SepsisHBPNCT02533011
Evaluation of the Heparin Binding Protein Levels in Sepsis
An observational study of Sepsis and Infection, run by Christiana Care Health Services at 1 site in United States.
Trial summary
Present criteria used to define sepsis are non-specific, making it difficult to both distinguish sepsis from other diseases and to predict which patients are likely to become more severely ill. Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Sepsis, Infection, Septic Shock
- What is being tested?
- HBP lab test
- How many people
- 1,055 participants
- Where
- 1 siteUnited States
- Study dates
- Jul 2015to Jul 2017
- 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: Patients admitted through the emergency department with infection.
Who may be able to join
- Clinical diagnosis of a bacterial or viral infection
- 18 years or older
- Meet the sepsis alert criterion (Hypotension (BP < 90 after 2 L of fluids or lactate ≥ 4) OR
- PIRO (Predispose, Infection, Response, Organ dysfunction ) score ≥ 15 .
Who cannot join
- Minors (less than 18 years of age)
- Patients who do not meet sepsis criteria as described above
Trial locations and contacts
1 site in 1 country.
United States1 site
Christiana Care Health System
Newark, Delaware, 19718
About this study
Official title: Heparin Binding Protein (HBP) in Sepsis for the Prediction of Disease Progression
Present criteria used to define sepsis are non-specific, making it difficult to both distinguish sepsis from other diseases and to predict which patients are likely to become more severely ill. In standard care, patients at risk of becoming more severely ill are neither identified nor indicated for resuscitative efforts until they develop hemodynamic insufficiency or organ failure; after progression to severe disease, mortality increases significantly. The identification of risk patients can lead to earlier initiation of resuscitation therapies and potentially lead to reduced morbidity and mortality. This study aims to determine whether Heparin-binding protein (HBP), which is secreted from neutrophils during infection and a mediator of vascular leakage, can act as a biomarker for the progression to severe sepsis with circulatory failure.
The objective of this study is to validate the utility of HBP to predict the development of delayed onset organ dysfunction in sepsis in patients and to compare the performance of HBP relative to currently used prognostic biomarkers in sepsis.
Read the detailed description
Sepsis is a heterogeneous disorder caused by an invasive infection that results in host inflammatory response. The underlying pathogenesis is complex and dependent on the etiologic microorganism, site of infection, and host factors. Present criteria defining sepsis (including change of body temperature, increased heart and respiration rates, and leukocytosis/leukopenia) are non-specific making it difficult to distinguish sepsis from other diseases and in particular to predict which patients are likely to become more severely ill. The consensus definition of sepsis has been debated over the past years and one suggested approach is to focus more on the presence of organ dysfunction. In standard care, patients at risk of becoming more seriously ill are not identified nor indicated for resuscitative efforts until they develop hemodynamic insufficiency or organ failure. However, after progression to severe disease mortality increases significantly. A recent study showed that almost a quarter of patients presenting with uncomplicated sepsis in an Emergency Department (ED) developed severe sepsis or septic shock within 72 hours. Delayed in-hospital progression to increased organ dysfunction was associated with increased transfer to the intensive care unit (ICU) and increased hospital length of stay. The identification of risk patients can lead to earlier initiation of resuscitation therapies and potentially lead to reduced morbidity and mortality. There are also increasing evidence that a single episode of severe sepsis has negative impact on quality of life and mortality several years after the actual incident. Also, recent studies indicate that less severe organ dysfunction, such as small increases in serum creatinine, are associated with increased long-term mortality among sepsis survivors.
Mechanisms that trigger the release of heparin-binding protein (HBP) from neutrophils in the presence of bacteria have previously been reported. HBP has several functions such as a chemo-attractant and as an activator of monocytes and macrophages. Also, it induces vascular leakage by interacting with the capillary endothelium and breaking cell barriers. In vivo studies have demonstrated that HBP released by the complex formed by the group A streptococcal M1 protein and fibrinogen induces a massive tissue edema contributing to severe organ damage. In clinical investigations, the release of HBP has been demonstrated in various infectious diseases caused by a wide array of bacteria. A recent single-center study of patients admitted for suspected infection and fever showed that plasma levels of HBP were significantly higher among patients who presented with or developed severe sepsis with circulatory failure.
