PneumoniaNCT03473119
Evaluation of Plasma Sphingosine-1-Phosphate as A Diagnostic and Prognostic Biomarkers of Community-Acquired Pneumonia
An observational study of Pneumonia and Chronic Obstructive Pulmonary Disease, run by Taipei Medical University WanFang Hospital at 1 site in Taiwan.
Trial summary
Pneumonia is a major infectious cause of death worldwide and imposes a considerable burden on healthcare resources. Obstructive lung diseases (COPD and Asthma) are increasingly important causes of morbidity and mortality worldwide. Read more about this study
- Who is it for?
- Ages 18 years and olderHealthy volunteers can take part
- Conditions the study is for
- Pneumonia, Chronic Obstructive Pulmonary Disease, Asthma
- How many people
- 600 participants
- Where
- 1 siteTaiwan
- Study dates
- 19 Mar 2016to 19 Mar 2021
- 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: The individuals who have the target diseases (CAP, Asthma, Asthma with CAP COPD, and COPD with CAP) and healthy controls will be recruited at the emergency department (ED) of Wan Fang Hospital (Taipei, Taiwan). The hospital is affiliated with Taipei Medical University and is located in the metropolitan area of Taipei City, Taiwan, at Wenshan District, and has had more than 65,000 emergency visits annually.
Who may be able to join
- Clinical diagnosis of chronic obstructive pulmonary disease (COPD; ICD-9 codes 490-492, 494, 496)
- Clinical diagnosis of Asthma (ICD-9 code 493),
- Clinical diagnosis of pneumonia (ICD-9 codes 480-488).
Who cannot join
- Underage incapacity
- Pregnant women,
- Psychiatric history
- Unfamiliar with Chinese
Trial locations and contacts
1 site in 1 country.
Chin-Wang Hsu, MD contact
Taiwan1 site, 1 recruiting
- Recruiting
The Emergency Department of Wan Fang Hospital
Taipei, Wenshan District
Shih-Chang Hsu, MD, 29307930 ext. 1279, 1980bradhsu@gmail.com
About this study
Official title: Acute Effects of Particulate Matter on Pulmonary Diseases: Discovery Its Chemo-signatures
Pneumonia is a major infectious cause of death worldwide and imposes a considerable burden on healthcare resources. Obstructive lung diseases (COPD and Asthma) are increasingly important causes of morbidity and mortality worldwide. The patients with community-acquired pneumonia (CAP), and acute exacerbations of obstructive lung diseases commonly present with similar signs and symptoms. For antibiotic use, the rapid and accurate differentiation of clinically relevant of bacterial lower respiratory tract infections from other mimics is essential. Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid has both extracellular and intracellular effects in mammalian cells. S1P is involved in many physiological processes including immune responses and endothelial barrier integrity. In term of endothelial barrier integrity, S1P plays a crucial role in protecting lungs from the pulmonary leak and lung injury. Because of the involvement in lung injury, S1P would be the potential biomarker of pneumonia. Based on the above evidence, S1P plays an essential role in the pathobiology of pneumonia was hypothesized.
Read the detailed description
The study was a branch of our PM2.5 observational study (Acute Effects of Particulate Matter on Pulmonary Diseases) and mainly focus on lipid biomarker for the target diseases. Lower respiratory tract infections are the most frequent infectious cause of death worldwide[1] and impose a considerable burden on healthcare resources. Despite the advancement in treatment and diagnostic technique, the overall 30-day mortality rate of community-acquired pneumonia (CAP) is as high as 12.1% for patients who aged 65 years and older admitted to hospital[2]. Obstructive lung diseases (COPD and Asthma) are increasingly important causes of morbidity and mortality worldwide. The patients with CAP, and acute exacerbations of obstructive lung diseases commonly present with similar signs and symptoms.
The use of conventional diagnostic markers, such as complete blood count (CBC) with differential and C-reactive protein is the current mainstream method for differentiating clinically relevant to bacterial lower respiratory tract infections from other mimics. However, for patients with a clinical suspicion of infection, those conventional methods have suboptimal sensitivity and specificity[3,4] The limitations often cause the ambiguity of the initiation of antibiotic treatment. As a result, unnecessary use of antibiotics adversely affects patient outcomes. Also, inappropriate antibiotic therapy increases antibiotic resistance in patients, which poses a public health problem. Current strategies to reduce antibiotic usage have included the development of biomarker-directed treatment algorithms. However, a recent study suggested that procalcitonin-guided therapy has not been effective in reducing antibiotic use[5]. Therefore, developing new biomarkers may be the answer to the problems.
Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid has both extracellular and intracellular effects in mammalian cells[6-9]. S1P is synthesized by two sphingosine kinases (SphK1 and SphK 2) and degraded by S1P lyase (S1PL)[6] S1P is a ligand for five G protein-coupled receptors, S1P receptors1-5[6,7], and also acts as an intracellular second messenger[10,11]. S1P is involved in many physiological processes including immune responses and endothelial barrier integrity[12-15]. In term of endothelial barrier integrity, S1P plays a crucial role in protecting lungs from the pulmonary leak and lung injury. [16-19] Previous research suggests that S1P signaling through S1PR1 is crucial for endothelial barrier function. [20] The S1P induces actin polymerization and then results in the spreading of endothelial cells which fills intercellular gaps. Also, the S1P-signaling can stabilize the endothelial cell-cell junctions such as adherens junction and tight junction. [21-23] Both actin-dependent outward spreading of endothelial cells and cell junction stabilization enhance the endothelial barrier function. Because of the involvement in lung injury and endothelial barrier function, S1P would be the potential biomarker of pneumonia.
For the study, a case-control design was utilized for collecting clinical samples. the investigators plan to enroll 150 individuals for each targeted disease (CAP, Asthma, Asthma with CAP, COPD, and COPD with CAP) and control. Peripheral blood will be collected from the patients presenting at the emergency department (ED) of Wan Fang Hospital for an acute event of the candidate diseases. Each recruited individual will fill out a specific questionnaire, which will include lifestyle, occupation, habits, and general dietary information. The initial peripheral blood sample will be obtained in the emergency department, and if the patients were admitted, the individual's blood sample would be collected one day before a planned discharge again. The following parameters will be recorded for each participant: sex, age, body weight, body temperature, vital signs at the ED, and clinical characteristics of the disease. The laboratory testing will include baseline analyses (hematocrit, white blood count with differential, serum sodium, and chloride), ALT, AST, CRP, BUN, and creatinine. The plasma S1P will also be tested and will be measured by ELISA. The questionnaire will provide the individual's basic information of living area, occupational environment, personal habits and family history for further analysis.
- Conditions
- Pneumonia, Chronic Obstructive Pulmonary Disease, Asthma
- Keywords
- Sphingosine-1-phosphate
- Medical subject headings
- Pneumonia, Pulmonary Disease, Chronic Obstructive, Asthma
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| Control | Healthy individuals | |
| Asthma | Asthma acute exacerbations | |
| Asthma with CAP | Asthma acute exacerbations with community-acquired pneumonia | |
| COPD | Acute exacerbations of chronic obstructive pulmonary disease | |
| COPD with CAP | Acute exacerbations of chronic obstructive pulmonary disease with community-acquired pneumonia | |
| CAP | Community-acquired pneumonia |
What is being measured
The primary outcome is the main question the study is designed to answer.
Mortality
3 months mortality
Measured: 3 months
Secondary outcomes (4)
ICU
ICU admission
Measured: During the hospital admission
ETT
On Tracheal tube
Measured: During the hospital admission
BiPAP
Using Bilevel Positive Airway Pressure
Measured: During the hospital admission
Length of Stay
length of hospital stay
Measured: During the hospital admission
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted22 Mar 2018
- Study start19 Mar 2016
- Primary completion19 Mar 2021 (estimated)
- Study completion19 Mar 2021 (estimated)
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 PneumoniaStudies 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
- Case-control
- Time perspective
- Prospective
- Enrolment
- 600 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Taipei Medical University WanFang Hospital
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT03473119
- Sponsor's protocol ID
- N201602089
- Status last verified
- Apr 2019
- First submitted
- 14 Mar 2018
- Last updated
- 10 Jul 2019
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Metersky ML, Waterer G, Nsa W, Bratzler DW. Predictors of in-hospital vs postdischarge mortality in pneumonia. Chest. 2012 Aug;142(2):476-481. doi: 10.1378/chest.11-2393.
