Allergic rhinitis can be a debilitating condition which, if untreated, can result in considerable health-related and economic consequences. A review of the published literature was conducted, with quantitative/qualitative analysis as appropriate, to explore the direct, indirect, and hidden costs of allergic rhinitis, as well as the quality-of-life burdens that the disease presents to patients and to the healthcare system. Lack of treatment, undertreatment, or nonadherence to treatment in allergic rhinitis were seen to increase direct and indirect costs, reinforcing the need for patient education and for physicians to implement existing evidence-based guidelines for prevention and treatment. It was concluded that greater awareness of the total economic burden of allergic rhinitis should encourage appropriate intervention and ultimately ensure clinically favorable and cost-effective outcomes.

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Establishing a reliable estimate of the prevalence of allergic rhinitis is difficult; prevalence estimates range from as low as 4% to more than 40%. Epidemiology studies suggest the prevalence of allergic rhinitis in the United States and around the world is increasing. The cause of this increase is unknown; however, contributing factors may include higher concentrations of airborne pollution, rising dust mite populations, less ventilation in homes and offices, dietary factors, and the trend toward more sedentary lifestyles. Allergic rhinitis symptoms typically begin in childhood and adolescence and continue into adulthood. In general, allergic rhinitis symptoms slowly improve and skin-test reactivity tends to wane with increasing age. There is a significant trend for symptom improvement with younger age of onset of allergic rhinitis. As the complicated etiology of allergic rhinitis becomes better understood, it may be possible to reverse the trend for increased prevalence.

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Fluticasone propionate (FP) administered via metered-dose inhaler is a potent corticosteroid effective in the treatment of asthma. To evaluate the efficacy and safety of FP powder administered via a breath-activated inhaler (Diskhaler), a multicenter, double-blind, randomized, placebo-controlled, parallel-group study was conducted in adolescent and adult patients (n = 331) with mild-to-moderate asthma previously treated with beta 2-agonist therapy alone. Patients received FP powder 50, 100, or 250 micrograms or placebo twice daily for 12 weeks. FP-treated patients compared with placebo-treated patients had significantly (p < 0.001) greater improvements in morning predose forced expiratory volume in 1 sec (21-22% increase vs. 9%). Improvement in morning peak flow rate were also significantly (p < 0.001) greater with FP than with placebo (8-10% increase vs. 2% increase). There was also a significant overall treatment difference in the frequency of inhaled albuterol use (p < 0.001) and number of nighttime awakenings due to asthma (p = 0.005). There were no statistically significant difference among the FP treatment groups in any outcome measure. Physicians' global assessments also indicated significant (p < 0.001) differences in efficacy, with 67-74% of FP-treated patients rated as having "effective" or "very effective" treatment compared with 41% of placebo-treated patients. Significant beneficial effects of FP were observed in lung function and diary card parameters after just 1 week of treatment. Adverse events were similar across treatment groups and primarily related to local irritation. Effect on hypothalamic-pituitary-adrenal axis function was minimal. In summary, all three dosages of inhaled FP powder were well tolerated and improved various asthma-related variables. Improvements in pulmonary function, beyond those achieved with beta 2-agonist therapy alone, were maintained for the duration of the 12-week study.

Three adults with osteogenesis imperfecta and associated cardiovascular lesions are reported. Two presented with aortic insufficiency due to dilatation of the aortic root for which none of the usual causes is apparent. The third patient was found to have lesions involving pulmonary, aortic, and mitral valves in addition to microscopic changes in the pulmonary artery and aorta. It is suggested that in osteogenesis imperfecta, as in other heritable disorders of connective tissue, cardiovascular defects may become apparent after the passage of time and play a dominant role in the natural history of the disease process.

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