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Effect of Fostair® on Biomarkers of Platelet Adhesion in Idiopathic Pulmonary Fibrosis

NCT02048644 · Status: COMPLETED · Phase: PHASE2 · Type: INTERVENTIONAL · Enrollment: 20

Last updated 2019-07-15

No results posted yet for this study

Summary

The investigator has recently studied markers of platelet activation in idiopathic pulmonary fibrosis (IPF) and found that in IPF patients there is a significantly increased platelet reactivity when compared with controls which is demonstrated by a concentration dependent increase in platelet-monocyte complex formation, platelet P-selectin expression and platelet fibrinogen binding in the presence of' the platelet agonists Adenosine diphosphate and L- Threonyl- L- phenylalanyl- L- leucyl- L- leucyl- L-argininamide (TFLLR).

During platelet activation the platelets degranulate releasing numerous profibrotic cytokines including Transforming growth factor beta and Platelet derived growth factor that are recognised to be important in the pathogenesis of IPF. It is therefore plausible that the observed increased platelet reactivity in IPF contributes to the fibrotic process through local activation and degranulation with release of proinflammatory and profibrotic mediators within the pulmonary circulation.

There is evidence that corticosteroid treatment may alter platelet adhesion, in a study of spontaneously hypertensive rat (SHR) increased circulating glucocorticoid, suppressed p-selectin expression. p selectin is a transmembrane protein present in the α granules of platelets. P selectin has a crucial role in platelet aggregation and platelet-leukocyte interactions, which are both potentially important mechanisms in the initiation and/or progression of tissue injury and development of thrombosis. In a study of patients with chronic obstructive pulmonary disease (COPD) exacerbation these were treated with either β agonists alone or β agonist and 40mg prednisolone and compared with a control group. At presentation the COPD patients had higher pulmonary artery pressure (PAP) higher p selectin and fibrinogen levels but lower Antithrombin III levels (AT III). The pulmonary artery pressure and fibrinogen levels were found to be significantly decreased in the steroid treated group whilst the p-selectin levels further increased in the non steroidal therapy patients.

Rationale for the Current Study

There is a significant unmet medical need for the treatment of IPF; the only medication approved for treatment of IPF in the United Kingdom (UK) is Pirfenidone and outside the UK there is none. The main goal of the current study is to evaluate the effect of Fostair on the biomarkers of platelet activation in IPF disease which the investigator believes play a pivotal role in the pathogenesis of IPF and whether this translates in to a clinically beneficial effect of Fostair on IPF disease.

Conditions

Interventions

DRUG

fostair

beclometasone dipropionate 200mcg and formoterol 12 mcg delivered by inhaler, twice a day for 28 days

DRUG

placebo

placebo matched inhaler 2puffs to be taken twice a day for 28 days

Sponsors & Collaborators

  • Chiesi Farmaceutici S.p.A.

    collaborator INDUSTRY

  • Hull University Teaching Hospitals NHS Trust

    lead OTHER_GOV

Principal Investigators

  • Simon Hart, MD · Hull University Teaching Hospitals NHS Trust

Study Design

Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
DOUBLE
Model
CROSSOVER

Eligibility

Min Age
40 Years
Max Age
85 Years
Sex
ALL
Healthy Volunteers
No

Timeline & Regulatory

Start
2014-03-31
Primary Completion
2015-04-30
Completion
2015-05-31

Countries

  • United Kingdom

Study Locations

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Drugs
Diseases

Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT02048644 on ClinicalTrials.gov