SepsisNCT02963480
Investigation of Inflammatory Parameters in a Perioperative Closed-meshed Standard Progress in CPB Patients
An observational study of Sepsis, run by Medical University of Vienna at 1 site in Austria.
Trial summary
Similar to poly-trauma, acute myocardial infarction, or stroke, the speed and appropriateness of therapy administered in the initial hours after severe sepsis develops are likely to influence outcome. Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Sepsis
- What is being tested?
- Cardiac Surgery
- Type of treatment
- Surgery or procedure
- How many people
- 100 participants
- Where
- 1 siteAustria
- Study dates
- 30 Oct 2016to 5 Feb 2018
- Phase
- Observational
- 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 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: Prospective observational cohort study in patients with elective cardiac surgery.
Who may be able to join
None listed.
Who cannot join
- Emergency procedures
- Heart transplantation
- Elective left ventricular assist device (LVAD) implantation
- Pulmonary thrombendarterectomy
- Declined informed consent
- Chronic renal failure on renal replacement therapy
Show all 14Show fewer
- Body mass index < 18
- Age < 18 years
- Pregnant woman
- Receiving chemotherapy or diagnosed with any disease state (e.g., AIDS)
- that has produced leukopenia
- Receiving anti-leucocyte drugs, immunosuppression or TNF-α Blockers
- CRP > 2mg.dl-1
- Patients receiving postoperative extracorporeal membrane oxygenation (ECMO)
Trial locations and contacts
1 site in 1 country.
Austria1 site
Divison of Cardiothoracic Anaesthesia and Intensive Care, Medical University of Vienna
Vienna, 1090
About this study
Similar to poly-trauma, acute myocardial infarction, or stroke, the speed and appropriateness of therapy administered in the initial hours after severe sepsis develops are likely to influence outcome. However, the crux of matter is the "early diagnosis" lacking of high sensitive and specific test, in contrary to, for instance, the acute coronary syndrome, where the highly sensitive Troponin T is measured and increased values are fix component of the diagnosis and definition of acute myocardial infarction. Cardiac surgery can initiate a systemic inflammatory response syndrome (SIRS) induced by extrinsic and intrinsic factors, which are associated in the pathogenesis of postoperative complications. SIRS is closely related to sepsis, but in contrast sepsis is induced by infection. This strong inflammatory response induces malfunction of the peripheral circulation with increased lactate levels, pronounced fluid accumulation and increased need of vasopressors.
The investigators want to assess the timing dynamic of release of IL-6 apart from established markers like CRP, leukocytes, PCT. Target of this is to estimate the time-scope and -advance of an "IL-6 axis panel" toward the measurement of standard inflammation parameters in inflammatory response to surgical trauma as a pre-figuration of non-infectious SIRS and to search for a eligible "cut-off" of IL-6.
Read the detailed description
Similarly for early detection of SIRS/Sepsis, interleukin 6 (IL-6) assays have been brought up for discussion and have been studied extensively over last years. IL-6 is pro-and anti-inflammatory cytokine with multimodal functions in physiology and patho- physiology: As a major regulator of hepatic acute phase response, IL-6 induces the expression of C- reactive protein, fibrinogen and serum amyloid-A protein among others. However, along with pro-inflammatory effects IL-6 is described as an anti- inflammatory agent. Especially in systemic inflammatory response syndrome (SIRS) and sepsis the pro-inflammatory impact of IL-6 is of paramount interest: Via trans-signaling using the soluble IL-6 receptor (sIL-6R) pathway adherent junctions of endothelial VE-cadherin are disconnected causing a loss of barrier function. Increased endothelial permeability results in trans-endothelial flow of fluid and interstitial oedema with consecutive impairment of tissue oxygenation and increased blood viscosity.
Recent publications suggest, that regenerative or anti-inflammatory activities of IL-6 are mediated by classic signalling via a membrane bound IL-6 receptor, whereas pro-inflammatory responses of interleukin-6 are rather mediated by trans-signalling using soluble IL-6.
The IL-6, sIL-6R, soluble glycoprotein 130- buffer:
Since all cells in body express glycoprotein (gp) 130, one of the crucial molecules in signal-transduction of IL-6, they all are susceptible to activation by the complex of IL-6 and sIL-6-Receptor. Thus, under steady state conditions there must be a control mechanism, which prevents IL-6/sIL-6R trans-signalling and hence unbounded activation of pro- inflammatory axis conterminously with a kind of "buffer system" for the IL-6 activity. For such a buffer, at least three different molecules have been taken into account: IL-6 itself, the -above mentioned- sIL-6Receptor and the soluble form of gp130 (sgp130).
