two cohorts of male patients with severe AGHD; one with normal and the other with subnormal age-related serum IGF-I values. The GH receptor antagonist - pegvisomant was be used to specifically inhibit GH action and the changes in markers of the GH axis, such as serum IGF-I, IGFBP-3, GH and GHBP were measured.
Read the detailed description
There is an increasing reliance on serum insulin-like factor-I (IGF-I) in the management of disturbances of the growth hormone (GH) axis. IGF-I is predominantly, but not exclusively, regulated by GH secreted from the pituitary, with the majority of circulating IGF-I being hepatic in origin.
In parallel with the age-related decline in GH secretion, circulating levels of IGF-I fall with age (1). For a given GH level women have lower serum IGF-I levels than men, indicative of a relative GH resistance (1,2). Nutrition-related factors are known to affect GH, IGF-I and their relationship. Obesity is associated with low GH production, but increased GH sensitivity resulting in relatively high IGF-I for given GH (3-6). Deprivation of important nutrients during fasting is known to stimulate GH, whilst reducing IGF-I (7-9). In vitro studies demonstrated complex role of insulin in IGF-I generation. Insulin stimulates hepatic IGF-I production directly by increasing IGF-I mRNA synthesis and indirectly by enhancing the effect of GH (10,11). By decreasing insulin-like growth factor 1 and 2 (IGFBP1-2), insulin may also affect bioavailability of IGF-I (12-13).
In acromegaly, IGF-I is an important marker for diagnosis and monitoring of disease activity. If patients are treated with a GH receptor antagonist, IGF-I becomes the only useful biochemical marker for monitoring disease activity.
GH deficiency in adults is associated with increased morbidity (14-16). In patients with pituitary disease there has been great progress in the recognition and treatment of this disorder. There is increasing awareness of GH deficiency, not only as a complication of the long-recognised causes of hypopituitarism, but also in the setting of traumatic brain injury and subarachnoid haemorrhage (17). The phenotype of severe adult GHD has been described but many of the features lack specificity and biochemical confirmation of the diagnosis is necessary. The Port Stevens consensus on severe adult GHD relies on the measurement of stimulated GH secretion for confirmation of the diagnosis with a peak GH of <3 µg/L, in one or two stimulation tests, depending on the number of other pituitary hormone deficiencies (18) GH replacement therapy relies on measurement of serum IGF-I for dose titration, with the biochemical goal being of placing circulating IGF-I within age- and gender-related reference range, preferably between 0 and +1 SDS (19). The Port Stephens consensus recognises the apparent paradox that approximately 50% of middle-aged patients diagnosed with severe GHD by a peak stimulated GH levels of <3 µg/L have a pre-treatment IGF-I within the reference range. In untreated severe GHD of adult onset and predominately in men, serum IGF-I may even be in the upper half of reference range. In other words, before treatment these patients already have an IGF-I that would be regarded as satisfactory response to GH replacement therapy. Prima facia, it is difficult to reconcile a serum IGF-I within the reference range and a diagnosis of GHD. Inevitably, it poses the question if factors other than GH are regulating circulating IGF-I levels in such patients.
Pegvisomant is a GH analogue that binds to, but does not activate the GH receptor and has been shown to normalise IGF-I in up to 97% of patients with acromegaly (20). We used pegvisomant to study the relationship between GH and IGF-I in patients with severe adult GHD and investigate whether IGF-I in such patients, is particularly GH-dependent.
- Conditions
- Severe Adult Growth Hormone Deficiency
- Being tested
- pegvisomant/placebo loading dose 80mg sc, thereafter 20mg daily for 2 weeks, GH sampling - every 20 min over 24 hours after each limb (pegvisomant/placebo), blood sampling before and after pegvisomant/placebo, arginine stimulation test after each limb
- Keywords
- Growth hormone, insulin-like growth factor 1, pegvisomant
- Medical subject headings
- Dwarfism, Pituitary
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
pegvisomant/placebo loading dose 80mg sc, thereafter 20mg daily for 2 weeksDrug
GH sampling - every 20 min over 24 hours after each limb (pegvisomant/placebo)Procedure or surgery
blood sampling before and after pegvisomant/placeboProcedure or surgery
arginine stimulation test after each limbProcedure or surgery
What is being measured
The primary outcome is the main question the study is designed to answer.
change in IGF-I
Measured: 2 weeks per limb
Secondary outcomes (1)
change in basal and stimulated GH Change in IGFBP-3 Change in GHBP
Measured: 2 weeks per limb
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted3 May 2007 (estimated)
- Study startDec 2004
- Study completionJul 2005
Why it stopped: recruitment completed
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (1)Papers the sponsor has linked to this study.