A prospective observational study in a tertiary care Emergency Department. Patients must be identified and enrolled within 72 hours of qualifying inclusion criteria. At this time, unused blood samples collected for routine testing will be examined and the plasma level of HBP will be recorded; only blood samples processed by the lab within 3 hours of collection will be used. In addition, physiologic variables detailed in the data elements section, including mental status, metabolic, renal, heme, hepatic, respiratory, cardiovascular, resuscitation, and vasopressor use will be recorded. Patients who meet the inclusion criteria will be identified. Researchers will collect and record a resuscitation summary for a span of 4 hours; this data, outlined in the data elements section, will be linked to the quality improvement (QI) database of Sepsis Research. Additionally, the patient's HBP plasma levels will be measured from unused blood samples collected for routine lab testing time (T) 24, 48, and 72-hours (T24, T48, T72) after meeting the inclusion criteria (T0); resuscitation summaries will also be collected at T24, T48, T72. For patients meeting sepsis alert criteria, T0 will be defined as the time that the patient qualified; those enrolled based on Predisposition, Injury, Response, Organ dysfunction (PIRO) score will have T0 defined as the time hospital admission was ordered. Patients will be followed throughout their time in the hospital and their outcomes will be recorded.
- Conditions
- Sepsis, Infection, Septic Shock
- Being tested
- HBP lab test
- Keywords
- Sepsis, Heparin Binding Protein
- Medical subject headings
- Sepsis, Infections, Shock, Septic
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
HBP lab testOther
Also called Plasma level of heparin binding protein
Plasma level of Heparin Binding Protein will be evaluated on extra blood specimens already collected as part of standard of care.
| Study group | Role | What they receive |
|---|---|---|
| 24 Hours | HBP lab test performed 24 hours after meeting sepsis inclusion criteria. Receives: Other: HBP lab test | |
| 48 Hours | HBP lab test performed 48 hours after meeting sepsis inclusion criteria. Receives: Other: HBP lab test | |
| 72 Hours | HBP lab test performed 72 hours after meeting sepsis inclusion criteria. Receives: Other: HBP lab test |
What is being measured
The primary outcome is the main question the study is designed to answer.
Infection with organ dysfunction, defined as PIRO (Predisposition, Insult, Response, Organ Dysfunction) Score greater than 5
Patients with septic shock or severe sepsis
Measured: 72 hours after meeting sepsis criteria
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted26 Aug 2015 (estimated)
- Study startJul 2015
- Primary completionDec 2016
- Study completionJul 2017
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (22)Papers the sponsor has linked to this study.
- Other trials for SepsisStudies 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
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 1,055 participants (actual)
Sponsor and investigators
- Lead sponsor
- Christiana Care Health Services
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
- Investigators
- Ryan C. Arnold, MD, Principal investigator, Christiana Care Health Services
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02533011
- Sponsor's protocol ID
- 602986
- Acronym
- HBP
- Status last verified
- Sep 2017
- First submitted
- 16 Jul 2015
- Last updated
- 25 Sep 2017
- Results posted
- No
- Data monitoring committee
- No
Publications
Dremsizov T, Clermont G, Kellum JA, Kalassian KG, Fine MJ, Angus DC. Severe sepsis in community-acquired pneumonia: when does it happen, and do systemic inflammatory response syndrome criteria help predict course? Chest. 2006 Apr;129(4):968-78. doi: 10.1378/chest.129.4.968.
PubMed 16608946Shapiro N, Howell MD, Bates DW, Angus DC, Ngo L, Talmor D. The association of sepsis syndrome and organ dysfunction with mortality in emergency department patients with suspected infection. Ann Emerg Med. 2006 Nov;48(5):583-90, 590.e1. doi: 10.1016/j.annemergmed.2006.07.007.
PubMed 17052559Vincent JL, Opal SM, Marshall JC, Tracey KJ. Sepsis definitions: time for change. Lancet. 2013 Mar 2;381(9868):774-5. doi: 10.1016/S0140-6736(12)61815-7. No abstract available.