Under steady-state and non- inflammatory conditions levels of sIL-6R and sgp130 are almost 1000 fold higher than IL-6, meaning IL-6 is once secreted, it will form a complex with sIL-6R and consecutively will be neutralized by association to sgp130. The immunological impact of circulating IL-6 is a function of the serum IL-6, sIL-6R and sgp130 concentration, respectively of the proportion of the proteins to each other.
Kinetic of IL-6 and the impact of procalcitonin:
In the early nineties, the use of procalcitonin (PCT) has been described by Assicot et al. for the diagnosis of, in particular, bacterial sepsis. However, for discrimination of the acute inflammatory pattern of sepsis from other causes of generalized inflammation (e.g., postoperative, other forms of shock) no recommendation has been given for the use PCT to distinguish between severe infection and other acute inflammatory states in the actual guidelines. Nevertheless, conflicting to this reference, a recent high impact meta-analysis concluded that PCT can differentiate effectively between sepsis and systemic inflammatory response syndrome (SIRS) of non- infectious origin with a cut-off of between 1·0 and 2·0 ng/mL.
The drawback of PCT and e.g. C-reactive Protein (CRP) in relation to members of the IL-6 axis is, that these molecules are downstream of the IL-6 axis and therefore the increase caused by endotoxin or for instance by surgical trauma is delayed.
- Conditions
- Sepsis
- Being tested
- Cardiac Surgery
- Medical subject headings
- Sepsis
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Cardiac SurgeryProcedure or surgery
| Study group | Role | What they receive |
|---|---|---|
| Sepsis | Patients, who developed postoperative sepsis Receives: Procedure: Cardiac Surgery | |
| SIRS | Patients, who developed postoperative SIRS Receives: Procedure: Cardiac Surgery |
What is being measured
The primary outcome is the main question the study is designed to answer.
Change of IL-6
Change of IL-6 over the observation period, peak and nadir comparison
Measured: 10 days
Secondary outcomes (2)
Change of PCT
Change of PCT over the observation period, peak and nadir comparison
Measured: 10 days
Change of bioelectrical impedance analysis
Change of percent Total Body Water, Fat Free Mass over the observation period
Measured: 10 days
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted15 Nov 2016 (estimated)
- Study start30 Oct 2016
- Primary completion26 Jan 2018
- Study completion5 Feb 2018
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (14)Papers the sponsor has linked to this study.
- Other trials for SepsisStudies of the same condition, open and under way.
- More trials run by Medical University of ViennaThe 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
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 100 participants (actual)
Sponsor and investigators
- Lead sponsor
- Medical University of Vienna
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Dr. Martin Bernardi, Medical University of Vienna
- Investigators
- Martin H Bernardi, MD, Principal investigator, Medical University of Vienna, Dept. of Cardiothoracic and Vascular Anesthesia and Intensive Care
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02963480
- Sponsor's protocol ID
- 1518/2016
- Status last verified
- Feb 2018
- First submitted
- 6 Jul 2016
- Last updated
- 19 Feb 2018
- Results posted
- No
- Data monitoring committee
- Yes
- Individual data sharing
- Undecided
Publications
Dellinger RP, Levy MM, Rhodes A, Annane D, Gerlach H, Opal SM, Sevransky JE, Sprung CL, Douglas IS, Jaeschke R, Osborn TM, Nunnally ME, Townsend SR, Reinhart K, Kleinpell RM, Angus DC, Deutschman CS, Machado FR, Rubenfeld GD, Webb SA, Beale RJ, Vincent JL, Moreno R; Surviving Sepsis Campaign Guidelines Committee including the Pediatric Subgroup. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013 Feb;41(2):580-637. doi: 10.1097/CCM.0b013e31827e83af.
PubMed 23353941Marshall JC, Reinhart K; International Sepsis Forum. Biomarkers of sepsis. Crit Care Med. 2009 Jul;37(7):2290-8. doi: 10.1097/CCM.0b013e3181a02afc.
PubMed 19487943Alpert JS, Thygesen K, Antman E, Bassand JP. Myocardial infarction redefined--a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol. 2000 Sep;36(3):959-69. doi: 10.1016/s0735-1097(00)00804-4.
PubMed 10987628Bernardi MH, Rinoesl H, Dragosits K, Ristl R, Hoffelner F, Opfermann P, Lamm C, Preissing F, Wiedemann D, Hiesmayr MJ, Spittler A. Effect of hemoadsorption during cardiopulmonary bypass surgery - a blinded, randomized, controlled pilot study using a novel adsorbent. Crit Care. 2016 Apr 9;20:96. doi: 10.1186/s13054-016-1270-0.
