ArticleClinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology2010
Suppression of gastric acid increases the risk of developing immunoglobulin E-mediated drug hypersensitivity: human diclofenac sensitization and a murine sensitization model.
Article in Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 36 citations in OpenAlex.
- Safety of first-line triple therapy with a potassium-competitive acid blocker for Helicobacter pylori eradication in children.Journal of gastroenterology · 2018Trial
- Proton pump inhibitors and the risk of acquiring a penicillin allergy label.Internal medicine journal · 2023Article
- Country-wide medical records infer increased allergy risk of gastric acid inhibition.Nature communications · 2019Article
- Acid suppressant medications and the risk of allergic diseases.Expert review of clinical immunology · 2018Article
- Review
- Association Between Use of Acid-Suppressive Medications and Antibiotics During Infancy and Allergic Diseases in Early Childhood.JAMA pediatrics · 2018Article
- Importance of hypersensitivity in adverse reactions to drugs in the elderly.Clinical and molecular allergy : CMA · 2018Article
- Allergic diseases and asthma in pregnancy, a secondary publication.The World Allergy Organization journal · 2017Review
- The Efficacy and Tolerability of a Triple Therapy Containing a Potassium-Competitive Acid Blocker Compared With a 7-Day PPI-Based Low-Dose Clarithromycin Triple Therapy.The American journal of gastroenterology · 2016Article
- Acid suppression therapy and allergic reactions.Allergo journal international · 2015Article
- Immediate-type hypersensitivity drug reactions.British journal of clinical pharmacology · 2014Review
- Development of food allergies in patients with gastroesophageal reflux disease treated with gastric acid suppressive medications.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2013Article
- Diclofenac hypersensitivity: antibody responses to the parent drug and relevant metabolites.PloS one · 2010Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundHypersensitivity reactions towards non-steroidal anti-inflammatory drugs (NSAID) are common, although true allergies are detectable only in a subgroup of patients. The current study was prompted by a case observation, where a patient experienced generalized urticaria following his second course of diclofenac and proton pump inhibitor medication, and was found to have diclofenac-specific IgE. During recent years, our group has been investigating the importance of gastric digestion in the development of food allergies, demonstrating anti-acid medication as a risk factor for sensitization against food proteins.
objectiveHere, we aimed to investigate whether the mechanism of food allergy induction described can also be causative in NSAID allergy, using diclofenac as a paradigm.
methodsWe subjected BALB/c mice to several oral immunization regimens modelled after the patient's medication intake. Diclofenac was applied with or without gastric acid suppression, in various doses, alone or covalently coupled to albumin, a protein abundant in gastric juices. Immune responses were assessed on the antibody level, and functionally examined by in vitro and in vivo crosslinking assays.
resultsOnly mice receiving albumin-coupled diclofenac under gastric acid suppression developed anti-diclofenac IgG1 and IgE, whereas no immune responses were induced by the drug alone or without gastric acid suppression. Antibody induction was dose dependent with the group receiving the higher dose of the drug showing sustained anti-diclofenac titres. The antibodies induced triggered basophil degranulation in vitro and positive skin tests in vivo.
conclusionGastric acid suppression was found to be a causative mechanism in the induction of IgE-mediated diclofenac allergy.
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