SepsisGPR43SepsisNCT02699905
Neutrophil FFA2/GPR43 Receptor Expression in Patients With the Diagnosis of Sepsis
An observational study of Sepsis and Septic Shock, run by Milton S. Hershey Medical Center.
Trial summary
This study seeks to elucidate the quantitative expression of G - protein receptor 43/free fatty acid (GPR43/FFA2) receptors in patients with the diagnosis of sepsis and specifically, its expression as it relates to the severity of sepsis. Read more about this study
- Who is it for?
- Ages 18 years and olderHealthy volunteers can take part
- Conditions the study is for
- Sepsis, Septic Shock, Multiple Organ Dysfunction
- What is being tested?
- phlebotomy
- How many people
- 0 participants
- Where
- No sites listed yet
- Study dates
- Aug 2016to Nov 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
- Healthy volunteers accepted
- Adult, Older adult
Study population: Adult patients with the diagnosis of sepsis or septic shock admitted to the intensive care unit at Penn State Hershey Medical Center, Hershey PA 17033.
Who may be able to join
- Diagnosis of sepsis or septic shock
- Age greater than eighteen years old.
- Ability to give informed consent (as determined by the attending physician) or presence of designated healthcare proxy that can give informed consent.
Who cannot join
- Patients or designated healthcare proxy with the inability to give informed consent.
- Patients under the age of eighteen
About this study
This study seeks to elucidate the quantitative expression of G - protein receptor 43/free fatty acid (GPR43/FFA2) receptors in patients with the diagnosis of sepsis and specifically, its expression as it relates to the severity of sepsis. The investigators hypothesize that patients with more severe sepsis, as defined by a higher SOFA (Sequential Organ Failure Assessment Score), will have decreased expression of the GPR43/FFA2 as compared to patients with lower SOFA scores, consistent with a less exuberant immune response to infection.
Patients admitted to Penn State Hershey Medical Center with a diagnosis of sepsis of any cause will undergo blood testing of leukocytes to determine the expressed quantity of GP43 during standardized time points of their illness and recovery. No interventions will be made in the standard clinical management of the patient. Additionally, healthy volunteers will be recruited to exam baseline GPR43 receptor expression between sepsis and control groups.
Read the detailed description
Despite advancements in recognition and treatment, sepsis continues to be a frequently fatal condition comprising 750,000 cases in the US with an estimated death rate of 28-38%. Bacterial sepsis complications are the result of a cascade of inflammatory mediators secondary to the immune system's recognition and response to invading bacteria, intracellular constituents and metabolites. Bacterial recognition results in the widespread activation of biological mediators essential to the immune response such as cytokines, chemokines, prostaglandins and reactive oxygen species. These compounds result in the activation and up-regulation of neutrophils, monocytes at the cellular level as well as the physiological changes of sepsis such as hyperpyrexia, vasodilation, and tachycardia. Despite this generally coordinated response, it is likely that marked complications are related to the sequela of the uncontrolled immune response leading to significant injury to the lungs (Acute Respiratory Distress Syndrome), and other organs (acute renal failure, shock liver). In addition, there is question that impairment of the gut mucosal barrier may result in translocation of bacteria and perpetuate the multiple organ failure.
