Benralizumab induces remission in 77% of patients with eosinophilic gastritis
Click Here to Manage Email Alerts
Key takeaways:
- Patients on benralizumab had more significant change from baseline in peak gastric eosinophil counts.
- Persistence of other indicators of disease suggest involvement of an additional pathogenic mechanism.
Benralizumab induced histological remission at 12 weeks in more than three-fourths of patients with eosinophilic gastritis, although other biomarkers of disease persisted, according to data in The Lancet Gastroenterology & Hepatology.
“Previous studies of eosinophilic gastrointestinal diseases have primarily focused on eosinophilic esophagitis, which is the most prevalent of these diseases,” Kara L. Kliewer, PhD, of the division of allergy and immunology at Cincinnati Children’s Hospital Medical Center, and colleagues wrote. “Eosinophilic gastritis is less understood ... Benralizumab is approved for the treatment of severe eosinophilic asthma for individuals aged 12 years or older and has shown promise in other eosinophil-associated diseases.”
They continued: “However, to our knowledge, no randomized trials have evaluated benralizumab in eosinophilic gastritis.”
In a randomized, phase 2 trial, Kliewer and colleagues assessed the safety and efficacy of benralizumab in 26 patients (mean age, 19.5 years; 73% men) with symptomatic, histologically active eosinophilic gastritis at Cincinnati Children’s Hospital Medical Center.
Patients received either benralizumab 30 mg (n = 13) or placebo (n = 13) subcutaneously once every 4 weeks for a 12-week double-blind period, after which patients were eligible for open-label extension periods of benralizumab up to 88 weeks.
The primary studied outcome was histological remission, defined as peak gastric eosinophil count less than 30 eos/hpf.
At 12 weeks, 77% (95% CI, 50-92) of patients in the treatment group and 8% (95% CI, 1-33) of patients in the placebo group achieved histological remission (difference = 69 percentage points; 95% CI, 32-85).
Results also showed patients in the treatment arm had significantly greater changes from baseline compared with placebo in mean peak gastric eosinophil counts (–137 eos/hpf; 95% CI, –186 to –88 vs. –38 eos/hpf; 95% CI, – 94 to 18), mean eosinophilic gastritis histology total score (–0.31; 95% CI, –0.42 to –0.2 vs. –0.02; 95% CI, –0.16 to 0.12), mean histology inflammatory score (–0.46; 95% CI, –0.6 to –0.31 vs. –0.04; 95% CI, –0.22 to 0.13) and median blood eosinophil counts (–1,060 eos/µL vs. –160 eos/µL).
However, there were no significant differences between groups for changes in mean eosinophilic gastritis histology structural score (–0.07; 95% CI, –0.19 to 0.05 vs. 0.03; 95% CI, –0.09 to 0.15), mean Eosinophilic Gastritis Endoscopic Reference System score (–1; 95% CI, –2.3 to 0.3 vs. –0.5; 95% CI, –2 to 1) or in patient-reported outcomes.
Researchers reported treatment-emergent adverse events in 85% of patients in the treatment arm and 46% in the placebo arm during the double-blind period, including headache, nausea and vomiting. Two patients had serious adverse events during the open label extension period unrelated to benralizumab.
“Treatment with benralizumab resulted in histological remission, as defined by the absence of tissue eosinophilia, in most patients with active eosinophilic gastritis,” Kliewer and colleagues concluded. “Nonetheless, the persistence of signs, symptoms and biomarkers of eosinophilic gastritis suggests the co-existence of an eosinophil-independent pathogenic mechanism in many patients.”
They continued, “As such, successful management of eosinophilic gastritis might require therapies that inhibit pathways that more broadly reduce type 2 inflammation, rather than only targeting eosinophils.”
Collapse
Read more about
Click Here to Manage Email Alerts