HypoglycaemiaNCT01347801
Mechanisms of Insulin Resistance in Critical Illness: Role of Systemic Inflammation and GLP-1
A study testing GLP-1, TNF-alfa and OGTT in people with Hypoglycaemia, run by Copenhagen University Hospital, Rigshospitalet at 2 sites in Denmark.
Trial summary
The purpose of this study is to determine the role of inflammation and the insulin regulating hormone GLP-1 during critical illness. Read more about this study
- Who is it for?
- Ages 18 to 40 years, men onlyHealthy volunteers can take part
- Conditions the study is for
- Hypoglycaemia
- What is being tested?
- GLP-1, TNF-alfa and OGTT
- Type of treatment
- Pill or oral medicine, Injection or infusion
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 40 participants
- Where
- 2 sitesDenmark
- Study dates
- Mar 2011to Sep 2014
- 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 40 years
- Men only
- Healthy volunteers accepted
- Adult
Who may be able to join
- Healthy (assessed by medical history and clinical examination)
- Age 18-40years
- BMI < 30kg/m2
- Age>18 years
- HbA1C<6,5%
- Admission to the ICU within the last 72 hours
Who cannot join
- Previous resection of the small intestine (not including the appendix)
- presence of any inflammatory illness during the fortnight preceding the study
Trial locations and contacts
2 sites in 1 country.
Denmark2 sites
Centre of Inflammation and Metabolism - Rigshospitalet 7641
Copenhagen, 2100
University of Copenhagen
Copenhagen, 2400
About this study
The purpose of this study is to determine the role of inflammation and the insulin regulating hormone GLP-1 during critical illness.
Read the detailed description
Critically ill patients often exhibit hyperglycaemia. Although the cause of this hyperglycaemia is probably multifactorial, peripheral insulin resistance is a major contributor, similar to type 2 diabetes mellitus (T2D). There are several similarities between critical illness and T2D, including the presence of systemic inflammation and increased plasma free fatty acids (FFA), all of which may induce insulin resistance in healthy volunteers. In critical illness, elevated catecholamines, cortisol, growth hormone and glucagon may also contribute to insulin resistance.
The degree of hyperglycaemia correlates with mortality in ICU patients. van den Berghe et al. found that IV infusion of insulin to obtain strict normoglycaemia reduced mortality as well as morbidity in critically ill surgical patients and in some medical ICU patients.
However, insulin increases the risk of hypoglycaemia; this is a major obstacle to strict euglycaemia in ICU patients and may explain the inability of others to reproduce the benefits reported by van den Berghe et al. Thus, alternatives to insulin for controlling plasma glucose (PG) in ICU patients are warranted.
Aim:
To study the role of the incretin hormone, glucagon-like peptide (GLP)-1 for glycaemic, metabolic, hormonal and inflammatory profile in
- critically ill patients in the intensive care unit (ICU) and
- healthy volunteers exposed to a standardised systemic inflammation
- Conditions
- Hypoglycaemia
- Being tested
- GLP-1, Placebo (Saline), TNF-alfa, OGTT, IVGTT
- Keywords
- GLP-1, Inflammation, Glucose
- Medical subject headings
- Hypoglycemia, Inflammation
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
GLP-1Drug
GLP-1 1,2pmol/kg/min i.v. infusion for 4 hours
Placebo (Saline)Drug
Normal saline (NaCl 0,9%)
TNF-alfaDrug
1000ng/m2 BSA/hour i.v. infusion for 4-6 hours
OGTTOther
Oral glucose tolerance test with 75 g glucose
IVGTTOther
Intravenous glucose tolerance test with infusion of 20% glucose matching the glucose profile of the corresponding OGTT
| Study group | Role | What they receive |
|---|---|---|
| 2C - 1 | Placebo comparator | TNF and OGTT and saline Receives: Drug: Placebo (Saline); Drug: TNF-alfa; Other: OGTT |
| 2C - 2 | Active comparator | TNF and OGTT and GLP-1 Receives: Drug: GLP-1; Drug: TNF-alfa; Other: OGTT |
| 2C - 3 | Placebo comparator | TNF and IVGTT and saline Receives: Drug: Placebo (Saline); Drug: TNF-alfa; Other: IVGTT |
| 2C - 4 | Active comparator | TNF and IVGTT and GLP-1 Receives: Drug: GLP-1; Drug: TNF-alfa; Other: IVGTT |
| 2A-1 | Placebo comparator | Saline infusion and OGTT Receives: Drug: Placebo (Saline); Other: OGTT |
| 2A-2 | Placebo comparator | Saline and IVGTT Receives: Drug: Placebo (Saline); Other: IVGTT |
| 2A-3 | Active comparator | TNF and OGTT Receives: Drug: TNF-alfa; Other: OGTT |
| 2A-4 | Active comparator | TNF and IVGTT Receives: Drug: TNF-alfa; Other: IVGTT |
| 1C | Experimental | OGTT and corresponding IVGTT Receives: Other: OGTT; Other: IVGTT |
What is being measured
The primary outcome is the main question the study is designed to answer.
