Effect of Fostair® on Biomarkers of Platelet Adhesion in Idiopathic Pulmonary Fibrosis
Condition: Idiopathic Pulmonary Fibrosis
MeSH terms: Pulmonary Fibrosis; Idiopathic Pulmonary Fibrosis; Fibrosis; Tissue Adhesions
Study type: Interventional
Phase: Phase 2

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.
    


Intervention name(s): fostair; placebo
Intervention type(s): Drug; Drug
Intervention description(s): beclometasone dipropionate 200mcg and formoterol 12 mcg delivered by inhaler, twice a day for 28 days; placebo matched inhaler 2puffs to be taken twice a day for 28 days
Other intervention name(s): beclometasone dipropionate and formoterol fumarate
Intervention MeSH terms: Beclomethasone; Formoterol Fumarate
Allocation: Randomized
Intervention model: Crossover Assignment
Masking: Double (Participant, Investigator)
Primary purpose: Treatment
Keywords: Platelets adhesion