- Other trials for Severe Adult Growth Hormone DeficiencyStudies 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 N/A
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Double blind
Sponsor and investigators
- Lead sponsor
- The Christie NHS Foundation Trust
- Sponsor type
- University, hospital or other
- Investigators
- Peter J Trainer, MD FRCP, Principal investigator, Christie Hospital NHS
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT00468624
- Sponsor's protocol ID
- 04_ENDO_41
- Status last verified
- May 2007
- First submitted
- 2 May 2007
- Last updated
- 3 May 2007
- Results posted
- No
- Data monitoring committee
- No
Publications
1. Svensson J, Johannsson G, Bengtsson BA 1997 Insulin-like growth factor-I in growth hormone-deficient adults: relationship to population-based normal values, body composition and insulin tolerance test. Clin Endocrinol (Oxf) 46:579-586 2. Veldhuis JD 1996 Gender differences in secretory activity of the human somatotropic (growth hormone) axis. Eur J Endocrinol 134:287-295 3. Caufriez A, Golstein J, Lebrun P, Herchuelz A, Furlanetto R, Copinschi G 1984 Relations between immunoreactive somatomedin C, insulin and T3 patterns during fasting in obese subjects. Clin Endocrinol (Oxf) 20:65-70 4. Copeland KC, Colletti RB, Devlin JT, McAuliffe TL 1990 The relationship between insulin-like growth factor-I, adiposity, and aging. Metabolism 39: 584-587 5. Yamamoto H, Kato Y 1993 Relationship between plasma insulin-like growth factor I (IGF-I) levels and body mass index (BMI) in adults. Endocr J 40:41-45 6. Rasmussen MH, Ho KK, Kjems L, Hilsted J 1996 Serum growth hormone-binding protein in obesity: effect of a short-term, very low calorie diet and diet-induced weight loss. J Clin Endocrinol Metab 81:1519-1524 7. Ho KY, Veldhuis JD, Johnson ML, Furlanetto R, Evans WS, Alberti KG, Thorner MO 1988 Fasting enhances growth hormone secretion and amplifies the complex rhythms of growth hormone secretion in man. J Clin Invest 81:968-975 8. Maccario M, Aimaretti G, Grottoli S, Gauna C, Tassone F, Corneli G, Rossetto R, Wu Z, Strasburger CJ, Ghigo E 2001 Effects of 36 hour fasting on GH/IGF-I axis and metabolic parameters in patients with simple obesity. Comparison with normal subjects and hypopituitary patients with severe GH deficiency. Int J Obes Relat Metab Disord 25:1233-1239 9. Darzy KH, Murray RD, Gleeson HK, Pezzoli SS, Thorner MO, Shalet SM 2006: The impact of short-term fasting on the dynamics of 24-hour growth hormone (GH) secretion in patients with severe radiation-induced GH deficiency.J Clin Endocrinol Metab. 91(3):987-94. 10. Boni Schnetzler M, Schmid C, Meier PJ, Froesch ER 1991 Insulin regulates insulin-like growth factor I mRNA in rat hepatocytes, Am J Physiol 260: 846-51. 11. Leung KC, Doyle N, Ballesteros M, Waters MJ, Ho KK. 2000 Insulin regulation of human hepatic growth hormone receptors: divergent effects on biosynthesis and surface translocation, J Clin Endocrinol Metab 85:4712-20. 12. Cox GN, McDermott MJ, Merkel E, Stroh CA, Ko SC, Squires CH, Gleason TM, Russell D. 1994 Recombinant human insulin-like growth factor (IGF)-binding protein-1 inhibits somatic growth stimulated by IGF-I and growth hormone in hypophysectomized rats, Endocrinology 135: 1913-20. 13. Wolf E, Lahm H, Wu M, Wanke R,. Hoeflich A, 2000 Effects of IGFBP-2 overexpression in vitro and in vivo, Pediatr Nephrol 14: 572-8. 14. Bates JA, Van't Hoff W, Jones PJ, Clayton RN. 1996 The effect of hypopituitarism on life expectancy. J Clin Endocrinol Metab 81:1169-72 15. Rosen T, Bengtsson B-A. 1990 Premaature mortality due to cardiovascular disease in hypopituitarism. Lancet 336: 285-8 16. Tomlinson JW, Holden N, Hills RK, Wheatley K, Clayton RN, Bates AS, Sheppard MC, Stewart PM. Association between premature mortality and hypopituitarism. West midlands prospective hypopituitary study group. 2001 Lancet 357:425-31. 