Substudy 2C (12 Healthy volunteers): GLP-1
Increased plasma insulin and C-peptide (intact insulinotropic effect of GLP-1) during GLP-1 infusion in healthy volunteers.
Measured: 6 weeks after intervention
Substudy 2A (12 Healthy volunteers): Insulin, C-peptide and incretin hormone response
Insulin, c-peptide and incretin hormone response to glucose stimulation during standardized systemic inflammation (TNF infusion) compared to placebo (saline infusion)
Measured: 6 weeks after intervention
Substudy 1C(8 patients, 8 healthy controls): Insulin, C-peptide and incretin hormone response
Insulin, c-peptide and incretin hormone response to glucose stimulation during IVGTT compared to OGTT in critically ill patients admitted to the ICU
Measured: 6 weeks after intervention
Secondary outcomes (3)
Substudy 2C (12 Healthy volunteers): Clamp
Enhanced insulin response (AUC) and reduced difference between the AUC obtained during OGTT and IGGTT (reduced endogenous incretin effect) during an isoglycaemic intravenous glucose tolerance test (IVGTT) in healthy volunteers receiving TNF-infusion.
Measured: 6 weeks after intervention
Substudy 2A (12 Healthy volunteers): The incretin effect
The difference between the plasma insulin AUC obtained during OGTT and IVGTT (endogenous incretin effect).
Measured: 6 weeks after intervention
Substudy 1C (8 patients, 8 healthy controls): The incretin effect
The difference between the plasma insulin AUC obtained during OGTT and IVGTT (endogenous incretin effect)in non-diabetic critically ill patients admitted to the ICU.
Measured: 6 weeks after intervention
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted4 May 2011 (estimated)
- Study startMar 2011
- Primary completionSep 2014
- Study completionSep 2014
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (36)Papers the sponsor has linked to this study.
- Other trials for HypoglycaemiaStudies of the same condition, open and under way.
- More trials run by Copenhagen University Hospital, RigshospitaletThe sponsor's other registered studies.
- 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
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- None (open label)
- Enrolment
- 40 participants (actual)
Sponsor and investigators
- Lead sponsor
- Copenhagen University Hospital, Rigshospitalet
- Sponsor type
- University, hospital or other
- Collaborators
- University of Copenhagen, Novo Nordisk A/S
- Responsible party
- Principal investigator, Kirsten Moller, Copenhagen University Hospital, Rigshospitalet
- Investigators
- Kirsten Møller, MD, Ph.D., DMSc, Principal investigator, Centre of Inflammation and Metabolism
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT01347801
- Sponsor's protocol ID
- HS:H-3-2009-108
- Status last verified
- Sep 2014
- First submitted
- 2 May 2011
- Last updated
- 22 Sep 2014
- Results posted
- No
- Data monitoring committee
- No
Publications
McCowen KC, Malhotra A, Bistrian BR. Stress-induced hyperglycemia. Crit Care Clin. 2001 Jan;17(1):107-24. doi: 10.1016/s0749-0704(05)70154-8.
PubMed 11219223Mizock BA. Alterations in fuel metabolism in critical illness: hyperglycaemia. Best Pract Res Clin Endocrinol Metab. 2001 Dec;15(4):533-51. doi: 10.1053/beem.2001.0168.
PubMed 11800522Rusavy Z, Sramek V, Lacigova S, Novak I, Tesinsky P, Macdonald IA. Influence of insulin on glucose metabolism and energy expenditure in septic patients. Crit Care. 2004 Aug;8(4):R213-20. doi: 10.1186/cc2868. Epub 2004 May 26.
PubMed 15312220Beal AL, Cerra FB. Multiple organ failure syndrome in the 1990s. Systemic inflammatory response and organ dysfunction. JAMA. 1994 Jan 19;271(3):226-33.
PubMed 8080494Schmidt MI, Duncan BB, Sharrett AR, Lindberg G, Savage PJ, Offenbacher S, Azambuja MI, Tracy RP, Heiss G. Markers of inflammation and prediction of diabetes mellitus in adults (Atherosclerosis Risk in Communities study): a cohort study. Lancet. 1999 May 15;353(9165):1649-52. doi: 10.1016/s0140-6736(99)01046-6.
