From the Lancet RespiratoryMedicine:
Pulmonary vascular leakage occurs early in acute respiratory distress syndrome (ARDS). Mortality is high (35–45%), but no eff ective pharmacotherapy exists. Production of anti-infl ammatory adenosine by ecto-5ΘΈ-nucleotidase (CD73) helps maintain endothelial barrier function. We tested whether interferon-beta-1a (IFN-beta-1a), which increases CD73 synthesis, can reduce vascular leakage and mortality in patients with ARDS...
We then tested the safety, tolerability, and effi cacy of intravenous human recombinant IFN- beta-1a (FP-1201) in patients with ARDS in an open-label study (comprising dose-escalation and expansion phases). We recruited patients from eight intensive care units in the UK. Eligible patients were aged 18 years or older, had ARDS, and were being treated with assisted ventilation. We established an optimal tolerated dose (OTD) in the first, dose-escalation phase. Once established, we gave all subsequently enrolled patients the OTD of intravenous FP-1201 for 6 days...
By day 28, 3 (8%) of 37 patients in the treatment cohort and 19 (32%) of 59 patients in the control cohort had died—thus, treatment with FP-1201 was associated with an 81% reduction in odds of 28-day mortality (odds ratio 0·19 [95% CI 0·03–0·72]; p=0·01).
It's only a phase II trial and it looks
too good to be true. If it is confirmed in high level studies it
will be a breakthrough in the treatment of ARDS.
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