17. Aimaretti G, Ambrosio MR, Di Somma C, Fusco A, Cannavo S, Gasperi M, Scaroni C, De Marinis L, Benvanga S, degli Uberti EC, Lombardi G, Mantero F, Martino E, Giordano G, Ghigo E. Traumatic brain injury and subarachnoid haemorrhage are conditions at high risk for hypopituitarism: screening study at 3 months after the brain injury. 2004 Clin Endo (Oxf.) 61(3):320-6 18. Consensus Guidelines for the Diagnosis and Treatment of Adults with Growth Hormone Deficiency: Summary Statement of the Growth Hormone Research Society Workshop on Adult Growth Hormone Deficiency 1998 JCE&M; 83(2):379-81 19. Mukherjee A, Monson JP, Jonsson PJ, Trainer PJ, Shalet SM 2003 Seeking the optimal target range for insulin-like growth factor I during the treatment of adult growth hormone disorders. J Clin Endocrinol Metab 88:5865-5870 20. Van der Lely AJ, Hutson RK, Trainer PJ, Besser GM, Barkan AL, Katznelson L, Klibanski A, Herman-Bonert V, Melmed S, Vance ML, Freda PU, Stewart PM, Friend KE, Clemmons DR, Johannsson G, Stavrou S, Cook DM, Phillips LS, Strasburger CJ, Hackett S, Zib KA, Davis RJ, Scarlett JA, Thorner MO. 2001 Long-term treatment of acromegaly with pegvisomant, a growth hormone receptor antagonist. Lancet 358: 1754-59
Study at a glance
From the registry record, last updated by the sponsor on 3 May 2007. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- A Study of the Relationship Between Serum Growth Hormone (GH) and Insulin-Like Growth Factor One (IGF-I) in Patients With Severe Adult Growth Hormone Deficiency (AGHD)
- ClinicalTrials.gov ID
- NCT00468624
- Acronym / sponsor ID
- 04_ENDO_41
- Conditions
- Severe Adult Growth Hormone Deficiency
- Keywords
- Growth hormone, insulin-like growth factor 1, pegvisomant
- Study type
- Interventional
- Recruitment status
- TerminatedReason stopped: recruitment completed
- Lead sponsor
- The Christie NHS Foundation TrustUniversity, hospital or other
- Study start
- Dec 2004
- Study completion
- Jul 2005 (actual)
- First posted
- 3 May 2007 (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.
Approximately 50% of middle-aged patients with severe AGHD have a normal age-related serum IGF-I. It remains unclear if in these individuals serum IGF-I is GH dependent or independent. This study compared the relationship between GH and serum IGF-I in two cohorts of male patients with severe AGHD; one with normal and the other with subnormal age-related serum IGF-I values. The GH receptor antagonist - pegvisomant was be used to specifically inhibit GH action and the changes in markers of the GH axis, such as serum IGF-I, IGFBP-3, GH and GHBP were measured.
Detailed description
There is an increasing reliance on serum insulin-like factor-I (IGF-I) in the management of disturbances of the growth hormone (GH) axis. IGF-I is predominantly, but not exclusively, regulated by GH secreted from the pituitary, with the majority of circulating IGF-I being hepatic in origin.
In parallel with the age-related decline in GH secretion, circulating levels of IGF-I fall with age (1). For a given GH level women have lower serum IGF-I levels than men, indicative of a relative GH resistance (1,2). Nutrition-related factors are known to affect GH, IGF-I and their relationship. Obesity is associated with low GH production, but increased GH sensitivity resulting in relatively high IGF-I for given GH (3-6). Deprivation of important nutrients during fasting is known to stimulate GH, whilst reducing IGF-I (7-9). In vitro studies demonstrated complex role of insulin in IGF-I generation. Insulin stimulates hepatic IGF-I production directly by increasing IGF-I mRNA synthesis and indirectly by enhancing the effect of GH (10,11). By decreasing insulin-like growth factor 1 and 2 (IGFBP1-2), insulin may also affect bioavailability of IGF-I (12-13).
In acromegaly, IGF-I is an important marker for diagnosis and monitoring of disease activity. If patients are treated with a GH receptor antagonist, IGF-I becomes the only useful biochemical marker for monitoring disease activity.