G protein-coupled receptors (GPCRs) comprise one of the largest collections of transmembrane proteins in the mammalian genome. Recently, a subfamily of G protein coupled receptors have been identified that utilize short chain free fatty acids as ligands, FFA1 (GPR40), FFA2 (GPR43) and FFA3 (GPR41). Research has intimated that these receptors are involved in essential biological crosstalk between colonic bacteria, host and immune defenses. Although highly conserved in structure, members of this sub family demonstrate differences in fatty acid specificity, intracellular signaling mechanisms and tissue localization. Specifically, FFA2 (GPR43)4 expression has been shown to be expressed in higher magnitudes within immune cells, has been hypothesized to be involved in the modulation of pro- and anti-inflammatory mediators, such as prostaglandin E2 and is involved in neutrophil chemotaxis in mice. GPR43 is involved in the process of differentiation of progenitor immune cells into monocytes and macrophages, a key component of host defense. In addition, highly selective expression of GPR43 in polymorphonuclear cells point to strong role in chemotaxis and recruitment of immune cells to foci of bacterial infection. Short chain fatty acids also activate GPR43 receptors on intestinal epithelial cells with rapid production of secondary chemokine and cytokines after being challenged with inflammation and infection, and likely aid in the coordinated immune response. GP43 is likely an essential component of the phagocytic chemotaxis that maintains normal intestinal immune defense. In a model of acute colitis, GPR43 knockout mice demonstrated increased mortality. The authors concluded that GPR43 deficiency likely suppressed the role of immune cells within the gut immune milieu leading to death from sepsis related complications. Conversely, in a chronic colitis model, GPR43 deficient knockout mice demonstrated reduced colonic inflammation, without overwhelming infection, the authors concluded that GPR43 has an unfavorable role in the manifestation of chronic inflammatory conditions. These findings were confirmed with at least one later study. In humans, fetal membrane expression of GPR43 was higher in parturients in preterm labor with signs of infection.
- Being tested
- phlebotomy
- Keywords
- Sepsis, Septic Shock, Multiple Organ Dysfunction, FFA2, GPR43
- Medical subject headings
- Sepsis, Shock, Septic
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
phlebotomyOther
phlebotomy
| Study group | Role | What they receive |
|---|---|---|
| Sepsis | Patients with the diagnosis of sepsis or septic shock Receives: Other: phlebotomy | |
| Control | Healthy control with no evidence of active infection, or recent infection in the past 4 weeks. Receives: Other: phlebotomy |
What is being measured
The primary outcome is the main question the study is designed to answer.
Quantitative FFA2/GPR43 receptor expression as a function of SOFA score
Quantitative expression of FFA2/GPR43 will be measured at specific time intervals and compared to SOFA score.
Measured: Time of diagnosis, 24, 72, 168 hour intervals
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted7 Mar 2016 (estimated)
- Study startAug 2016
- Primary completionAug 2017 (estimated)
- Study completionNov 2017 (estimated)
Why it stopped: data was received from another source, therefore phlebotomy was not necessary
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (13)Papers the sponsor has linked to this study.
- Other trials for SepsisStudies of the same condition, open and under way.
- More trials run by Milton S. Hershey Medical CenterThe 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
- 0 participants (actual)
Sponsor and investigators
- Lead sponsor
- Milton S. Hershey Medical Center
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Zyad J. Carr, M.D., Milton S. Hershey Medical Center
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02699905
- Sponsor's protocol ID
- STUDY00004607
- Acronym
- GPR43Sepsis
- Status last verified
- Jan 2017
- First submitted
- 1 Mar 2016
- Last updated
- 13 Jan 2017
- Results posted
- No
- Data monitoring committee
- Yes
- Individual data sharing
- Yes
Publications
Covington DK, Briscoe CA, Brown AJ, Jayawickreme CK. The G-protein-coupled receptor 40 family (GPR40-GPR43) and its role in nutrient sensing. Biochem Soc Trans. 2006 Nov;34(Pt 5):770-3. doi: 10.1042/BST0340770.
PubMed 17052194Brown AJ, Goldsworthy SM, Barnes AA, Eilert MM, Tcheang L, Daniels D, Muir AI, Wigglesworth MJ, Kinghorn I, Fraser NJ, Pike NB, Strum JC, Steplewski KM, Murdock PR, Holder JC, Marshall FH, Szekeres PG, Wilson S, Ignar DM, Foord SM, Wise A, Dowell SJ. The Orphan G protein-coupled receptors GPR41 and GPR43 are activated by propionate and other short chain carboxylic acids. J Biol Chem. 2003 Mar 28;278(13):11312-9. doi: 10.1074/jbc.M211609200. Epub 2002 Dec 19.
PubMed 12496283Cox MA, Jackson J, Stanton M, Rojas-Triana A, Bober L, Laverty M, Yang X, Zhu F, Liu J, Wang S, Monsma F, Vassileva G, Maguire M, Gustafson E, Bayne M, Chou CC, Lundell D, Jenh CH. Short-chain fatty acids act as antiinflammatory mediators by regulating prostaglandin E(2) and cytokines. World J Gastroenterol. 2009 Nov 28;15(44):5549-57. doi: 10.3748/wjg.15.5549.
