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Clinical Trials/NCT02922673
NCT02922673
Completed
Not Applicable

The Effects of Acetylsalicylic Acid on Immunoparalysis Following Human Endotoxemia

Radboud University Medical Center1 site in 1 country30 target enrollmentStarted: September 2016Last updated:
ConditionsEndotoxemia
InterventionsAspirinPlacebo

Overview

Phase
Not Applicable
Status
Completed
Enrollment
30
Locations
1
Primary Endpoint
Change in concentration plasma TNFalpha (pg/ml)

Overview

Brief Summary

Rationale:

The last years, research focus has moved to immunostimulatory agents in order to restore or increase the functionality of the immune system during sepsis-induced immunoparalysis. Epidemiologic data show that prehospital use of low dose acetylsalicylic acid (ASA) is associated with improved outcome of sepsis. Experimental data indicate that ASA exerts pro-inflammatory effects during systemic inflammation. However, it remains to be determined whether treatment with ASA improves immune function once immunoparalysis has developed and whether prehospital use of low dose ASA prevents the development of immunoparalysis. In the former case, ASA is a potential immunostimulatory therapy that can treat sepsis-induced immunoparalysis. In the latter case, ASA may have a broader indication as an immunomodulating agent. Taken together, ASA might be a promising, cheap, well-known, and globally available agent to reduce the incidence of secondary infections and improve patient outcome in sepsis.

Objective:

  • To determine whether acetylsalicylic acid treatment can reverse endotoxin tolerance, which is expressed as a decrease in pro-inflammatory cytokine levels between the first and second endotoxin challenge.
  • To determine whether acetylsalicylic acid prophylaxis can prevent endotoxin tolerance, which is expressed as a decrease in pro-inflammatory cytokine levels between the first and second endotoxin challenge.

Study design:

Double-blind randomized placebo-controlled pilot study in 30 healthy male volunteers during repeated experimental endotoxemia. All subjects will receive a 14 day course of study medication (low-dose ASA or placebo) and undergo experimental endotoxemia (lipopolysacharide (LPS), E.Coli type O113) on day 7 and on day 14. LPS is administrated using an initial bolus of 1ng/kg followed by continuous infusion at 1ng/kg/hr during 3 hours.

Subjects are randomized in three study arms:

  1. Treatment group: 7 days placebo / first endotoxemia / 7 days ASA 80 mg (loading dose on first day of 160mg) / second endotoxemia
  2. Prophylaxis group: 7 days ASA 80 mg (loading dose on first day of 160mg) / first endotoxemia / 7 days ASA 80 mg / second endotoxemia
  3. Placebo group: 7 days placebo / first endotoxemia / 7 days placebo / second endotoxemia

Study Design

Study Type
Interventional
Allocation
Randomized
Intervention Model
Parallel
Primary Purpose
Basic Science
Masking
Quadruple (Participant, Care Provider, Investigator, Outcomes Assessor)

Eligibility Criteria

Ages
18 Years to 35 Years (Adult)
Sex
Male
Accepts Healthy Volunteers
Yes

Inclusion Criteria

  • Written informed consent
  • Age ≥18 and ≤35 yrs
  • Healthy (as confirmed by medical history, examination, ECG, blood sampling)

Exclusion Criteria

  • Use of any medication
  • Use of COX-inhibitors within 6 weeks prior to the first endotoxemia day
  • Known anaphylaxis or hypersensitivity to acetylsalicylic acid or non-investigational products
  • History or signs of atopic syndrome (asthma, rhinitis with medication and/or eczema)
  • History of peptic ulcer disease
  • History or signs of hematological disease
  • Thrombocytopenia (\<150\*10\^9/ml) or anemia (hemoglobin \< 8.0 mmol/L)
  • History of glucose-6-phosphate dehydrogenase deficiency
  • History of intracranial hemorrhage
  • History, signs or symptoms of cardiovascular disease, in particular:

Arms & Interventions

Treatment group

Experimental

7 day treatment with placebo - first LPS challenge - 7 day treatment with ASA 80 mg (with a loading dose of 160 mg on the first day) - second LPS challenge

Intervention: Aspirin (Drug)

Treatment group

Experimental

7 day treatment with placebo - first LPS challenge - 7 day treatment with ASA 80 mg (with a loading dose of 160 mg on the first day) - second LPS challenge

Intervention: Placebo (Drug)

Prophylaxis group

Active Comparator

7 day treatment with ASA 80 mg (with a loading dose of 160 mg on the first day) - first LPS challenge - 7 day treatment with ASA (no loading dose on first day) - second LPS challenge

Intervention: Aspirin (Drug)

Placebo group

Placebo Comparator

7 day treatment with placebo - first LPS challenge - 7 day treatment with placebo - second LPS challenge

Intervention: Placebo (Drug)

Outcomes

Primary Outcomes

Change in concentration plasma TNFalpha (pg/ml)

Time Frame: Measured after the first and second LPS-challenge (on day 7 and day 14)

measured with Luminex assay

Secondary Outcomes

  • Kidney damage markers in urine (NGAL, KIM-1 and L-FABP)(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Change in transcriptional activity of leukocytes(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Change in concentration plasma IL-6 (pg/ml)(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Change in plasma concentration of IFN-gamma (pg/ml)(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Change in plasma concentration of IL-10 (pg/ml)(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Change in temperature(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Change in plasma concentration of IL-1beta (pg/ml)(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Change in plasma concentration of MIP-1alpha (pg/ml)(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Change in plasma concentration of MIP-1beta (pg/ml)(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Change in monocytic HLA-DR expression (mHLA-DR)(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Change in blood pressure(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Change in cerebral blood flow using Transcranial Doppler (TCD) measurements and Near Infrared Spectroscopy (NIRS)(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Change in platelet monocyte complexes(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Change in concentration plasma IL-8 (pg/ml)(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Change in heart rate(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Prostaglandin E2 (PGE-M)(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Change in symptoms during endotoxin day(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Arterial bloodgas(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Thromboxane B2(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Change in plasma enkephalin(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Change in lymphocyte surface antigen expression of PD-1 and IL7-RA(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Change in plasma concentration of IL-1RA (pg/ml)(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Change in plasma concentration of MCP-1 (pg/ml)(Measured after the first and second LPS-challenge)
  • Change in monocyte surface antigen expression of PD-L1(Measured after the first and second LPS-challenge (on day 7 and day 14))
  • Change in leukocyte count (and differentiation)(Measured after the first and second LPS-challenge (on day 7 and day 14))

Investigators

Sponsor Class
Other
Responsible Party
Sponsor

Study Sites (1)

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