GH deficiency in adults is associated with increased morbidity (14-16). In patients with pituitary disease there has been great progress in the recognition and treatment of this disorder. There is increasing awareness of GH deficiency, not only as a complication of the long-recognised causes of hypopituitarism, but also in the setting of traumatic brain injury and subarachnoid haemorrhage (17). The phenotype of severe adult GHD has been described but many of the features lack specificity and biochemical confirmation of the diagnosis is necessary. The Port Stevens consensus on severe adult GHD relies on the measurement of stimulated GH secretion for confirmation of the diagnosis with a peak GH of <3 µg/L, in one or two stimulation tests, depending on the number of other pituitary hormone deficiencies (18) GH replacement therapy relies on measurement of serum IGF-I for dose titration, with the biochemical goal being of placing circulating IGF-I within age- and gender-related reference range, preferably between 0 and +1 SDS (19). The Port Stephens consensus recognises the apparent paradox that approximately 50% of middle-aged patients diagnosed with severe GHD by a peak stimulated GH levels of <3 µg/L have a pre-treatment IGF-I within the reference range. In untreated severe GHD of adult onset and predominately in men, serum IGF-I may even be in the upper half of reference range. In other words, before treatment these patients already have an IGF-I that would be regarded as satisfactory response to GH replacement therapy. Prima facia, it is difficult to reconcile a serum IGF-I within the reference range and a diagnosis of GHD. Inevitably, it poses the question if factors other than GH are regulating circulating IGF-I levels in such patients.
Pegvisomant is a GH analogue that binds to, but does not activate the GH receptor and has been shown to normalise IGF-I in up to 97% of patients with acromegaly (20). We used pegvisomant to study the relationship between GH and IGF-I in patients with severe adult GHD and investigate whether IGF-I in such patients, is particularly GH-dependent.
Study design
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Double blind
Who may qualify
- Ages
- 18 to 70 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (5 listed)
- Over 18 years of age
- Confirmed severe AGHD
- GH response <9 mU/l (preferably <4) to insulin-induced hypoglycaemia or glucagon stimulation test plus (These tests will have taken place as part of routine management).
- Full, stable pituitary replacement therapy
- Willing to provide informed consent
Key exclusion criteria (4 listed)
- Unwilling to provide written consent
- Current GH therapy
- Pharmacological doses of glucocorticoids
- Any acute illness
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 |
|---|---|---|
| pegvisomant/placebo loading dose 80mg sc, thereafter 20mg daily for 2 weeks | Drug | – |
| GH sampling - every 20 min over 24 hours after each limb (pegvisomant/placebo) | Procedure or surgery | – |
| blood sampling before and after pegvisomant/placebo | Procedure or surgery | – |
| arginine stimulation test after each limb | Procedure or surgery | – |
Primary outcome
change in IGF-I
Time frame: 2 weeks per limb
1 secondary outcome
change in basal and stimulated GH Change in IGFBP-3 Change in GHBP
Time frame: 2 weeks per limb
Results and safety
The study was stopped early (reason given: recruitment completed). Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 3 May 2007.
- Background1. Svensson J, Johannsson G, Bengtsson BA 1997 Insulin-like growth factor-I in growth hormone-deficient adults: relationship to population-based normal values, body composition and insulin tolerance test. Clin Endocrinol (Oxf) 46:579-586 2. Veldhuis JD 1996 Gender differences in secretory activity of the human somatotropic (growth hormone) axis. Eur J Endocrinol 134:287-295 3. Caufriez A, Golstein J, Lebrun P, Herchuelz A, Furlanetto R, Copinschi G 1984 Relations between immunoreactive somatomedin C, insulin and T3 patterns during fasting in obese subjects. Clin Endocrinol (Oxf) 20:65-70 4. Copeland KC, Colletti RB, Devlin JT, McAuliffe TL 1990 The relationship between insulin-like growth factor-I, adiposity, and aging. Metabolism 39: 584-587 5. Yamamoto H, Kato Y 1993 Relationship between plasma insulin-like growth factor I (IGF-I) levels and body mass index (BMI) in adults. Endocr J 40:41-45 6. Rasmussen MH, Ho KK, Kjems L, Hilsted J 1996 Serum growth hormone-binding protein in obesity: effect of a