PubMed 19938193Vinolo MA, Ferguson GJ, Kulkarni S, Damoulakis G, Anderson K, Bohlooly-Y M, Stephens L, Hawkins PT, Curi R. SCFAs induce mouse neutrophil chemotaxis through the GPR43 receptor. PLoS One. 2011;6(6):e21205. doi: 10.1371/journal.pone.0021205. Epub 2011 Jun 15.
PubMed 21698257Sina C, Gavrilova O, Forster M, Till A, Derer S, Hildebrand F, Raabe B, Chalaris A, Scheller J, Rehmann A, Franke A, Ott S, Hasler R, Nikolaus S, Folsch UR, Rose-John S, Jiang HP, Li J, Schreiber S, Rosenstiel P. G protein-coupled receptor 43 is essential for neutrophil recruitment during intestinal inflammation. J Immunol. 2009 Dec 1;183(11):7514-22. doi: 10.4049/jimmunol.0900063. Epub 2009 Nov 16.
PubMed 19917676Masui R, Sasaki M, Funaki Y, Ogasawara N, Mizuno M, Iida A, Izawa S, Kondo Y, Ito Y, Tamura Y, Yanamoto K, Noda H, Tanabe A, Okaniwa N, Yamaguchi Y, Iwamoto T, Kasugai K. G protein-coupled receptor 43 moderates gut inflammation through cytokine regulation from mononuclear cells. Inflamm Bowel Dis. 2013 Dec;19(13):2848-56. doi: 10.1097/01.MIB.0000435444.14860.ea.
PubMed 24141712Kim MH, Kang SG, Park JH, Yanagisawa M, Kim CH. Short-chain fatty acids activate GPR41 and GPR43 on intestinal epithelial cells to promote inflammatory responses in mice. Gastroenterology. 2013 Aug;145(2):396-406.e1-10. doi: 10.1053/j.gastro.2013.04.056. Epub 2013 May 7.
PubMed 23665276Senga T, Iwamoto S, Yoshida T, Yokota T, Adachi K, Azuma E, Hamaguchi M, Iwamoto T. LSSIG is a novel murine leukocyte-specific GPCR that is induced by the activation of STAT3. Blood. 2003 Feb 1;101(3):1185-7. doi: 10.1182/blood-2002-06-1881. Epub 2002 Sep 19.
PubMed 12393494Le Poul E, Loison C, Struyf S, Springael JY, Lannoy V, Decobecq ME, Brezillon S, Dupriez V, Vassart G, Van Damme J, Parmentier M, Detheux M. Functional characterization of human receptors for short chain fatty acids and their role in polymorphonuclear cell activation. J Biol Chem. 2003 Jul 11;278(28):25481-9. doi: 10.1074/jbc.M301403200. Epub 2003 Apr 23.
PubMed 12711604Bindels LB, Dewulf EM, Delzenne NM. GPR43/FFA2: physiopathological relevance and therapeutic prospects. Trends Pharmacol Sci. 2013 Apr;34(4):226-32. doi: 10.1016/j.tips.2013.02.002. Epub 2013 Mar 13.
PubMed 23489932Vincent JL, Moreno R, Takala J, Willatts S, De Mendonca A, Bruining H, Reinhart CK, Suter PM, Thijs LG. The SOFA (Sepsis-related Organ Failure Assessment) score to describe organ dysfunction/failure. On behalf of the Working Group on Sepsis-Related Problems of the European Society of Intensive Care Medicine. Intensive Care Med. 1996 Jul;22(7):707-10. doi: 10.1007/BF01709751. No abstract available.
PubMed 8844239Yao YM, Redl H, Bahrami S, Schlag G. The inflammatory basis of trauma/shock-associated multiple organ failure. Inflamm Res. 1998 May;47(5):201-10. doi: 10.1007/s000110050318.
