Background: Because nonsteroidal anti-inflammatory drug (NSAID) intolerance depends on COX-1 inhibition, preferential or selective COX-2 inhibitors have been thought to be well tolerated by these patients.
Objective: The aim of this study is to evaluate tolerability to nabumetone and meloxicam in patients with NSAID intolerance.
Methods: Seventy patients intolerant to NSAIDs were selected. Thirty subjects were patients with asthma with respiratory (rhinitis-asthma) intolerance to NSAIDs (group A); 40 patients (group B) had cutaneous-mucous (urticaria-angioedema) NSAID intolerance. Diagnosis was based on clinical histories in all patients, and it was confirmed by positive single-blind placebo-controlled oral challenge test in 36 patients. After written informed consent, a single-blind placebo-controlled oral challenge test with nabumetone in all patients (2 g except for 11 patients who reached 1 g) and meloxicam (15 mg) in 51 patients was performed.
Results: Of the total selected, 94.3% tolerated 1 g nabumetone. In those who reached the 2-g dose, the tolerability was 83.6%. With respect to meloxicam, 96.1% of patients, tolerated 15 mg. No significant difference in nabumetone and meloxicam tolerability was observed between groups A and B.
Conclusion: The results of this study confirm a high percentage of tolerability to the maximum therapeutic dosage of nabumetone and meloxicam in patients with NSAID intolerance, both in those with cutaneous/mucous manifestations and in those with respiratory disease.
Clinical Implications: Nabumetone and meloxicam are safe alternatives in NSAID-intolerant patients.
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http://dx.doi.org/10.1016/j.jaci.2006.12.616 | DOI Listing |
Data Brief
April 2021
Department of Neurosurgery, Johns Hopkins University School of Medicine, 600 N. Wolfe St., Meyer 7-113, Baltimore, MD 21287, USA.
Here we describe the dataset of the first report of pharmacogenomics profiling in an outpatient spine setting with the primary aims to catalog: 1) the genes, alleles, and associated rs Numbers (accession numbers for specific single-nucleotide polymorphisms) analysed and 2) the genotypes and corresponding phenotypes of the genes involved in metabolizing 37 commonly used analgesic medications. The present description applies to analgesic medication-metabolizing enzymes and may be especially valuable to investigators who are exploring strategies to optimize pharmacologic pain management (e.g.
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Allergy Service, Hospital Universitario de Canarias, La Laguna, Spain.
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