short-term, very low calorie diet and diet-induced weight loss. J Clin Endocrinol Metab 81:1519-1524 7. Ho KY, Veldhuis JD, Johnson ML, Furlanetto R, Evans WS, Alberti KG, Thorner MO 1988 Fasting enhances growth hormone secretion and amplifies the complex rhythms of growth hormone secretion in man. J Clin Invest 81:968-975 8. Maccario M, Aimaretti G, Grottoli S, Gauna C, Tassone F, Corneli G, Rossetto R, Wu Z, Strasburger CJ, Ghigo E 2001 Effects of 36 hour fasting on GH/IGF-I axis and metabolic parameters in patients with simple obesity. Comparison with normal subjects and hypopituitary patients with severe GH deficiency. Int J Obes Relat Metab Disord 25:1233-1239 9. Darzy KH, Murray RD, Gleeson HK, Pezzoli SS, Thorner MO, Shalet SM 2006: The impact of short-term fasting on the dynamics of 24-hour growth hormone (GH) secretion in patients with severe radiation-induced GH deficiency.J Clin Endocrinol Metab. 91(3):987-94. 10. Boni Schnetzler M, Schmid C, Meier PJ, Froesch ER 1991 Insulin regulates insulin-like growth factor I mRNA in rat hepatocytes, Am J Physiol 260: 846-51. 11. Leung KC, Doyle N, Ballesteros M, Waters MJ, Ho KK. 2000 Insulin regulation of human hepatic growth hormone receptors: divergent effects on biosynthesis and surface translocation, J Clin Endocrinol Metab 85:4712-20. 12. Cox GN, McDermott MJ, Merkel E, Stroh CA, Ko SC, Squires CH, Gleason TM, Russell D. 1994 Recombinant human insulin-like growth factor (IGF)-binding protein-1 inhibits somatic growth stimulated by IGF-I and growth hormone in hypophysectomized rats, Endocrinology 135: 1913-20. 13. Wolf E, Lahm H, Wu M, Wanke R,. Hoeflich A, 2000 Effects of IGFBP-2 overexpression in vitro and in vivo, Pediatr Nephrol 14: 572-8. 14. Bates JA, Van't Hoff W, Jones PJ, Clayton RN. 1996 The effect of hypopituitarism on life expectancy. J Clin Endocrinol Metab 81:1169-72 15. Rosen T, Bengtsson B-A. 1990 Premaature mortality due to cardiovascular disease in hypopituitarism. Lancet 336: 285-8 16. Tomlinson JW, Holden N, Hills RK, Wheatley K, Clayton RN, Bates AS, Sheppard MC, Stewart PM. Association between premature mortality and hypopituitarism. West midlands prospective hypopituitary study group. 2001 Lancet 357:425-31. 17. Aimaretti G, Ambrosio MR, Di Somma C, Fusco A, Cannavo S, Gasperi M, Scaroni C, De Marinis L, Benvanga S, degli Uberti EC, Lombardi G, Mantero F, Martino E, Giordano G, Ghigo E. Traumatic brain injury and subarachnoid haemorrhage are conditions at high risk for hypopituitarism: screening study at 3 months after the brain injury. 2004 Clin Endo (Oxf.) 61(3):320-6 18. Consensus Guidelines for the Diagnosis and Treatment of Adults with Growth Hormone Deficiency: Summary Statement of the Growth Hormone Research Society Workshop on Adult Growth Hormone Deficiency 1998 JCE&M; 83(2):379-81 19. Mukherjee A, Monson JP, Jonsson PJ, Trainer PJ, Shalet SM 2003 Seeking the optimal target range for insulin-like growth factor I during the treatment of adult growth hormone disorders. J Clin Endocrinol Metab 88:5865-5870 20. Van der Lely AJ, Hutson RK, Trainer PJ, Besser GM, Barkan AL, Katznelson L, Klibanski A, Herman-Bonert V, Melmed S, Vance ML, Freda PU, Stewart PM, Friend KE, Clemmons DR, Johannsson G, Stavrou S, Cook DM, Phillips LS, Strasburger CJ, Hackett S, Zib KA, Davis RJ, Scarlett JA, Thorner MO. 2001 Long-term treatment of acromegaly with pegvisomant, a growth hormone receptor antagonist. Lancet 358: 1754-59
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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.
Peter J Trainer, MD FRCP principal investigator
Christie Hospital NHS
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing arginine stimulation test after each limb in people with Severe Adult Growth Hormone Deficiency, run by The Christie NHS Foundation Trust at 1 site in United Kingdom.
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 5 inclusion and 4 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: stopped early, as of the sponsor's last update on 3 May 2007. 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 United Kingdom. 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.
Are results available for this study?
The study was stopped early (reason given: recruitment completed). Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
change in IGF-I (time frame: 2 weeks per limb). 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 NCT00468624, which also lists 1 linked publication.
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 3 May 2007.