PubMed 23472921Glickman SW, Cairns CB, Otero RM, Woods CW, Tsalik EL, Langley RJ, van Velkinburgh JC, Park LP, Glickman LT, Fowler VG Jr, Kingsmore SF, Rivers EP. Disease progression in hemodynamically stable patients presenting to the emergency department with sepsis. Acad Emerg Med. 2010 Apr;17(4):383-90. doi: 10.1111/j.1553-2712.2010.00664.x.
PubMed 20370777Arnold RC, Sherwin R, Shapiro NI, O'Connor JL, Glaspey L, Singh S, Medado P, Trzeciak S, Jones AE; Emergency Medicine Shock Research Network (EM Shock Net) Investigators. Multicenter observational study of the development of progressive organ dysfunction and therapeutic interventions in normotensive sepsis patients in the emergency department. Acad Emerg Med. 2013 May;20(5):433-40. doi: 10.1111/acem.12137.
PubMed 23672356Bastani A, Galens S, Rocchini A, Walch R, Shaqiri B, Palomba K, Milewski AM, Falzarano A, Loch D, Anderson W. ED identification of patients with severe sepsis/septic shock decreases mortality in a community hospital. Am J Emerg Med. 2012 Oct;30(8):1561-6. doi: 10.1016/j.ajem.2011.09.029. Epub 2011 Dec 26.
PubMed 22204997Kumar A, Roberts D, Wood KE, Light B, Parrillo JE, Sharma S, Suppes R, Feinstein D, Zanotti S, Taiberg L, Gurka D, Kumar A, Cheang M. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med. 2006 Jun;34(6):1589-96. doi: 10.1097/01.CCM.0000217961.75225.E9.
PubMed 16625125Rivers EP, Katranji M, Jaehne KA, Brown S, Abou Dagher G, Cannon C, Coba V. Early interventions in severe sepsis and septic shock: a review of the evidence one decade later. Minerva Anestesiol. 2012 Jun;78(6):712-24. Epub 2012 Mar 23.
PubMed 22447123Yende S, D'Angelo G, Kellum JA, Weissfeld L, Fine J, Welch RD, Kong L, Carter M, Angus DC; GenIMS Investigators. Inflammatory markers at hospital discharge predict subsequent mortality after pneumonia and sepsis. Am J Respir Crit Care Med. 2008 Jun 1;177(11):1242-7. doi: 10.1164/rccm.200712-1777OC. Epub 2008 Mar 27.
PubMed 18369199Cuthbertson BH, Elders A, Hall S, Taylor J, MacLennan G, Mackirdy F, Mackenzie SJ; Scottish Critical Care Trials Group; Scottish Intensive Care Society Audit Group. Mortality and quality of life in the five years after severe sepsis. Crit Care. 2013 Apr 16;17(2):R70. doi: 10.1186/cc12616.
PubMed 23587132Murugan R, Karajala-Subramanyam V, Lee M, Yende S, Kong L, Carter M, Angus DC, Kellum JA; Genetic and Inflammatory Markers of Sepsis (GenIMS) Investigators. Acute kidney injury in non-severe pneumonia is associated with an increased immune response and lower survival. Kidney Int. 2010 Mar;77(6):527-35. doi: 10.1038/ki.2009.502. Epub 2009 Dec 23.
PubMed 20032961Linder A, Fjell C, Levin A, Walley KR, Russell JA, Boyd JH. Small acute increases in serum creatinine are associated with decreased long-term survival in the critically ill. Am J Respir Crit Care Med. 2014 May 1;189(9):1075-81. doi: 10.1164/rccm.201311-2097OC.
PubMed 24601781Herwald H, Cramer H, Morgelin M, Russell W, Sollenberg U, Norrby-Teglund A, Flodgaard H, Lindbom L, Bjorck L. M protein, a classical bacterial virulence determinant, forms complexes with fibrinogen that induce vascular leakage. Cell. 2004 Feb 6;116(3):367-79. doi: 10.1016/s0092-8674(04)00057-1.
