Biomedical subjects

Donald D Stevenson

Publications and source records attributed to Donald D Stevenson.

21 records · Page 2Linked to original sources

PubMed2002

Improvement of aspirin-intolerant asthma by montelukast, a leukotriene antagonist: a randomized, double-blind, placebo-controlled trial.

Leukotriene antagonists block the proinflammatory actions of leukotrienes (LT) and have been introduced as new treatments for asthma. Conventional therapy with glucocorticosteroids does not inhibit the biosynthesis of leukotrienes. We therefore tested whether addition of the leukotriene receptor antagonist montelukast was of therapeutic benefit in a group of aspirin-intolerant patients with asthma of whom 90% already were treated with moderate to high doses of glucocorticosteroids. Under double-blind conditions, 80 aspirin-intolerant patients with asthma were randomized to receive 4 wk oral treatment of either 10 mg of montelukast or placebo once daily at bedtime. Pulmonary function was measured as forced expiratory volume in 1 s (FEV(1)) once a week in the clinic and daily as morning and evening peak expiratory flow rate (PEFR). Asthma symptoms and use of rescue bronchodilator were also recorded daily. Asthma specific quality of life (QoL) was assessed before and after the treatments. The group receiving montelukast showed a remarkable improvement of their asthma, whereas the group given placebo showed no change. Thus, from equal baseline values, the mean difference between the groups over the 4-wk treatment period was 10.2% for FEV(1) and 28.0 L for morning PEFR (p for both < 0.001). The improved pulmonary function in the group receiving montelukast occurred at the same time as 27% less bronchodilator was used (p < 0.05), and it was associated with fewer asthma symptoms than in the group given placebo, including 1.3 nights more of sleep per week and 54% fewer asthma exacerbations (p < 0.05). There was also an improvement in asthma-specific QoL (p < 0.05). The therapeutic response to montelukast was consistent across patients with different baseline characteristics and did not correlate with baseline urinary LTE(4). Addition of a leukotriene receptor antagonist such as montelukast improves asthma in aspirin-intolerant patients over and above what can be achieved by glucocorticosteroids.

Acetates↗

PubMed2002

The safety of celecoxib in patients with aspirin-sensitive asthma.

OBJECTIVE: To determine whether celecoxib, a selective cyclooxygenase 2 (COX-2) inhibitor, cross-reacts in patients with aspirin-exacerbated respiratory disease (AERD) with asthma. METHODS: Sixty patients with asthma underwent double-blinded, placebo-controlled oral challenges with celecoxib (100 mg, 200 mg, and 2 placebos) over 48 hours in our General Clinical Research Center. The next day, sensitivity to acetylsalicylic acid (ASA) was proven in all patients with the use of single-blinded ASA challenges. RESULTS: None of the 60 patients experienced any symptoms, changes in nasal examinations, or declines in forced expiratory volume in 1 second during the celecoxib challenges. All 60 patients experienced oculonasal and/or asthmatic reactions to ASA, with a mean provoking dose of 69 mg. The exact 1-sided confidence interval for the probability of celecoxib inducing cross-reactions in AERD patients was calculated to be between 0% and 5%. CONCLUSION: Cross-reactivity between ASA and celecoxib does not occur in patients with AERD. These results do not preclude the possibility of other types of immune reactions occurring with celecoxib after prior exposure. Our results add to the growing body of evidence that inhibition of COX-1 is a critical initiating event in the precipitation of respiratory reactions in AERD patients following ingestion of nonsteroidal antiinflammatory drugs.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2002

The natural history and clinical characteristics of aspirin-exacerbated respiratory disease.

BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is a clinical syndrome characterized by chronic rhinitis, nasal polyps, asthma, and precipitation of asthma and rhinitis attacks after ingestion of aspirin (ASA) and most nonsteroidal anti-inflammatory drugs (NSAIDs). Most information about the disease in the United States has come from small samples of patients. OBJECTIVE: The purpose of this study was to examine the natural history and clinical characteristics of 300 AERD patients, referred to our institution for aspirin desensitization. METHODS: All potential AERD patients were evaluated using a standard questionnaire that included information about clinical characteristics and natural progression of their disease, previous history of reactions to ASA and other NSAIDs, current use of medications, and ethnic backgrounds. All patients underwent oral ASA challenges to prove they had AERD. RESULTS: From patients' history we found that the average age at onset of AERD was 34 years, and that 57% were female. Counting ASA as an NSAID, 33% had previously reacted on two occasions to NSAIDs and 36% on more than three occasions to NSAIDs, whereas only 27% had reacted to one NSAID before they came to us for evaluation. Our patients had averaged 5.5 episodes of sinusitis per year. There were no significant differences in the clinical characteristics or use of medications between genders. Ethnicity was heterogeneous in most participants. CONCLUSIONS: AERD begins in the third decade of life and in both sexes. The disease progressed over the 13 years between historical onset and current evaluation, with more sinusitis and need for controller medications over time. There was no ethnic or familial distribution of AERD.

Acute Disease↗