PubMed 27059056Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, Bellomo R, Bernard GR, Chiche JD, Coopersmith CM, Hotchkiss RS, Levy MM, Marshall JC, Martin GS, Opal SM, Rubenfeld GD, van der Poll T, Vincent JL, Angus DC. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):801-10. doi: 10.1001/jama.2016.0287.
PubMed 26903338Evans BJ, Haskard DO, Finch JR, Hambleton IR, Landis RC, Taylor KM. The inflammatory effect of cardiopulmonary bypass on leukocyte extravasation in vivo. J Thorac Cardiovasc Surg. 2008 May;135(5):999-1006. doi: 10.1016/j.jtcvs.2007.08.071.
PubMed 18455576Chalaris A, Garbers C, Rabe B, Rose-John S, Scheller J. The soluble Interleukin 6 receptor: generation and role in inflammation and cancer. Eur J Cell Biol. 2011 Jun-Jul;90(6-7):484-94. doi: 10.1016/j.ejcb.2010.10.007. Epub 2010 Dec 8.
PubMed 21145125Wolsk E, Mygind H, Grondahl TS, Pedersen BK, van Hall G. IL-6 selectively stimulates fat metabolism in human skeletal muscle. Am J Physiol Endocrinol Metab. 2010 Nov;299(5):E832-40. doi: 10.1152/ajpendo.00328.2010. Epub 2010 Sep 7.
PubMed 20823453Kruttgen A, Rose-John S. Interleukin-6 in sepsis and capillary leakage syndrome. J Interferon Cytokine Res. 2012 Feb;32(2):60-5. doi: 10.1089/jir.2011.0062. Epub 2011 Dec 2.
PubMed 22136372Scheller J, Chalaris A, Schmidt-Arras D, Rose-John S. The pro- and anti-inflammatory properties of the cytokine interleukin-6. Biochim Biophys Acta. 2011 May;1813(5):878-88. doi: 10.1016/j.bbamcr.2011.01.034. Epub 2011 Feb 4.
PubMed 21296109Jones SA, Scheller J, Rose-John S. Therapeutic strategies for the clinical blockade of IL-6/gp130 signaling. J Clin Invest. 2011 Sep;121(9):3375-83. doi: 10.1172/JCI57158. Epub 2011 Sep 1.
PubMed 21881215Rose-John S. IL-6 trans-signaling via the soluble IL-6 receptor: importance for the pro-inflammatory activities of IL-6. Int J Biol Sci. 2012;8(9):1237-47. doi: 10.7150/ijbs.4989. Epub 2012 Oct 24.
PubMed 23136552Assicot M, Gendrel D, Carsin H, Raymond J, Guilbaud J, Bohuon C. High serum procalcitonin concentrations in patients with sepsis and infection. Lancet. 1993 Feb 27;341(8844):515-8. doi: 10.1016/0140-6736(93)90277-n.
PubMed 8094770Wacker C, Prkno A, Brunkhorst FM, Schlattmann P. Procalcitonin as a diagnostic marker for sepsis: a systematic review and meta-analysis. Lancet Infect Dis. 2013 May;13(5):426-35. doi: 10.1016/S1473-3099(12)70323-7. Epub 2013 Feb 1.
PubMed 23375419
Study at a glance
From the registry record, last updated by the sponsor on 19 Feb 2018. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Investigation of Inflammatory Parameters in a Perioperative Closed-meshed Standard Progress in CPB Patients
- ClinicalTrials.gov ID
- NCT02963480
- Acronym / sponsor ID
- 1518/2016
- Conditions
- Sepsis
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 100 participants (actual)
- Lead sponsor
- Medical University of ViennaUniversity, hospital or other
- Study start
- 30 Oct 2016 (actual)
- Primary completion
- 26 Jan 2018 (actual)
- Study completion
- 5 Feb 2018 (actual)
- First posted
- 15 Nov 2016 (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.
Similar to poly-trauma, acute myocardial infarction, or stroke, the speed and appropriateness of therapy administered in the initial hours after severe sepsis develops are likely to influence outcome. However, the crux of matter is the "early diagnosis" lacking of high sensitive and specific test, in contrary to, for instance, the acute coronary syndrome, where the highly sensitive Troponin T is measured and increased values are fix component of the diagnosis and definition of acute myocardial infarction. Cardiac surgery can initiate a systemic inflammatory response syndrome (SIRS) induced by extrinsic and intrinsic factors, which are associated in the pathogenesis of postoperative complications. SIRS is closely related to sepsis, but in contrast sepsis is induced by infection. This strong inflammatory response induces malfunction of the peripheral circulation with increased lactate levels, pronounced fluid accumulation and increased need of vasopressors.