PubMed 15016372McNamara C, Zinkernagel AS, Macheboeuf P, Cunningham MW, Nizet V, Ghosh P. Coiled-coil irregularities and instabilities in group A Streptococcus M1 are required for virulence. Science. 2008 Mar 7;319(5868):1405-8. doi: 10.1126/science.1154470.
PubMed 18323455Macheboeuf P, Buffalo C, Fu CY, Zinkernagel AS, Cole JN, Johnson JE, Nizet V, Ghosh P. Streptococcal M1 protein constructs a pathological host fibrinogen network. Nature. 2011 Apr 7;472(7341):64-8. doi: 10.1038/nature09967.
PubMed 21475196
Study at a glance
From the registry record, last updated by the sponsor on 25 Sep 2017. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Heparin Binding Protein (HBP) in Sepsis for the Prediction of Disease Progression
- ClinicalTrials.gov ID
- NCT02533011
- Acronym / sponsor ID
- HBP / 602986
- Conditions
- Sepsis, Infection, Septic Shock
- Keywords
- Sepsis, Heparin Binding Protein
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 1,055 participants (actual)
- Lead sponsor
- Christiana Care Health ServicesUniversity, hospital or other
- Study start
- Jul 2015
- Primary completion
- Dec 2016 (actual)
- Study completion
- Jul 2017 (actual)
- First posted
- 26 Aug 2015 (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.
Present criteria used to define sepsis are non-specific, making it difficult to both distinguish sepsis from other diseases and to predict which patients are likely to become more severely ill. In standard care, patients at risk of becoming more severely ill are neither identified nor indicated for resuscitative efforts until they develop hemodynamic insufficiency or organ failure; after progression to severe disease, mortality increases significantly. The identification of risk patients can lead to earlier initiation of resuscitation therapies and potentially lead to reduced morbidity and mortality. This study aims to determine whether Heparin-binding protein (HBP), which is secreted from neutrophils during infection and a mediator of vascular leakage, can act as a biomarker for the progression to severe sepsis with circulatory failure.
The objective of this study is to validate the utility of HBP to predict the development of delayed onset organ dysfunction in sepsis in patients and to compare the performance of HBP relative to currently used prognostic biomarkers in sepsis.
Detailed description
Sepsis is a heterogeneous disorder caused by an invasive infection that results in host inflammatory response. The underlying pathogenesis is complex and dependent on the etiologic microorganism, site of infection, and host factors. Present criteria defining sepsis (including change of body temperature, increased heart and respiration rates, and leukocytosis/leukopenia) are non-specific making it difficult to distinguish sepsis from other diseases and in particular to predict which patients are likely to become more severely ill. The consensus definition of sepsis has been debated over the past years and one suggested approach is to focus more on the presence of organ dysfunction. In standard care, patients at risk of becoming more seriously ill are not identified nor indicated for resuscitative efforts until they develop hemodynamic insufficiency or organ failure. However, after progression to severe disease mortality increases significantly. A recent study showed that almost a quarter of patients presenting with uncomplicated sepsis in an Emergency Department (ED) developed severe sepsis or septic shock within 72 hours. Delayed in-hospital progression to increased organ dysfunction was associated with increased transfer to the intensive care unit (ICU) and increased hospital length of stay. The identification of risk patients can lead to earlier initiation of resuscitation therapies and potentially lead to reduced morbidity and mortality. There are also increasing evidence that a single episode of severe sepsis has negative impact on quality of life and mortality several years after the actual incident. Also, recent studies indicate that less severe organ dysfunction, such as small increases in serum creatinine, are associated with increased long-term mortality among sepsis survivors.
Mechanisms that trigger the release of heparin-binding protein (HBP) from neutrophils in the presence of bacteria have previously been reported. HBP has several functions such as a chemo-attractant and as an activator of monocytes and macrophages. Also, it induces vascular leakage by interacting with the capillary endothelium and breaking cell barriers. In vivo studies have demonstrated that HBP released by the complex formed by the group A streptococcal M1 protein and fibrinogen induces a massive tissue edema contributing to severe organ damage. In clinical investigations, the release of HBP has been demonstrated in various infectious diseases caused by a wide array of bacteria. A recent single-center study of patients admitted for suspected infection and fever showed that plasma levels of HBP were significantly higher among patients who presented with or developed severe sepsis with circulatory failure.