PubMed 22383662Hausfater P. Biomarkers and infection in the emergency unit. Med Mal Infect. 2014 Apr;44(4):139-45. doi: 10.1016/j.medmal.2014.01.002. Epub 2014 Feb 17.
PubMed 24556451Mitsuma SF, Mansour MK, Dekker JP, Kim J, Rahman MZ, Tweed-Kent A, Schuetz P. Promising new assays and technologies for the diagnosis and management of infectious diseases. Clin Infect Dis. 2013 Apr;56(7):996-1002. doi: 10.1093/cid/cis1014. Epub 2012 Dec 7.
PubMed 23223587Lindenauer PK, Shieh MS, Stefan MS, Fisher KA, Haessler SD, Pekow PS, Rothberg MB, Krishnan JA, Walkey AJ. Hospital Procalcitonin Testing and Antibiotic Treatment of Patients Admitted for Chronic Obstructive Pulmonary Disease Exacerbation. Ann Am Thorac Soc. 2017 Dec;14(12):1779-1785. doi: 10.1513/AnnalsATS.201702-133OC.
PubMed 28795838Rosen H, Goetzl EJ. Sphingosine 1-phosphate and its receptors: an autocrine and paracrine network. Nat Rev Immunol. 2005 Jul;5(7):560-70. doi: 10.1038/nri1650.
PubMed 15999095Anliker B, Chun J. Cell surface receptors in lysophospholipid signaling. Semin Cell Dev Biol. 2004 Oct;15(5):457-65. doi: 10.1016/j.semcdb.2004.05.005.
PubMed 15271291Meyer zu Heringdorf D, Liliom K, Schaefer M, Danneberg K, Jaggar JH, Tigyi G, Jakobs KH. Photolysis of intracellular caged sphingosine-1-phosphate causes Ca2+ mobilization independently of G-protein-coupled receptors. FEBS Lett. 2003 Nov 20;554(3):443-9. doi: 10.1016/s0014-5793(03)01219-5.
PubMed 14623109Usatyuk PV, He D, Bindokas V, Gorshkova IA, Berdyshev EV, Garcia JG, Natarajan V. Photolysis of caged sphingosine-1-phosphate induces barrier enhancement and intracellular activation of lung endothelial cell signaling pathways. Am J Physiol Lung Cell Mol Physiol. 2011 Jun;300(6):L840-50. doi: 10.1152/ajplung.00404.2010. Epub 2011 Apr 8.
PubMed 21478254Blom T, Slotte JP, Pitson SM, Tornquist K. Enhancement of intracellular sphingosine-1-phosphate production by inositol 1,4,5-trisphosphate-evoked calcium mobilisation in HEK-293 cells: endogenous sphingosine-1-phosphate as a modulator of the calcium response. Cell Signal. 2005 Jul;17(7):827-36. doi: 10.1016/j.cellsig.2004.11.022. Epub 2005 Jan 7.
PubMed 15763425Itagaki K, Yun JK, Hengst JA, Yatani A, Hauser CJ, Spolarics Z, Deitch EA. Sphingosine 1-phosphate has dual functions in the regulation of endothelial cell permeability and Ca2+ metabolism. J Pharmacol Exp Ther. 2007 Oct;323(1):186-91. doi: 10.1124/jpet.107.121210. Epub 2007 Jul 12.
PubMed 17626797Pappu R, Schwab SR, Cornelissen I, Pereira JP, Regard JB, Xu Y, Camerer E, Zheng YW, Huang Y, Cyster JG, Coughlin SR. Promotion of lymphocyte egress into blood and lymph by distinct sources of sphingosine-1-phosphate. Science. 2007 Apr 13;316(5822):295-8. doi: 10.1126/science.1139221. Epub 2007 Mar 15.
PubMed 17363629Rivera J, Proia RL, Olivera A. The alliance of sphingosine-1-phosphate and its receptors in immunity. Nat Rev Immunol. 2008 Oct;8(10):753-63. doi: 10.1038/nri2400.
PubMed 18787560Schuchardt M, Tolle M, Prufer J, van der Giet M. Pharmacological relevance and potential of sphingosine 1-phosphate in the vascular system. Br J Pharmacol. 2011 Jul;163(6):1140-62. doi: 10.1111/j.1476-5381.2011.01260.x.