PubMed 9657252Angus DC, Linde-Zwirble WT, Lidicker J, Clermont G, Carcillo J, Pinsky MR. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Crit Care Med. 2001 Jul;29(7):1303-10. doi: 10.1097/00003246-200107000-00002.
PubMed 11445675
Study at a glance
From the registry record, last updated by the sponsor on 13 Jan 2017. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Neutrophil FFA2/GPR43 Receptor Expression in Patients With the Diagnosis of Sepsis
- ClinicalTrials.gov ID
- NCT02699905
- Acronym / sponsor ID
- GPR43Sepsis / STUDY00004607
- Keywords
- Sepsis, Septic Shock, Multiple Organ Dysfunction, FFA2, GPR43
- Study type
- Observational
- Recruitment status
- WithdrawnReason stopped: data was received from another source, therefore phlebotomy was not necessary
- Enrolment
- 0 participants (actual)
- Lead sponsor
- Milton S. Hershey Medical CenterUniversity, hospital or other
- Study start
- Aug 2016
- Primary completion
- Aug 2017 (estimated)
- Study completion
- Nov 2017 (estimated)
- First posted
- 7 Mar 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.
This study seeks to elucidate the quantitative expression of G - protein receptor 43/free fatty acid (GPR43/FFA2) receptors in patients with the diagnosis of sepsis and specifically, its expression as it relates to the severity of sepsis. The investigators hypothesize that patients with more severe sepsis, as defined by a higher SOFA (Sequential Organ Failure Assessment Score), will have decreased expression of the GPR43/FFA2 as compared to patients with lower SOFA scores, consistent with a less exuberant immune response to infection.
Patients admitted to Penn State Hershey Medical Center with a diagnosis of sepsis of any cause will undergo blood testing of leukocytes to determine the expressed quantity of GP43 during standardized time points of their illness and recovery. No interventions will be made in the standard clinical management of the patient. Additionally, healthy volunteers will be recruited to exam baseline GPR43 receptor expression between sepsis and control groups.
Detailed description
Despite advancements in recognition and treatment, sepsis continues to be a frequently fatal condition comprising 750,000 cases in the US with an estimated death rate of 28-38%. Bacterial sepsis complications are the result of a cascade of inflammatory mediators secondary to the immune system's recognition and response to invading bacteria, intracellular constituents and metabolites. Bacterial recognition results in the widespread activation of biological mediators essential to the immune response such as cytokines, chemokines, prostaglandins and reactive oxygen species. These compounds result in the activation and up-regulation of neutrophils, monocytes at the cellular level as well as the physiological changes of sepsis such as hyperpyrexia, vasodilation, and tachycardia. Despite this generally coordinated response, it is likely that marked complications are related to the sequela of the uncontrolled immune response leading to significant injury to the lungs (Acute Respiratory Distress Syndrome), and other organs (acute renal failure, shock liver). In addition, there is question that impairment of the gut mucosal barrier may result in translocation of bacteria and perpetuate the multiple organ failure.