PubMed 10335783Wolfe RR, Martini WZ. Changes in intermediary metabolism in severe surgical illness. World J Surg. 2000 Jun;24(6):639-47. doi: 10.1007/s002689910105.
PubMed 10773115Boden G, Shulman GI. Free fatty acids in obesity and type 2 diabetes: defining their role in the development of insulin resistance and beta-cell dysfunction. Eur J Clin Invest. 2002 Jun;32 Suppl 3:14-23. doi: 10.1046/j.1365-2362.32.s3.3.x.
PubMed 12028371Thijs LG, Hack CE. Time course of cytokine levels in sepsis. Intensive Care Med. 1995 Nov;21 Suppl 2:S258-63. doi: 10.1007/BF01740764.
PubMed 8636533Krogh-Madsen R, Plomgaard P, Moller K, Mittendorfer B, Pedersen BK. Influence of TNF-alpha and IL-6 infusions on insulin sensitivity and expression of IL-18 in humans. Am J Physiol Endocrinol Metab. 2006 Jul;291(1):E108-14. doi: 10.1152/ajpendo.00471.2005. Epub 2006 Feb 7.
PubMed 16464907Roden M, Price TB, Perseghin G, Petersen KF, Rothman DL, Cline GW, Shulman GI. Mechanism of free fatty acid-induced insulin resistance in humans. J Clin Invest. 1996 Jun 15;97(12):2859-65. doi: 10.1172/JCI118742.
PubMed 8675698Voerman BJ, Strack van Schijndel RJ, Groeneveld AB, de Boer H, Nauta JP, Thijs LG. Effects of human growth hormone in critically ill nonseptic patients: results from a prospective, randomized, placebo-controlled trial. Crit Care Med. 1995 Apr;23(4):665-73. doi: 10.1097/00003246-199504000-00014.
PubMed 7712756Finney SJ, Zekveld C, Elia A, Evans TW. Glucose control and mortality in critically ill patients. JAMA. 2003 Oct 15;290(15):2041-7. doi: 10.1001/jama.290.15.2041.
PubMed 14559958van den Berghe G, Wouters P, Weekers F, Verwaest C, Bruyninckx F, Schetz M, Vlasselaers D, Ferdinande P, Lauwers P, Bouillon R. Intensive insulin therapy in critically ill patients. N Engl J Med. 2001 Nov 8;345(19):1359-67. doi: 10.1056/NEJMoa011300.
PubMed 11794168Van den Berghe G, Wilmer A, Hermans G, Meersseman W, Wouters PJ, Milants I, Van Wijngaerden E, Bobbaers H, Bouillon R. Intensive insulin therapy in the medical ICU. N Engl J Med. 2006 Feb 2;354(5):449-61. doi: 10.1056/NEJMoa052521.
PubMed 16452557Brunkhorst FM, Engel C, Bloos F, Meier-Hellmann A, Ragaller M, Weiler N, Moerer O, Gruendling M, Oppert M, Grond S, Olthoff D, Jaschinski U, John S, Rossaint R, Welte T, Schaefer M, Kern P, Kuhnt E, Kiehntopf M, Hartog C, Natanson C, Loeffler M, Reinhart K; German Competence Network Sepsis (SepNet). Intensive insulin therapy and pentastarch resuscitation in severe sepsis. N Engl J Med. 2008 Jan 10;358(2):125-39. doi: 10.1056/NEJMoa070716.
PubMed 18184958
Study at a glance
From the registry record, last updated by the sponsor on 22 Sep 2014. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Mechanisms of Insulin Resistance in Critical Illness: Role of Systemic Inflammation and GLP-1
- ClinicalTrials.gov ID
- NCT01347801
- Acronym / sponsor ID
- HS:H-3-2009-108
- Conditions
- Hypoglycaemia
- Keywords
- GLP-1, Inflammation, Glucose
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 40 participants (actual)
- Lead sponsor
- Copenhagen University Hospital, RigshospitaletUniversity, hospital or other
- Collaborators
- University of Copenhagen, Novo Nordisk A/S
- Study start
- Mar 2011
- Primary completion
- Sep 2014 (actual)
- Study completion
- Sep 2014 (actual)
- First posted
- 4 May 2011 (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.
The purpose of this study is to determine the role of inflammation and the insulin regulating hormone GLP-1 during critical illness.
Detailed description
Critically ill patients often exhibit hyperglycaemia. Although the cause of this hyperglycaemia is probably multifactorial, peripheral insulin resistance is a major contributor, similar to type 2 diabetes mellitus (T2D). There are several similarities between critical illness and T2D, including the presence of systemic inflammation and increased plasma free fatty acids (FFA), all of which may induce insulin resistance in healthy volunteers. In critical illness, elevated catecholamines, cortisol, growth hormone and glucagon may also contribute to insulin resistance.