PubMed 21309759Xiong Y, Hla T. S1P control of endothelial integrity. Curr Top Microbiol Immunol. 2014;378:85-105. doi: 10.1007/978-3-319-05879-5_4.
PubMed 24728594Dudek SM, Jacobson JR, Chiang ET, Birukov KG, Wang P, Zhan X, Garcia JG. Pulmonary endothelial cell barrier enhancement by sphingosine 1-phosphate: roles for cortactin and myosin light chain kinase. J Biol Chem. 2004 Jun 4;279(23):24692-700. doi: 10.1074/jbc.M313969200. Epub 2004 Mar 31.
PubMed 15056655
Study at a glance
From the registry record, last updated by the sponsor on 10 Jul 2019. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Acute Effects of Particulate Matter on Pulmonary Diseases: Discovery Its Chemo-signatures
- ClinicalTrials.gov ID
- NCT03473119
- Acronym / sponsor ID
- N201602089
- Conditions
- Pneumonia, Chronic Obstructive Pulmonary Disease, Asthma
- Keywords
- Sphingosine-1-phosphate
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 600 participants (estimated)
- Lead sponsor
- Taipei Medical University WanFang HospitalUniversity, hospital or other
- Study start
- 19 Mar 2016 (actual)
- Primary completion
- 19 Mar 2021 (estimated)
- Study completion
- 19 Mar 2021 (estimated)
- First posted
- 22 Mar 2018 (actual)
- 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.
Pneumonia is a major infectious cause of death worldwide and imposes a considerable burden on healthcare resources. Obstructive lung diseases (COPD and Asthma) are increasingly important causes of morbidity and mortality worldwide. The patients with community-acquired pneumonia (CAP), and acute exacerbations of obstructive lung diseases commonly present with similar signs and symptoms. For antibiotic use, the rapid and accurate differentiation of clinically relevant of bacterial lower respiratory tract infections from other mimics is essential. Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid has both extracellular and intracellular effects in mammalian cells. S1P is involved in many physiological processes including immune responses and endothelial barrier integrity. In term of endothelial barrier integrity, S1P plays a crucial role in protecting lungs from the pulmonary leak and lung injury. Because of the involvement in lung injury, S1P would be the potential biomarker of pneumonia. Based on the above evidence, S1P plays an essential role in the pathobiology of pneumonia was hypothesized.
Detailed description
The study was a branch of our PM2.5 observational study (Acute Effects of Particulate Matter on Pulmonary Diseases) and mainly focus on lipid biomarker for the target diseases. Lower respiratory tract infections are the most frequent infectious cause of death worldwide[1] and impose a considerable burden on healthcare resources. Despite the advancement in treatment and diagnostic technique, the overall 30-day mortality rate of community-acquired pneumonia (CAP) is as high as 12.1% for patients who aged 65 years and older admitted to hospital[2]. Obstructive lung diseases (COPD and Asthma) are increasingly important causes of morbidity and mortality worldwide. The patients with CAP, and acute exacerbations of obstructive lung diseases commonly present with similar signs and symptoms.
The use of conventional diagnostic markers, such as complete blood count (CBC) with differential and C-reactive protein is the current mainstream method for differentiating clinically relevant to bacterial lower respiratory tract infections from other mimics. However, for patients with a clinical suspicion of infection, those conventional methods have suboptimal sensitivity and specificity[3,4] The limitations often cause the ambiguity of the initiation of antibiotic treatment. As a result, unnecessary use of antibiotics adversely affects patient outcomes. Also, inappropriate antibiotic therapy increases antibiotic resistance in patients, which poses a public health problem. Current strategies to reduce antibiotic usage have included the development of biomarker-directed treatment algorithms. However, a recent study suggested that procalcitonin-guided therapy has not been effective in reducing antibiotic use[5]. Therefore, developing new biomarkers may be the answer to the problems.
Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid has both extracellular and intracellular effects in mammalian cells[6-9]. S1P is synthesized by two sphingosine kinases (SphK1 and SphK 2) and degraded by S1P lyase (S1PL)[6] S1P is a ligand for five G protein-coupled receptors, S1P receptors1-5[6,7], and also acts as an intracellular second messenger[10,11]. S1P is involved in many physiological processes including immune responses and endothelial barrier integrity[12-15]. In term of endothelial barrier integrity, S1P plays a crucial role in protecting lungs from the pulmonary leak and lung injury. [16-19] Previous research suggests that S1P signaling through S1PR1 is crucial for endothelial barrier function. [20] The S1P induces actin polymerization and then results in the spreading of endothelial cells which fills intercellular gaps. Also, the S1P-signaling can stabilize the endothelial cell-cell junctions such as adherens junction and tight junction. [21-23] Both actin-dependent outward spreading of endothelial cells and cell junction stabilization enhance the endothelial barrier function. Because of the involvement in lung injury and endothelial barrier function, S1P would be the potential biomarker of pneumonia.
For the study, a case-control design was utilized for collecting clinical samples. the investigators plan to enroll 150 individuals for each targeted disease (CAP, Asthma, Asthma with CAP, COPD, and COPD with CAP) and control. Peripheral blood will be collected from the patients presenting at the emergency department (ED) of Wan Fang Hospital for an acute event of the candidate diseases. Each recruited individual will fill out a specific questionnaire, which will include lifestyle, occupation, habits, and general dietary information. The initial peripheral blood sample will be obtained in the emergency department, and if the patients were admitted, the individual's blood sample would be collected one day before a planned discharge again. The following parameters will be recorded for each participant: sex, age, body weight, body temperature, vital signs at the ED, and clinical characteristics of the disease. The laboratory testing will include baseline analyses (hematocrit, white blood count with differential, serum sodium, and chloride), ALT, AST, CRP, BUN, and creatinine. The plasma S1P will also be tested and will be measured by ELISA. The questionnaire will provide the individual's basic information of living area, occupational environment, personal habits and family history for further analysis.
Study design
- Observational model
- Case-control
- Time perspective
- Prospective
- Number of arms
- 6
| Arm | Type | Receives |
|---|---|---|
| Control | – | –Healthy individuals |
| Asthma | – | –Asthma acute exacerbations |
| Asthma with CAP | – | –Asthma acute exacerbations with community-acquired pneumonia |
| COPD | – | –Acute exacerbations of chronic obstructive pulmonary disease |
| COPD with CAP | – | –Acute exacerbations of chronic obstructive pulmonary disease with community-acquired pneumonia |
| CAP | – | –Community-acquired pneumonia |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
- Study population
- The individuals who have the target diseases (CAP, Asthma, Asthma with CAP COPD, and COPD with CAP) and healthy controls will be recruited at the emergency department (ED) of Wan Fang Hospital (Taipei, Taiwan). The hospital is affiliated with Taipei Medical University and is located in the metropolitan area of Taipei City, Taiwan, at Wenshan District, and has had more than 65,000 emergency visits annually.
Key inclusion criteria (3 listed)
- Clinical diagnosis of chronic obstructive pulmonary disease (COPD; ICD-9 codes 490-492, 494, 496)
- Clinical diagnosis of Asthma (ICD-9 code 493),
- Clinical diagnosis of pneumonia (ICD-9 codes 480-488).
Key exclusion criteria (4 listed)
- Underage incapacity
- Pregnant women,
- Psychiatric history
- Unfamiliar with Chinese
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Mortality
Time frame: 3 months
3 months mortality
4 secondary outcomes
ICU
Time frame: During the hospital admission
ETT
Time frame: During the hospital admission
BiPAP
Time frame: During the hospital admission
Length of Stay
Time frame: During the hospital admission
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 10 Jul 2019.
- Background: PubMed 22383662Metersky ML, Waterer G, Nsa W, Bratzler DW. Predictors of in-hospital vs postdischarge mortality in pneumonia. Chest. 2012 Aug;142(2):476-481. doi: 10.1378/chest.11-2393.
- Background: PubMed 24556451Hausfater P. Biomarkers and infection in the emergency unit. Med Mal Infect. 2014 Apr;44(4):139-45. doi: 10.1016/j.medmal.2014.01.002. Epub 2014 Feb 17.