The investigators want to assess the timing dynamic of release of IL-6 apart from established markers like CRP, leukocytes, PCT. Target of this is to estimate the time-scope and -advance of an "IL-6 axis panel" toward the measurement of standard inflammation parameters in inflammatory response to surgical trauma as a pre-figuration of non-infectious SIRS and to search for a eligible "cut-off" of IL-6.
Detailed description
Similarly for early detection of SIRS/Sepsis, interleukin 6 (IL-6) assays have been brought up for discussion and have been studied extensively over last years. IL-6 is pro-and anti-inflammatory cytokine with multimodal functions in physiology and patho- physiology: As a major regulator of hepatic acute phase response, IL-6 induces the expression of C- reactive protein, fibrinogen and serum amyloid-A protein among others. However, along with pro-inflammatory effects IL-6 is described as an anti- inflammatory agent. Especially in systemic inflammatory response syndrome (SIRS) and sepsis the pro-inflammatory impact of IL-6 is of paramount interest: Via trans-signaling using the soluble IL-6 receptor (sIL-6R) pathway adherent junctions of endothelial VE-cadherin are disconnected causing a loss of barrier function. Increased endothelial permeability results in trans-endothelial flow of fluid and interstitial oedema with consecutive impairment of tissue oxygenation and increased blood viscosity.
Recent publications suggest, that regenerative or anti-inflammatory activities of IL-6 are mediated by classic signalling via a membrane bound IL-6 receptor, whereas pro-inflammatory responses of interleukin-6 are rather mediated by trans-signalling using soluble IL-6.
The IL-6, sIL-6R, soluble glycoprotein 130- buffer:
Since all cells in body express glycoprotein (gp) 130, one of the crucial molecules in signal-transduction of IL-6, they all are susceptible to activation by the complex of IL-6 and sIL-6-Receptor. Thus, under steady state conditions there must be a control mechanism, which prevents IL-6/sIL-6R trans-signalling and hence unbounded activation of pro- inflammatory axis conterminously with a kind of "buffer system" for the IL-6 activity. For such a buffer, at least three different molecules have been taken into account: IL-6 itself, the -above mentioned- sIL-6Receptor and the soluble form of gp130 (sgp130).
Under steady-state and non- inflammatory conditions levels of sIL-6R and sgp130 are almost 1000 fold higher than IL-6, meaning IL-6 is once secreted, it will form a complex with sIL-6R and consecutively will be neutralized by association to sgp130. The immunological impact of circulating IL-6 is a function of the serum IL-6, sIL-6R and sgp130 concentration, respectively of the proportion of the proteins to each other.
Kinetic of IL-6 and the impact of procalcitonin:
In the early nineties, the use of procalcitonin (PCT) has been described by Assicot et al. for the diagnosis of, in particular, bacterial sepsis. However, for discrimination of the acute inflammatory pattern of sepsis from other causes of generalized inflammation (e.g., postoperative, other forms of shock) no recommendation has been given for the use PCT to distinguish between severe infection and other acute inflammatory states in the actual guidelines. Nevertheless, conflicting to this reference, a recent high impact meta-analysis concluded that PCT can differentiate effectively between sepsis and systemic inflammatory response syndrome (SIRS) of non- infectious origin with a cut-off of between 1·0 and 2·0 ng/mL.
The drawback of PCT and e.g. C-reactive Protein (CRP) in relation to members of the IL-6 axis is, that these molecules are downstream of the IL-6 axis and therefore the increase caused by endotoxin or for instance by surgical trauma is delayed.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Sepsis | – | Procedure: Cardiac SurgeryPatients, who developed postoperative sepsis |
| SIRS | – | Procedure: Cardiac SurgeryPatients, who developed postoperative SIRS |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Prospective observational cohort study in patients with elective cardiac surgery.
Key inclusion criteria (0 listed)
Key exclusion criteria (14 listed)
- Emergency procedures
- Heart transplantation
- Elective left ventricular assist device (LVAD) implantation
- Pulmonary thrombendarterectomy
- Declined informed consent
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 |
|---|---|---|
| Cardiac Surgery | Procedure or surgery | SIRS, Sepsis |
Primary outcome
Change of IL-6
Time frame: 10 days
Change of IL-6 over the observation period, peak and nadir comparison
2 secondary outcomes
Change of PCT
Time frame: 10 days
Change of bioelectrical impedance analysis
Time frame: 10 days
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 19 Feb 2018.
