Introduction Severe Asthma, characterised by persistent symptoms despite maximal medical therapy, represents 5% of asthma cases. Bronchial Thermoplasty (BT) is a novel therapy, NICE approved for Severe Asthma patients uncontrolled despite step 4/5 of British Guideline on Asthma Management. BT delivers radiofrequency thermal energy to airways distal to the main-stem bronchi, permanently reducing airway smooth muscle mass. It is unknown whether treatment of smooth muscle hypertrophy impacts persistently upon systemic signs of allergic inflammation. Peripheral blood eosinophils (PBEs) are a marker of allergic inflammation in asthma. We asked: does BT modify signs of allergic inflammation as measured by PBEs and if so, does this effect persist over time?
Method A retrospective review of 15 consecutive Severe Asthma cases treated with BT was performed. Serial PBEs measured before and up to 1 year after BT were compared. Blood eosinophil levels taken peri-procedure were excluded from analysis due to standard protocol concomitant steroid therapy. For time to first detectable high PBE all available post-BT PBE levels were assessed.
Results 13 patients had PBE data before and after BT, with an average of 9 and 12 serial PBE levels pre and post-BT respectively. Mean PBE 1 year pre-BT was 0.33 × 109/L falling to a mean of 0.16 × 109/L 1 year post-BT (p < 0.05) (see Figure). 9 of 13 patients had a fall in mean PBE, in 2 of 13 levels rouse and 1 of 13 mean PBEs were unchanged post-BT. In 6 patients who converted from normal to high PBE post-BT, average time to first high PBE (>0.4 × 109/L) was 7 months (range 1–13 months). In 5 patients (38%) PBE remained within normal range persistently post BT.
Conclusion Severe Asthma patients undergoing BT had a significant reduction in average peripheral blood eosinophil levels from baseline. In over 1/3 of cases this effect was persistent 1 year post procedure. These findings support the concept that BT not only reduces asthma-associated smooth muscle hypertrophy but impacts upon systemic markers of allergic inflammation.