Early Severe Illness TrAnslational BioLogy InformaticS in Humans

NCT ID: NCT05591924

Last Updated: 2025-10-06

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

RECRUITING

Total Enrollment

1000 participants

Study Classification

OBSERVATIONAL

Study Start Date

2024-04-26

Study Completion Date

2034-12-31

Brief Summary

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Advanced stages of the response to life-threatening infection, severe trauma, or other physiological insults often lead to exhaustion of the homeostatic mechanisms that sustain normal blood pressure and oxygenation. These syndromic presentations often meet the diagnostic criteria of sepsis and/or the acute respiratory distress syndrome (ARDS), the two most common syndromes encountered in the intensive care unit (ICU). Although critical illness syndromes, such as sepsis and ARDS, have separate clinical definitions, they often overlap clinically and share several common injury mechanisms. Moreover, there are no specific therapies for critically ill patients, and as a consequence, approximately 1 in 4 patients admitted to the ICU will not survive.

The purpose of this observational study is to identify early patient biologic factors that are present at the time of ICU admission that will help diagnose critical illness syndromes earlier, identify who could benefit most from specific therapies, and enable the discovery of new treatments for syndromes such as sepsis and ARDS.

Detailed Description

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Background:

Critical illness syndromes, such as sepsis and ARDS, are associated with tremendous heterogeneity in patient predisposing risk factors, mechanisms of acute insult contributing to infection, presenting symptoms, response to therapies, as well as short and long-term outcomes. Since the first standardization of sepsis and ARDS definitions \>30 years ago, significant insight into biological mechanisms contributing to critical illness syndromes have been made. However, there are many important unanswered questions that prevent accurate diagnosis, treatment, and prognosis of patients who present to the ICU with early symptoms consistent with critical illness.

Of the many gaps about the biology of sepsis and ARDS that remain unanswered, the following are particularly important: (1) what constitutes immune system dysregulation; (2) how the immune system response depends on interaction with the infecting pathogens; (3) what biologic traits distinguish other diagnoses that mimic these syndromes; (4) what are the mechanisms of genetic polymorphisms in patient outcomes. To address these questions and to improve our understanding of these complex and heterogenous syndromes, a multifaceted and collaborative approach is needed. This study will investigate the biology of early sepsis in critically ill patients by developing a longitudinal prospective observational cohort called Early Severe illness TrAnslational BioLogy InformaticS in Humans (ESTABLISH).

Specific objectives:

Objective 1: To study biologic mechanisms of immune system regulation during early critical illness. The main questions that will be addressed include: (1) how immune function at the time of admission and over the course of the ICU stay is related to clinical complications; (2) how anatomic compartmentalization of immune responses is associated with clinical complications; (3) how immune responses in different anatomic locations contribute to endothelial cell injury; (4) how macrophages contribute to distal organ injury and long-term clinical complications.

Objective 2: To characterize the host-pathogen interaction during early critical illness. The main question that will be addressed include: (1) how the microbial composition at the time of ICU admission affects the immune response; (2) how the change in host-pathogen interactions over time influence clinical complications.

Objective 3: To identify biologic traits that distinguish patients with early sepsis and ARDS from other critically ill patients. The main questions that will be addressed include: (1) are biological trains unique to sepsis and/or ARDS, or are they shared by other clinical diagnoses that mimic these syndromes?; (2) can accurately prognosticate clinically important short and long-term patient outcomes?; (3) are biologic traits associated with differential responses to therapies?

Objective 4: To study the molecular mechanisms of genetic polymorphisms associated with critical illness using induced pluripotent stem cells (iPSCs) derived from polymorphonuclear cells (PBMCs) from critically ill patients. The main questions that will be addressed include: (1) how do autologous iPSC-derived cell lineages interact with autologous plasma?; (2) how do iPSC-derived cell lineages respond to treatment with drugs related to genetic polymorphisms function?; (3) how do iPSC-derived lineages respond to treatment with drugs commonly used in the ICU?

