D3.168 - Clinical Department of Allergy Center in Linköping
Case report
Background
Tezepelumab inhibits the thymic stromal lymphopoietin released by airway epithelial cells in response to viruses, pollutants, allergens. It has an impact on different inflammatory pathways and asthma phenotypes, including allergic asthma. A previous study has shown that tezepelumab reduced the rate of exacerbations over 52 weeks by 51% in patients with severe allergic asthma who had previously been treated with omalizumab. There are no head-to-head studies performed specifically in patients with allergic asthma to compare omalizumab to Tezepelumab and long-term comparative data are lacking.
Case report
A 61-year-old female with severe pollen-induced allergic rhino-conjunctivitis and oral steroid–dependent, predominantly allergic asthma presented to the allergy clinic. She had a successful childhood birch pollen immunotherapy and two prior timothy grass immunotherapy attempts (ages 11 and 23), both discontinued due to adverse effects. In vitro testing confirmed timothy grass sensitization. Peak fractional exhaled nitric oxide was 29 ppb, and maximum blood eosinophils 200 cells/µL. Omalizumab was initiated and subcutaneous immunotherapy (SCIT) for five-grass pollen was started. Asthma symptoms improved during the first 2 years. However, complete discontinuation of oral corticosteroids was not achievable despite multiple attempts. Low-dose prednisolone (2.5–7.5 mg/day) remained necessary during pollen seasons to maintain adequate control of both asthma and ARC. Omalizumab was administered continuously for one year, followed by a four-month discontinuation period during the winter season. Afterwards the treatment was reinitiated before the pollen seasons for the subsequent two consecutive years. During the third year, the patient’s asthma symptoms worsened markedly, prompting discontinuation of SCIT and escalation of oral corticosteroid therapy (methylprednisolone 36 mg/day). Omalizumab was subsequently switched to Tezepelumab, resulting in a marked clinical improvement after only two doses, and oral corticosteroids were successfully discontinued three months later. Over the following two years, no oral steroid courses were required and no exacerbations occurred. During periods of allergen exposure, high-dose inhaled corticosteroids remained necessary. However, during the winter season, asthma control was maintained with a medium-to-high inhaled corticosteroid dose.
Conclusion
Tezepelumab could provide rapid and sustained clinical effect in a patient with severe, oral steroid–dependent, predominantly allergic asthma who had an inadequate response to omalizumab. Treatment with Tezepelumab allowed complete discontinuation of oral corticosteroids and maintained asthma control over a two-year follow-up, highlighting its potential as an effective therapeutic option for severe allergic asthma.