- Background: PubMed 23353941Dellinger RP, Levy MM, Rhodes A, Annane D, Gerlach H, Opal SM, Sevransky JE, Sprung CL, Douglas IS, Jaeschke R, Osborn TM, Nunnally ME, Townsend SR, Reinhart K, Kleinpell RM, Angus DC, Deutschman CS, Machado FR, Rubenfeld GD, Webb SA, Beale RJ, Vincent JL, Moreno R; Surviving Sepsis Campaign Guidelines Committee including the Pediatric Subgroup. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013 Feb;41(2):580-637. doi: 10.1097/CCM.0b013e31827e83af.
- Background: PubMed 19487943Marshall JC, Reinhart K; International Sepsis Forum. Biomarkers of sepsis. Crit Care Med. 2009 Jul;37(7):2290-8. doi: 10.1097/CCM.0b013e3181a02afc.
- Background: PubMed 10987628Alpert JS, Thygesen K, Antman E, Bassand JP. Myocardial infarction redefined--a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol. 2000 Sep;36(3):959-69. doi: 10.1016/s0735-1097(00)00804-4.
- Background: PubMed 27059056Bernardi MH, Rinoesl H, Dragosits K, Ristl R, Hoffelner F, Opfermann P, Lamm C, Preissing F, Wiedemann D, Hiesmayr MJ, Spittler A. Effect of hemoadsorption during cardiopulmonary bypass surgery - a blinded, randomized, controlled pilot study using a novel adsorbent. Crit Care. 2016 Apr 9;20:96. doi: 10.1186/s13054-016-1270-0.
- Background: PubMed 26903338Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, Bellomo R, Bernard GR, Chiche JD, Coopersmith CM, Hotchkiss RS, Levy MM, Marshall JC, Martin GS, Opal SM, Rubenfeld GD, van der Poll T, Vincent JL, Angus DC. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):801-10. doi: 10.1001/jama.2016.0287.
- Background: PubMed 18455576Evans BJ, Haskard DO, Finch JR, Hambleton IR, Landis RC, Taylor KM. The inflammatory effect of cardiopulmonary bypass on leukocyte extravasation in vivo. J Thorac Cardiovasc Surg. 2008 May;135(5):999-1006. doi: 10.1016/j.jtcvs.2007.08.071.
- Background: PubMed 21145125Chalaris A, Garbers C, Rabe B, Rose-John S, Scheller J. The soluble Interleukin 6 receptor: generation and role in inflammation and cancer. Eur J Cell Biol. 2011 Jun-Jul;90(6-7):484-94. doi: 10.1016/j.ejcb.2010.10.007. Epub 2010 Dec 8.
- Background: PubMed 20823453Wolsk E, Mygind H, Grondahl TS, Pedersen BK, van Hall G. IL-6 selectively stimulates fat metabolism in human skeletal muscle. Am J Physiol Endocrinol Metab. 2010 Nov;299(5):E832-40. doi: 10.1152/ajpendo.00328.2010. Epub 2010 Sep 7.
- Background: PubMed 22136372Kruttgen A, Rose-John S. Interleukin-6 in sepsis and capillary leakage syndrome. J Interferon Cytokine Res. 2012 Feb;32(2):60-5. doi: 10.1089/jir.2011.0062. Epub 2011 Dec 2.
- Background: PubMed 21296109Scheller J, Chalaris A, Schmidt-Arras D, Rose-John S. The pro- and anti-inflammatory properties of the cytokine interleukin-6. Biochim Biophys Acta. 2011 May;1813(5):878-88. doi: 10.1016/j.bbamcr.2011.01.034. Epub 2011 Feb 4.
- Background: PubMed 21881215Jones SA, Scheller J, Rose-John S. Therapeutic strategies for the clinical blockade of IL-6/gp130 signaling. J Clin Invest. 2011 Sep;121(9):3375-83. doi: 10.1172/JCI57158. Epub 2011 Sep 1.
- Background: PubMed 23136552Rose-John S. IL-6 trans-signaling via the soluble IL-6 receptor: importance for the pro-inflammatory activities of IL-6. Int J Biol Sci. 2012;8(9):1237-47. doi: 10.7150/ijbs.4989. Epub 2012 Oct 24.
- Individual participant dataSharing planned: Undecided
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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.
Martin H Bernardi, MD principal investigator
Medical University of Vienna, Dept. of Cardiothoracic and Vascular Anesthesia and Intensive Care
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Sepsis, run by Medical University of Vienna at 1 site in Austria.
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 0 inclusion and 14 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 19 Feb 2018. 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 Austria. 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 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?
Change of IL-6 (time frame: 10 days). 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 NCT02963480, which also lists 14 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 19 Feb 2018.