G protein-coupled receptors (GPCRs) comprise one of the largest collections of transmembrane proteins in the mammalian genome. Recently, a subfamily of G protein coupled receptors have been identified that utilize short chain free fatty acids as ligands, FFA1 (GPR40), FFA2 (GPR43) and FFA3 (GPR41). Research has intimated that these receptors are involved in essential biological crosstalk between colonic bacteria, host and immune defenses. Although highly conserved in structure, members of this sub family demonstrate differences in fatty acid specificity, intracellular signaling mechanisms and tissue localization. Specifically, FFA2 (GPR43)4 expression has been shown to be expressed in higher magnitudes within immune cells, has been hypothesized to be involved in the modulation of pro- and anti-inflammatory mediators, such as prostaglandin E2 and is involved in neutrophil chemotaxis in mice. GPR43 is involved in the process of differentiation of progenitor immune cells into monocytes and macrophages, a key component of host defense. In addition, highly selective expression of GPR43 in polymorphonuclear cells point to strong role in chemotaxis and recruitment of immune cells to foci of bacterial infection. Short chain fatty acids also activate GPR43 receptors on intestinal epithelial cells with rapid production of secondary chemokine and cytokines after being challenged with inflammation and infection, and likely aid in the coordinated immune response. GP43 is likely an essential component of the phagocytic chemotaxis that maintains normal intestinal immune defense. In a model of acute colitis, GPR43 knockout mice demonstrated increased mortality. The authors concluded that GPR43 deficiency likely suppressed the role of immune cells within the gut immune milieu leading to death from sepsis related complications. Conversely, in a chronic colitis model, GPR43 deficient knockout mice demonstrated reduced colonic inflammation, without overwhelming infection, the authors concluded that GPR43 has an unfavorable role in the manifestation of chronic inflammatory conditions. These findings were confirmed with at least one later study. In humans, fetal membrane expression of GPR43 was higher in parturients in preterm labor with signs of infection.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Sepsis | – | Other: phlebotomyPatients with the diagnosis of sepsis or septic shock |
| Control | – | Other: phlebotomyHealthy control with no evidence of active infection, or recent infection in the past 4 weeks. |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
- Study population
- Adult patients with the diagnosis of sepsis or septic shock admitted to the intensive care unit at Penn State Hershey Medical Center, Hershey PA 17033.
Key inclusion criteria (3 listed)
- Diagnosis of sepsis or septic shock
- Age greater than eighteen years old.
- Ability to give informed consent (as determined by the attending physician) or presence of designated healthcare proxy that can give informed consent.
Key exclusion criteria (2 listed)
- Patients or designated healthcare proxy with the inability to give informed consent.
- Patients under the age of eighteen
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 |
|---|---|---|
| phlebotomyphlebotomy | Other | Control, Sepsis |
Primary outcome
Quantitative FFA2/GPR43 receptor expression as a function of SOFA score
Time frame: Time of diagnosis, 24, 72, 168 hour intervals
Quantitative expression of FFA2/GPR43 will be measured at specific time intervals and compared to SOFA score.
Results and safety
The study was withdrawn before enrolling participants, so there are no results.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 13 Jan 2017.
- Background: PubMed 17052194Covington DK, Briscoe CA, Brown AJ, Jayawickreme CK. The G-protein-coupled receptor 40 family (GPR40-GPR43) and its role in nutrient sensing. Biochem Soc Trans. 2006 Nov;34(Pt 5):770-3. doi: 10.1042/BST0340770.
- Background: PubMed 12496283Brown AJ, Goldsworthy SM, Barnes AA, Eilert MM, Tcheang L, Daniels D, Muir AI, Wigglesworth MJ, Kinghorn I, Fraser NJ, Pike NB, Strum JC, Steplewski KM, Murdock PR, Holder JC, Marshall FH, Szekeres PG, Wilson S, Ignar DM, Foord SM, Wise A, Dowell SJ. The Orphan G protein-coupled receptors GPR41 and GPR43 are activated by propionate and other short chain carboxylic acids. J Biol Chem. 2003 Mar 28;278(13):11312-9. doi: 10.1074/jbc.M211609200. Epub 2002 Dec 19.
- Background: PubMed 19938193Cox MA, Jackson J, Stanton M, Rojas-Triana A, Bober L, Laverty M, Yang X, Zhu F, Liu J, Wang S, Monsma F, Vassileva G, Maguire M, Gustafson E, Bayne M, Chou CC, Lundell D, Jenh CH. Short-chain fatty acids act as antiinflammatory mediators by regulating prostaglandin E(2) and cytokines. World J Gastroenterol. 2009 Nov 28;15(44):5549-57. doi: 10.3748/wjg.15.5549.
- Background: PubMed 21698257Vinolo MA, Ferguson GJ, Kulkarni S, Damoulakis G, Anderson K, Bohlooly-Y M, Stephens L, Hawkins PT, Curi R. SCFAs induce mouse neutrophil chemotaxis through the GPR43 receptor. PLoS One. 2011;6(6):e21205. doi: 10.1371/journal.pone.0021205. Epub 2011 Jun 15.