- Background: PubMed 23223587Mitsuma SF, Mansour MK, Dekker JP, Kim J, Rahman MZ, Tweed-Kent A, Schuetz P. Promising new assays and technologies for the diagnosis and management of infectious diseases. Clin Infect Dis. 2013 Apr;56(7):996-1002. doi: 10.1093/cid/cis1014. Epub 2012 Dec 7.
- Background: PubMed 28795838Lindenauer PK, Shieh MS, Stefan MS, Fisher KA, Haessler SD, Pekow PS, Rothberg MB, Krishnan JA, Walkey AJ. Hospital Procalcitonin Testing and Antibiotic Treatment of Patients Admitted for Chronic Obstructive Pulmonary Disease Exacerbation. Ann Am Thorac Soc. 2017 Dec;14(12):1779-1785. doi: 10.1513/AnnalsATS.201702-133OC.
- Background: PubMed 15999095Rosen H, Goetzl EJ. Sphingosine 1-phosphate and its receptors: an autocrine and paracrine network. Nat Rev Immunol. 2005 Jul;5(7):560-70. doi: 10.1038/nri1650.
- Background: PubMed 15271291Anliker B, Chun J. Cell surface receptors in lysophospholipid signaling. Semin Cell Dev Biol. 2004 Oct;15(5):457-65. doi: 10.1016/j.semcdb.2004.05.005.
- Background: PubMed 14623109Meyer zu Heringdorf D, Liliom K, Schaefer M, Danneberg K, Jaggar JH, Tigyi G, Jakobs KH. Photolysis of intracellular caged sphingosine-1-phosphate causes Ca2+ mobilization independently of G-protein-coupled receptors. FEBS Lett. 2003 Nov 20;554(3):443-9. doi: 10.1016/s0014-5793(03)01219-5.
- Background: PubMed 21478254Usatyuk PV, He D, Bindokas V, Gorshkova IA, Berdyshev EV, Garcia JG, Natarajan V. Photolysis of caged sphingosine-1-phosphate induces barrier enhancement and intracellular activation of lung endothelial cell signaling pathways. Am J Physiol Lung Cell Mol Physiol. 2011 Jun;300(6):L840-50. doi: 10.1152/ajplung.00404.2010. Epub 2011 Apr 8.
- Background: PubMed 15763425Blom T, Slotte JP, Pitson SM, Tornquist K. Enhancement of intracellular sphingosine-1-phosphate production by inositol 1,4,5-trisphosphate-evoked calcium mobilisation in HEK-293 cells: endogenous sphingosine-1-phosphate as a modulator of the calcium response. Cell Signal. 2005 Jul;17(7):827-36. doi: 10.1016/j.cellsig.2004.11.022. Epub 2005 Jan 7.
- Background: PubMed 17626797Itagaki K, Yun JK, Hengst JA, Yatani A, Hauser CJ, Spolarics Z, Deitch EA. Sphingosine 1-phosphate has dual functions in the regulation of endothelial cell permeability and Ca2+ metabolism. J Pharmacol Exp Ther. 2007 Oct;323(1):186-91. doi: 10.1124/jpet.107.121210. Epub 2007 Jul 12.
- Background: PubMed 17363629Pappu R, Schwab SR, Cornelissen I, Pereira JP, Regard JB, Xu Y, Camerer E, Zheng YW, Huang Y, Cyster JG, Coughlin SR. Promotion of lymphocyte egress into blood and lymph by distinct sources of sphingosine-1-phosphate. Science. 2007 Apr 13;316(5822):295-8. doi: 10.1126/science.1139221. Epub 2007 Mar 15.
- Background: PubMed 18787560Rivera J, Proia RL, Olivera A. The alliance of sphingosine-1-phosphate and its receptors in immunity. Nat Rev Immunol. 2008 Oct;8(10):753-63. doi: 10.1038/nri2400.
- Individual participant dataSharing planned: No
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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.
Chin-Wang Hsu, MD contact
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 Pneumonia and Chronic Obstructive Pulmonary Disease, run by Taipei Medical University WanFang Hospital at 1 site in Taiwan.
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 4 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 10 Jul 2019. 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 Taiwan. 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?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Contact Shih-Chang Hsu, MD (29307930 ext. 1279, 1980bradhsu@gmail.com), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Mortality (time frame: 3 months). 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 NCT03473119, 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 10 Jul 2019.