The degree of hyperglycaemia correlates with mortality in ICU patients. van den Berghe et al. found that IV infusion of insulin to obtain strict normoglycaemia reduced mortality as well as morbidity in critically ill surgical patients and in some medical ICU patients.
However, insulin increases the risk of hypoglycaemia; this is a major obstacle to strict euglycaemia in ICU patients and may explain the inability of others to reproduce the benefits reported by van den Berghe et al. Thus, alternatives to insulin for controlling plasma glucose (PG) in ICU patients are warranted.
Aim:
To study the role of the incretin hormone, glucagon-like peptide (GLP)-1 for glycaemic, metabolic, hormonal and inflammatory profile in
- critically ill patients in the intensive care unit (ICU) and
- healthy volunteers exposed to a standardised systemic inflammation
Study design
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- None (open label)
- Number of arms
- 9
| Arm | Type | Receives |
|---|---|---|
| 2C - 1 | Placebo comparator | Drug: Placebo (Saline), Drug: TNF-alfa, Other: OGTTTNF and OGTT and saline |
| 2C - 2 | Active comparator | Drug: GLP-1, Drug: TNF-alfa, Other: OGTTTNF and OGTT and GLP-1 |
| 2C - 3 | Placebo comparator | Drug: Placebo (Saline), Drug: TNF-alfa, Other: IVGTTTNF and IVGTT and saline |
| 2C - 4 | Active comparator | Drug: GLP-1, Drug: TNF-alfa, Other: IVGTTTNF and IVGTT and GLP-1 |
| 2A-1 | Placebo comparator | Drug: Placebo (Saline), Other: OGTTSaline infusion and OGTT |
| 2A-2 | Placebo comparator | Drug: Placebo (Saline), Other: IVGTTSaline and IVGTT |
| 2A-3 | Active comparator | Drug: TNF-alfa, Other: OGTTTNF and OGTT |
| 2A-4 | Active comparator | Drug: TNF-alfa, Other: IVGTTTNF and IVGTT |
| 1C | Experimental | Other: OGTT, Other: IVGTTOGTT and corresponding IVGTT |
Who may qualify
- Ages
- 18 to 40 years
- Sex
- Male only
- Healthy volunteers
- Accepted
- Age groups
- Adult
Key inclusion criteria (6 listed)
- Healthy (assessed by medical history and clinical examination)
- Age 18-40years
- BMI < 30kg/m2
- Age>18 years
- HbA1C<6,5%
Key exclusion criteria (2 listed)
- Previous resection of the small intestine (not including the appendix)
- presence of any inflammatory illness during the fortnight preceding the study
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 |
|---|---|---|
| GLP-1GLP-1 1,2pmol/kg/min i.v. infusion for 4 hours | Drug | 2C - 2, 2C - 4 |
| Placebo (Saline)Normal saline (NaCl 0,9%) | Drug | 2A-1, 2A-2, 2C - 1, 2C - 3 |
| TNF-alfa1000ng/m2 BSA/hour i.v. infusion for 4-6 hours | Drug | 2A-3, 2A-4, 2C - 1, 2C - 2, 2C - 3, 2C - 4 |
| OGTTOral glucose tolerance test with 75 g glucose | Other | 1C, 2A-1, 2A-3, 2C - 1, 2C - 2 |
| IVGTTIntravenous glucose tolerance test with infusion of 20% glucose matching the glucose profile of the corresponding OGTT | Other | 1C, 2A-2, 2A-4, 2C - 3, 2C - 4 |
Primary outcome
Substudy 2C (12 Healthy volunteers): GLP-1
Time frame: 6 weeks after intervention
Increased plasma insulin and C-peptide (intact insulinotropic effect of GLP-1) during GLP-1 infusion in healthy volunteers.
Substudy 2A (12 Healthy volunteers): Insulin, C-peptide and incretin hormone response
Time frame: 6 weeks after intervention
Insulin, c-peptide and incretin hormone response to glucose stimulation during standardized systemic inflammation (TNF infusion) compared to placebo (saline infusion)
Substudy 1C(8 patients, 8 healthy controls): Insulin, C-peptide and incretin hormone response
Time frame: 6 weeks after intervention
Insulin, c-peptide and incretin hormone response to glucose stimulation during IVGTT compared to OGTT in critically ill patients admitted to the ICU
3 secondary outcomes
Substudy 2C (12 Healthy volunteers): Clamp
Time frame: 6 weeks after intervention
Substudy 2A (12 Healthy volunteers): The incretin effect
Time frame: 6 weeks after intervention
Substudy 1C (8 patients, 8 healthy controls): The incretin effect
Time frame: 6 weeks after intervention
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 22 Sep 2014.