- Background: PubMed 19917676Sina C, Gavrilova O, Forster M, Till A, Derer S, Hildebrand F, Raabe B, Chalaris A, Scheller J, Rehmann A, Franke A, Ott S, Hasler R, Nikolaus S, Folsch UR, Rose-John S, Jiang HP, Li J, Schreiber S, Rosenstiel P. G protein-coupled receptor 43 is essential for neutrophil recruitment during intestinal inflammation. J Immunol. 2009 Dec 1;183(11):7514-22. doi: 10.4049/jimmunol.0900063. Epub 2009 Nov 16.
- Background: PubMed 24141712Masui R, Sasaki M, Funaki Y, Ogasawara N, Mizuno M, Iida A, Izawa S, Kondo Y, Ito Y, Tamura Y, Yanamoto K, Noda H, Tanabe A, Okaniwa N, Yamaguchi Y, Iwamoto T, Kasugai K. G protein-coupled receptor 43 moderates gut inflammation through cytokine regulation from mononuclear cells. Inflamm Bowel Dis. 2013 Dec;19(13):2848-56. doi: 10.1097/01.MIB.0000435444.14860.ea.
- Background: PubMed 23665276Kim MH, Kang SG, Park JH, Yanagisawa M, Kim CH. Short-chain fatty acids activate GPR41 and GPR43 on intestinal epithelial cells to promote inflammatory responses in mice. Gastroenterology. 2013 Aug;145(2):396-406.e1-10. doi: 10.1053/j.gastro.2013.04.056. Epub 2013 May 7.
- Background: PubMed 12393494Senga T, Iwamoto S, Yoshida T, Yokota T, Adachi K, Azuma E, Hamaguchi M, Iwamoto T. LSSIG is a novel murine leukocyte-specific GPCR that is induced by the activation of STAT3. Blood. 2003 Feb 1;101(3):1185-7. doi: 10.1182/blood-2002-06-1881. Epub 2002 Sep 19.
- Background: PubMed 12711604Le Poul E, Loison C, Struyf S, Springael JY, Lannoy V, Decobecq ME, Brezillon S, Dupriez V, Vassart G, Van Damme J, Parmentier M, Detheux M. Functional characterization of human receptors for short chain fatty acids and their role in polymorphonuclear cell activation. J Biol Chem. 2003 Jul 11;278(28):25481-9. doi: 10.1074/jbc.M301403200. Epub 2003 Apr 23.
- Background: PubMed 23489932Bindels LB, Dewulf EM, Delzenne NM. GPR43/FFA2: physiopathological relevance and therapeutic prospects. Trends Pharmacol Sci. 2013 Apr;34(4):226-32. doi: 10.1016/j.tips.2013.02.002. Epub 2013 Mar 13.
- Background: PubMed 8844239Vincent JL, Moreno R, Takala J, Willatts S, De Mendonca A, Bruining H, Reinhart CK, Suter PM, Thijs LG. The SOFA (Sepsis-related Organ Failure Assessment) score to describe organ dysfunction/failure. On behalf of the Working Group on Sepsis-Related Problems of the European Society of Intensive Care Medicine. Intensive Care Med. 1996 Jul;22(7):707-10. doi: 10.1007/BF01709751. No abstract available.
- Results publication: PubMed 9657252Yao YM, Redl H, Bahrami S, Schlag G. The inflammatory basis of trauma/shock-associated multiple organ failure. Inflamm Res. 1998 May;47(5):201-10. doi: 10.1007/s000110050318.
- Individual participant dataSharing planned: Yes
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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.
The record lists no contact. Use the official record to reach the sponsor.
Questions about this trial
What is this clinical trial studying?
An observational study of Sepsis and Septic Shock, run by Milton S. Hershey Medical Center.
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 3 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: withdrawn, as of the sponsor's last update on 13 Jan 2017. Status can change between updates, so confirm with the study contact before making plans.
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 withdrawn before enrolling participants, so there are no results.
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?
Quantitative FFA2/GPR43 receptor expression as a function of SOFA score (time frame: Time of diagnosis, 24, 72, 168 hour intervals). 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 NCT02699905, which also lists 13 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 13 Jan 2017.