Methods:

The ESTABLISH cohort will enroll patients within 48 hours of ICU admission who presented to the emergency department within 72 hours of ICU admission. Patients will be enrolled with deferred consent to enable the earliest possible collection of biological specimen. The biological specimen will include anticoagulated blood, a PAX gene tube, and a bronchioalveolar lavage fluid (BALF) sample (in mechanically ventilated patients, when bronchoscopy is clinically indicated) collected at the time of ICU admission (Day 0), and on 4 subsequent timepoints during the ICU admission (Days 1,3,7,14,21).

Data generated during ESTABLISH will be analyzed in batches on an ongoing, regular basis and will be objective-specific. Batch sample preparation and data analysis will minimize biological assay and methodological heterogeneity. Objective 1 and 2 data will be analyzed after enrollment of the first 50 patients, and every 50 patients after this. Objective 3 data will be analyzed after enrollment of the first 200 patients and every 200 patients after this.

Conditions

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Sepsis ARDS Critical Illness Neurocognitive Dysfunction Shock, Septic Ventilator Associated Pneumonia Immune Suppression Inflammation SIRS

Study Design

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Observational Model Type

COHORT

Study Time Perspective

PROSPECTIVE

Study Groups

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ESTABLISH

Adults over 18 years of age admitted to the ICU within 48 hours and whose presentation to the Emergency Department was within 72h of ICU admission.

Phelebotomy

Intervention Type PROCEDURE

Collection of 10mL of heparin anticoagulated blood, 10mL of EDTA anticoagulated blood, and 3mL of blood in a PAX gene tube

Broncheoalveolar Lavage

Intervention Type PROCEDURE

Bronchioalveolar lavage fluid (BALF) samples will be obtained from participants who are mechanically ventilated, and a bronchoscopy is indicated as part of routine clinical care. The BALF will be collected by a qualified ICU physician using standard clinical practice. Briefly, patients will receive appropriate sedation and analgesia, a flexible video-bronchoscope will be inserted into the patient's airway, and bronchial segments will be identified. The bronchoscope will be wedged in the most appropriate lung segment and 40-100mL of sterile normal saline (NS) as clinically indicated, will be injected into the bronchoscope port with using a 50mL syringe. Next, the instilled NS (i.e.: lavage fluid) will be collected in a sterile container using gentle suction. The BALF will then be partitioned and sent to clinical laboratories, and the remaining BALF (10-20mL) will be used in the ESTABLISH research study.

Tracheal Aspirate

Intervention Type PROCEDURE

Tracheal Aspirate (TA) will be obtained from participants who have an endotracheal tube or a tracheostomy in situ at the time of ICU admission through out the ICU admission on the study days, as long as distal airway access is available.

Rectal Swab

Intervention Type PROCEDURE

A Rectal will be obtained at the time of ICU admission and on all study days during the ICU admission

Healthy Controls

Adults over 18 years of age with no infectious symptoms, interaction with the health care system, or antimicrobial use in the past 14 days and no history of immunosuppression.

Phelebotomy

Intervention Type PROCEDURE

Collection of 10mL of heparin anticoagulated blood, 10mL of EDTA anticoagulated blood, and 3mL of blood in a PAX gene tube

Interventions

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Phelebotomy

Collection of 10mL of heparin anticoagulated blood, 10mL of EDTA anticoagulated blood, and 3mL of blood in a PAX gene tube

Intervention Type PROCEDURE

Broncheoalveolar Lavage

Bronchioalveolar lavage fluid (BALF) samples will be obtained from participants who are mechanically ventilated, and a bronchoscopy is indicated as part of routine clinical care. The BALF will be collected by a qualified ICU physician using standard clinical practice. Briefly, patients will receive appropriate sedation and analgesia, a flexible video-bronchoscope will be inserted into the patient's airway, and bronchial segments will be identified. The bronchoscope will be wedged in the most appropriate lung segment and 40-100mL of sterile normal saline (NS) as clinically indicated, will be injected into the bronchoscope port with using a 50mL syringe. Next, the instilled NS (i.e.: lavage fluid) will be collected in a sterile container using gentle suction. The BALF will then be partitioned and sent to clinical laboratories, and the remaining BALF (10-20mL) will be used in the ESTABLISH research study.