A prospective observational study in a tertiary care Emergency Department. Patients must be identified and enrolled within 72 hours of qualifying inclusion criteria. At this time, unused blood samples collected for routine testing will be examined and the plasma level of HBP will be recorded; only blood samples processed by the lab within 3 hours of collection will be used. In addition, physiologic variables detailed in the data elements section, including mental status, metabolic, renal, heme, hepatic, respiratory, cardiovascular, resuscitation, and vasopressor use will be recorded. Patients who meet the inclusion criteria will be identified. Researchers will collect and record a resuscitation summary for a span of 4 hours; this data, outlined in the data elements section, will be linked to the quality improvement (QI) database of Sepsis Research. Additionally, the patient's HBP plasma levels will be measured from unused blood samples collected for routine lab testing time (T) 24, 48, and 72-hours (T24, T48, T72) after meeting the inclusion criteria (T0); resuscitation summaries will also be collected at T24, T48, T72. For patients meeting sepsis alert criteria, T0 will be defined as the time that the patient qualified; those enrolled based on Predisposition, Injury, Response, Organ dysfunction (PIRO) score will have T0 defined as the time hospital admission was ordered. Patients will be followed throughout their time in the hospital and their outcomes will be recorded.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 3
| Arm | Type | Receives |
|---|---|---|
| 24 Hours | – | Other: HBP lab testHBP lab test performed 24 hours after meeting sepsis inclusion criteria. |
| 48 Hours | – | Other: HBP lab testHBP lab test performed 48 hours after meeting sepsis inclusion criteria. |
| 72 Hours | – | Other: HBP lab testHBP lab test performed 72 hours after meeting sepsis inclusion criteria. |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Patients admitted through the emergency department with infection.
Key inclusion criteria (4 listed)
- Clinical diagnosis of a bacterial or viral infection
- 18 years or older
- Meet the sepsis alert criterion (Hypotension (BP < 90 after 2 L of fluids or lactate ≥ 4) OR
- PIRO (Predispose, Infection, Response, Organ dysfunction ) score ≥ 15 .
Key exclusion criteria (2 listed)
- Minors (less than 18 years of age)
- Patients who do not meet sepsis criteria as described above
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 |
|---|---|---|
| HBP lab testAlso: Plasma level of heparin binding proteinPlasma level of Heparin Binding Protein will be evaluated on extra blood specimens already collected as part of standard of care. | Other | 24 Hours, 48 Hours, 72 Hours |
Primary outcome
Infection with organ dysfunction, defined as PIRO (Predisposition, Insult, Response, Organ Dysfunction) Score greater than 5
Time frame: 72 hours after meeting sepsis criteria
Patients with septic shock or severe sepsis
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 25 Sep 2017.
- Background: PubMed 16608946Dremsizov T, Clermont G, Kellum JA, Kalassian KG, Fine MJ, Angus DC. Severe sepsis in community-acquired pneumonia: when does it happen, and do systemic inflammatory response syndrome criteria help predict course? Chest. 2006 Apr;129(4):968-78. doi: 10.1378/chest.129.4.968.
- Background: PubMed 17052559Shapiro N, Howell MD, Bates DW, Angus DC, Ngo L, Talmor D. The association of sepsis syndrome and organ dysfunction with mortality in emergency department patients with suspected infection. Ann Emerg Med. 2006 Nov;48(5):583-90, 590.e1. doi: 10.1016/j.annemergmed.2006.07.007.
- Background: PubMed 23472921Vincent JL, Opal SM, Marshall JC, Tracey KJ. Sepsis definitions: time for change. Lancet. 2013 Mar 2;381(9868):774-5. doi: 10.1016/S0140-6736(12)61815-7. No abstract available.
