Impact of asthma controller medications on clinical, economic, and patient-reported outcomes.

OBJECTIVE: To comprehensively evaluate clinical, economic, and patient-reported outcomes associated with various therapeutic classes of asthma controller medications. PATIENTS AND METHODS: This observational study, which used administrative claims data from US commercial health plans, included patients with asthma aged 18 through 64 years who filled a prescription for at least 1 asthma controller medication from September 1, 2003, through August 31, 2005. Outcome metrics included the use of short-acting beta-agonists (SABAs), the use of oral corticosteroids, inpatient (INP)/emergency department (ED) visits, and asthma-related health care costs. A subset of 5000 patients was randomly selected for a survey using the Mini-Asthma Quality of Life Questionnaire, the Work Productivity and Activity Impairment questionnaire, and the Asthma Therapy Assessment Questionnaire. RESULTS: Of 56,168 eligible patients, 823 returned completed questionnaires. Compared with inhaled corticosteroids (ICSs), leukotriene modifiers (LMs) were associated with lower odds of INP/ED visits (odds ratio [OR], 0.80; P<.001), lower odds of using 6 or more SABA canisters (OR, 0.81; P<.001), and higher annual cost ($193; P<.001). In the subgroup analysis of adherent patients, LMs were associated with higher odds of INP/ED visits (OR, 1.74; P=.04), lower odds of using 6 or more SABA canisters (OR, 0.46; P<.001), and higher annual cost ($235; P<.001). Inhaled corticosteroids and LMs had a comparable impact on all patient-reported outcomes. For combination therapy, ICS plus a long-acting beta-agonist consistently showed at least equivalent or better outcomes in the use of SABAs and oral corticosteroids, the risk of INP/ED visits, cost, asthma control level, quality of life, and impairment in productivity and activity. CONCLUSION: Inhaled corticosteroids were associated with a lower risk of INP/ED visits, and a lower cost if adherence was achieved. When adherence cannot be achieved, LMs may be a reasonable alternative. Combination therapy with ICS plus a long-acting beta-agonist was associated with better or equivalent clinical, economic, and patient-reported outcomes.

Cardiac Manifestations from Non-FIP1L1-PDGFRα-Associated Hypereosinophilic Syndrome in a 13-Year-Old African American Boy.

Hypereosinophilic syndrome (HES) is a rare disorder typically seen in males, aged 20 to 50, with a predisposition for Caucasians. It is marked by overproduction of eosinophils (>1,500/µL) and multiorgan system damage due to eosinophilic infiltration and mediator release. There are multiple variants of HES. Cardiac complications are more common in myeloproliferative HES associated with the FIP1L1-PDGFRα mutation. Sequelae range from acute necrosis and thrombus formation to fibrosis of the endomyocardium. We describe a young boy who presented with chest pain and dyspnea. A diagnosis of HES was made after all other etiologies of eosinophilia were excluded. Although he was found to be negative for the FIP1L1-PDGFRα mutation, his cardiac complications included pericardial effusion and restrictive cardiomyopathy, without myocardial necrosis. Multi-organ involvement resulted in pericarditis, pleuritis, nephritis, and dermatitis. In this paper, we review his case and discuss the known subtypes of HES, the classic cardiac complications, and available treatment strategies.

Genetic aspects of the etiology and treatment of asthma.

This article provides a clinical review of the genetic aspects of the etiology and treatment of asthma for pediatric practitioners who are experienced in asthma diagnosis and management but lack expertise in genetics and immunology. Asthma is caused by the interaction of genetic susceptibility with environmental factors. The asthmatic response is characterized by elevated production of IgE, cytokines, and chemokines; mucus hypersecretion; airway obstruction; eosinophilia; and enhanced airway hyperreactivity to spasmogens. The genes most clearly associated with asthma include disintegrin and metalloprotease ADAM-33, dipeptidyl peptidase 10, PHD finger protein 11, and the prostanoid DP1 receptor. Within a few years, practitioners may apply sophisticated knowledge of cell and molecular biology to expand pharmacotherapeutic approaches and to personalize diagnosis and management.