Intervention Type PROCEDURE

Tracheal Aspirate

Tracheal Aspirate (TA) will be obtained from participants who have an endotracheal tube or a tracheostomy in situ at the time of ICU admission through out the ICU admission on the study days, as long as distal airway access is available.

Intervention Type PROCEDURE

Rectal Swab

A Rectal will be obtained at the time of ICU admission and on all study days during the ICU admission

Intervention Type PROCEDURE

Eligibility Criteria

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Inclusion Criteria

* Age ≥18 years old
* ≤48h since ICU admission
* ICU admission within 72h of presentation to the emergency department (ER)
* Clinical critical illness suspected on the basis of any one of the following:

1. Altered mental status (GCS\<15)
2. Cardiovascular collapse (presence of any: Heart rate \>90, systolic blood pressure \<90, presence of vasopressors, lactate \>2.0)
3. Respiratory collapse (presence of any: respiratory rate \>20, PaCO₂ \<32 mm Hg, supplemental oxygen, invasive or non-invasive ventilation)
4. Suspected severe infection (presence of any: temperature \>38°C or \<36°C, white blood cell (WBC) count \>12,000/mm³ or \<4,000/mm³, presence of 1 or more antibiotics at the time of ICU admission)

Exclusion Criteria

* Age \<18 years old
* \>72h since ICU admission
* Admission to ICU in patients \>72h after the presentation to the ER
* No evidence of critical illness (ICU admission due to bed-spacing)
Minimum Eligible Age

18 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

Yes

Sponsors

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London Health Sciences Centre

OTHER

Sponsor Role collaborator

Western University, Canada

OTHER

Sponsor Role collaborator

Western University

OTHER

Sponsor Role collaborator

London Health Sciences Centre Research Institute OR Lawson Research Institute of St. Joseph's

OTHER

Sponsor Role lead

Responsible Party

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Aleks Leligdowicz

Clinician Scientist

Responsibility Role PRINCIPAL_INVESTIGATOR

Principal Investigators

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Aleks Leligdowicz, MD PhD

Role: PRINCIPAL_INVESTIGATOR

Western University

Locations

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Aleks Leligdowicz

London, Ontario, Canada

Site Status RECRUITING

Countries

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Canada

Central Contacts

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Aleks Leligdowicz, MD PhD

Role: CONTACT

519-661-2111 ext. 87241

Facility Contacts

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Aleks Leligdowicz, MD PhD

Role: primary

519-661-2111 ext. 87241

References

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Reference Type BACKGROUND
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Reference Type BACKGROUND
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Reference Type BACKGROUND
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Reference Type BACKGROUND
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Tandon SP, Mishra MM. Effect of sodium, manganese and zinc on the activity of nitrobacter agilis. Zentralbl Bakteriol Parasitenkd Infektionskr Hyg. 1969;123(4):399-402. No abstract available.

Reference Type BACKGROUND
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Yoshino M, Murakami K. The regulatory role of spermine and fatty acid in the interaction of AMP deaminase with phosphofructokinase. Biochim Biophys Acta. 1982 Dec 17;719(3):474-9. doi: 10.1016/0304-4165(82)90235-5.

Reference Type BACKGROUND
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Aono R. Improvement of organic solvent tolerance level of Escherichia coli by overexpression of stress-responsive genes. Extremophiles. 1998 Aug;2(3):239-48. doi: 10.1007/s007920050066.

Reference Type BACKGROUND
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Kaplan A, Matsue H, Shibaki A, Kawashima T, Kobayashi H, Ohkawara A. The effects of cyclosporin A and FK506 on proliferation and IL-8 production of cultured human keratinocytes. J Dermatol Sci. 1995 Sep;10(2):130-8. doi: 10.1016/0923-1811(95)00395-9.

Reference Type BACKGROUND
PMID: 8534611 (View on PubMed)

Study Documents

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Document Type: C3RP Laboratory Website

View Document

Other Identifiers

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12145

Identifier Type: -

Identifier Source: org_study_id

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