- Background: PubMed 20370777Glickman SW, Cairns CB, Otero RM, Woods CW, Tsalik EL, Langley RJ, van Velkinburgh JC, Park LP, Glickman LT, Fowler VG Jr, Kingsmore SF, Rivers EP. Disease progression in hemodynamically stable patients presenting to the emergency department with sepsis. Acad Emerg Med. 2010 Apr;17(4):383-90. doi: 10.1111/j.1553-2712.2010.00664.x.
- Background: PubMed 23672356Arnold RC, Sherwin R, Shapiro NI, O'Connor JL, Glaspey L, Singh S, Medado P, Trzeciak S, Jones AE; Emergency Medicine Shock Research Network (EM Shock Net) Investigators. Multicenter observational study of the development of progressive organ dysfunction and therapeutic interventions in normotensive sepsis patients in the emergency department. Acad Emerg Med. 2013 May;20(5):433-40. doi: 10.1111/acem.12137.
- Background: PubMed 22204997Bastani A, Galens S, Rocchini A, Walch R, Shaqiri B, Palomba K, Milewski AM, Falzarano A, Loch D, Anderson W. ED identification of patients with severe sepsis/septic shock decreases mortality in a community hospital. Am J Emerg Med. 2012 Oct;30(8):1561-6. doi: 10.1016/j.ajem.2011.09.029. Epub 2011 Dec 26.
- Background: PubMed 16625125Kumar A, Roberts D, Wood KE, Light B, Parrillo JE, Sharma S, Suppes R, Feinstein D, Zanotti S, Taiberg L, Gurka D, Kumar A, Cheang M. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med. 2006 Jun;34(6):1589-96. doi: 10.1097/01.CCM.0000217961.75225.E9.
- Background: PubMed 22447123Rivers EP, Katranji M, Jaehne KA, Brown S, Abou Dagher G, Cannon C, Coba V. Early interventions in severe sepsis and septic shock: a review of the evidence one decade later. Minerva Anestesiol. 2012 Jun;78(6):712-24. Epub 2012 Mar 23.
- Background: PubMed 18369199Yende S, D'Angelo G, Kellum JA, Weissfeld L, Fine J, Welch RD, Kong L, Carter M, Angus DC; GenIMS Investigators. Inflammatory markers at hospital discharge predict subsequent mortality after pneumonia and sepsis. Am J Respir Crit Care Med. 2008 Jun 1;177(11):1242-7. doi: 10.1164/rccm.200712-1777OC. Epub 2008 Mar 27.
- Background: PubMed 23587132Cuthbertson BH, Elders A, Hall S, Taylor J, MacLennan G, Mackirdy F, Mackenzie SJ; Scottish Critical Care Trials Group; Scottish Intensive Care Society Audit Group. Mortality and quality of life in the five years after severe sepsis. Crit Care. 2013 Apr 16;17(2):R70. doi: 10.1186/cc12616.
- Background: PubMed 20032961Murugan R, Karajala-Subramanyam V, Lee M, Yende S, Kong L, Carter M, Angus DC, Kellum JA; Genetic and Inflammatory Markers of Sepsis (GenIMS) Investigators. Acute kidney injury in non-severe pneumonia is associated with an increased immune response and lower survival. Kidney Int. 2010 Mar;77(6):527-35. doi: 10.1038/ki.2009.502. Epub 2009 Dec 23.
- Background: PubMed 24601781Linder A, Fjell C, Levin A, Walley KR, Russell JA, Boyd JH. Small acute increases in serum creatinine are associated with decreased long-term survival in the critically ill. Am J Respir Crit Care Med. 2014 May 1;189(9):1075-81. doi: 10.1164/rccm.201311-2097OC.
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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.
Ryan C. Arnold, MD principal investigator
Christiana Care Health Services
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 and Infection, run by Christiana Care Health Services at 1 site in United States.
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 4 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 25 Sep 2017. 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 States. 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?
Infection with organ dysfunction, defined as PIRO (Predisposition, Insult, Response, Organ Dysfunction) Score greater than 5 (time frame: 72 hours after meeting sepsis criteria). 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 NCT02533011, which also lists 22 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 25 Sep 2017.