The oral steroid budesonide is effective in treatment of acute symptoms from gluten exposure in patients with celiac disease, researchers report in the January issue of Clinical Gastroenterology and Hepatology.
Budesonide is a corticosteroid that produces clinical and histologic responses in patients with refractory celiac disease and is used for the treatment of celiac crisis and as an adjuvant to the gluten-free diet at diagnosis.
Amelie Therrien et al investigated the effects of enteric-release budesonide in a retrospective study of 13 patients with acute symptoms following inadvertent ingestion of gluten. Twelve of the patients had biopsy-confirmed disease and 1 had potential celiac disease.
The patients were offered a trial of budesonide therapy because of diarrhea, abdominal pain, and nausea and/or vomiting that lasted from 2 days to 4 weeks following accidental gluten ingestion. The initial dose of enteric-release budesonide was 9 mg daily for most patients (85%), ranging from 3 to 28 days.
All patients reported a clinical response to budesonide, including 8 patients (62%) with substantial improvement in gastrointestinal symptoms. Most partial responses were related to extraintestinal manifestations. Two patients (15%) reported adverse events (headache and constipation). Nine patients (69%) took additional course(s) of budesonide, and all had a reduction in symptoms.
One patient, who used budesonide on multiple occasions, reported that it was most effective when taken at symptom onset.
Therrien et al do not advocate use of steroids for uncomplicated celiac disease; the patients included in this study were selected for a trial of budesonide because of severe, debilitating reactions due to inadvertent exposure to gluten.
The authors explain that budesonide is a micronized corticosteroid with large topical effects. It binds to the transcription factor nuclear factor-κB, which regulates transcription of genes that control inflammation. Budesonide also has direct anti-inflammatory effects on the intestinal mucosa following exposure to gliadin and the drug inhibits mast cells, eosinophils, and T-helper 2 cells.
The topical effects of budesonide might account for its greater efficacy on gastrointestinal symptoms compared with extra-intestinal manifestations, which might be related to systemic inflammation. Patients with extra-intestinal manifestations might benefit from a longer drug taper (3–4 weeks) than patients with predominantly gastrointestinal symptoms (3–9 days taper). Alternatively, extra-intestinal manifestations might require systemic therapy or be unrelated to celiac disease.
Short courses of budesonide were well tolerated and seldom associated with any systemic steroid side-effects, and several patients received multiple courses. Therrien et al note that prolonged treatment regimen of 3 mg, 3 times each day, including 2 open capsules to deliver the drug proximally, has been proposed to be more effective for patients with refractory celiac disease.
Although this retrospective study lacked objective endpoints and different treatment regimens were used, budesonide might be a therapeutic option for acute flares of symptoms related to gluten exposures in patients with celiac disease. Prospective studies are required.