- Background: PubMed 11219223McCowen KC, Malhotra A, Bistrian BR. Stress-induced hyperglycemia. Crit Care Clin. 2001 Jan;17(1):107-24. doi: 10.1016/s0749-0704(05)70154-8.
- Background: PubMed 11800522Mizock BA. Alterations in fuel metabolism in critical illness: hyperglycaemia. Best Pract Res Clin Endocrinol Metab. 2001 Dec;15(4):533-51. doi: 10.1053/beem.2001.0168.
- Background: PubMed 15312220Rusavy Z, Sramek V, Lacigova S, Novak I, Tesinsky P, Macdonald IA. Influence of insulin on glucose metabolism and energy expenditure in septic patients. Crit Care. 2004 Aug;8(4):R213-20. doi: 10.1186/cc2868. Epub 2004 May 26.
- Background: PubMed 8080494Beal AL, Cerra FB. Multiple organ failure syndrome in the 1990s. Systemic inflammatory response and organ dysfunction. JAMA. 1994 Jan 19;271(3):226-33.
- Background: PubMed 10335783Schmidt MI, Duncan BB, Sharrett AR, Lindberg G, Savage PJ, Offenbacher S, Azambuja MI, Tracy RP, Heiss G. Markers of inflammation and prediction of diabetes mellitus in adults (Atherosclerosis Risk in Communities study): a cohort study. Lancet. 1999 May 15;353(9165):1649-52. doi: 10.1016/s0140-6736(99)01046-6.
- Background: PubMed 10773115Wolfe RR, Martini WZ. Changes in intermediary metabolism in severe surgical illness. World J Surg. 2000 Jun;24(6):639-47. doi: 10.1007/s002689910105.
- Background: PubMed 12028371Boden G, Shulman GI. Free fatty acids in obesity and type 2 diabetes: defining their role in the development of insulin resistance and beta-cell dysfunction. Eur J Clin Invest. 2002 Jun;32 Suppl 3:14-23. doi: 10.1046/j.1365-2362.32.s3.3.x.
- Background: PubMed 8636533Thijs LG, Hack CE. Time course of cytokine levels in sepsis. Intensive Care Med. 1995 Nov;21 Suppl 2:S258-63. doi: 10.1007/BF01740764.
- Background: PubMed 16464907Krogh-Madsen R, Plomgaard P, Moller K, Mittendorfer B, Pedersen BK. Influence of TNF-alpha and IL-6 infusions on insulin sensitivity and expression of IL-18 in humans. Am J Physiol Endocrinol Metab. 2006 Jul;291(1):E108-14. doi: 10.1152/ajpendo.00471.2005. Epub 2006 Feb 7.
- Background: PubMed 8675698Roden M, Price TB, Perseghin G, Petersen KF, Rothman DL, Cline GW, Shulman GI. Mechanism of free fatty acid-induced insulin resistance in humans. J Clin Invest. 1996 Jun 15;97(12):2859-65. doi: 10.1172/JCI118742.
- Background: PubMed 7712756Voerman BJ, Strack van Schijndel RJ, Groeneveld AB, de Boer H, Nauta JP, Thijs LG. Effects of human growth hormone in critically ill nonseptic patients: results from a prospective, randomized, placebo-controlled trial. Crit Care Med. 1995 Apr;23(4):665-73. doi: 10.1097/00003246-199504000-00014.
- Background: PubMed 14559958Finney SJ, Zekveld C, Elia A, Evans TW. Glucose control and mortality in critically ill patients. JAMA. 2003 Oct 15;290(15):2041-7. doi: 10.1001/jama.290.15.2041.
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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.
Kirsten Møller, MD, Ph.D., DMSc principal investigator
Centre of Inflammation and Metabolism
2 sites in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing GLP-1, TNF-alfa and OGTT in people with Hypoglycaemia, run by Copenhagen University Hospital, Rigshospitalet at 2 sites in Denmark.
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 6 inclusion and 2 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: finished, as of the sponsor's last update on 22 Sep 2014. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 2 sites in Denmark. 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. Some participants in this study may receive a placebo. 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 is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
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?
Substudy 2C (12 Healthy volunteers): GLP-1 (time frame: 6 weeks after intervention). The study lists 3 primary outcomes in all. 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 NCT01347801, which also lists 36 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 22 Sep 2014.