The Journal of allergy and clinical immunology
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J. Allergy Clin. Immunol. · Jun 2008
Randomized Controlled Trial Multicenter Study Comparative StudyComparison of adjustable- and fixed-dose budesonide/formoterol pressurized metered-dose inhaler and fixed-dose fluticasone propionate/salmeterol dry powder inhaler in asthma patients.
The adjustable-dose budesonide/formoterol dry powder inhaler (DPI) has demonstrated similar or greater asthma control with less inhaled corticosteroid compared with the fixed-dose budesonide/formoterol DPI. ⋯ Adjustable-dose and fixed-dose budesonide/formoterol showed no differences in asthma control or tolerability versus fixed-dose fluticasone propionate/salmeterol.
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J. Allergy Clin. Immunol. · Mar 2008
Randomized Controlled TrialRapid corticosteroid effect on beta(2)-adrenergic airway and airway vascular reactivity in patients with mild asthma.
Long-term glucocorticoid therapy has been suggested to improve airway and airway vascular smooth muscle responsiveness to inhaled beta(2)-agonists in patients with asthma. ⋯ A single dose of an inhaled glucocorticoid restores beta(2)-adrenergic airway vasodilator responses in patients with mild asthma. The mechanism of this rapid glucocorticoid effect remains to be clarified.
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J. Allergy Clin. Immunol. · Jan 2008
Randomized Controlled TrialIntranasal noninhaled carbon dioxide for the symptomatic treatment of seasonal allergic rhinitis.
Noninhaled intranasal carbon dioxide (CO2) has been shown to be effective in the abortive treatment of migraine headache. Migraine headache is associated with trigeminal neuronal activation and release of calcitonin gene-related peptide, events also implicated in allergic rhinitis. Intranasal CO2 might inhibit trigeminal neuronal activation and suppress the release of calcitonin gene-related peptide. ⋯ Two 60-second intranasal CO2 treatments resulted in rapid (10 minutes) and sustained (24 hours) relief of seasonal allergic rhinitis symptoms.
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J. Allergy Clin. Immunol. · Aug 2007
Randomized Controlled Trial Multicenter StudyCritical role of kallikrein in hereditary angioedema pathogenesis: a clinical trial of ecallantide, a novel kallikrein inhibitor.
Hereditary angioedema (HAE) is a rare, autosomal-dominant disorder caused by C1 inhibitor gene mutation. Patients with HAE experience intermittent attacks of edema affecting the oropharynx, abdomen, gastrointestinal tract, and limbs. C1 inhibitor is the primary endogenous inhibitor of the kallikrein-kinin (contact) cascade. Unregulated kallikrein activation generates bradykinin, the likely mediator of the swelling and pain characterizing HAE attacks. Ecallantide, a novel, recombinant protein, potently inhibits kallikrein. This is the first placebo-controlled assessment in human beings of a therapeutic intervention to improve symptoms of HAE attacks under the hypothesis that the contact cascade is the putative pathway responsible for HAE pathology. ⋯ Ecallantide is a promising new therapy for HAE attacks.
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J. Allergy Clin. Immunol. · Jul 2007
Letter Randomized Controlled TrialEvaluation of BCG administration as an adjuvant to specific immunotherapy in asthmatic children with mite allergy.