Anaphylaxis in Children: Current Understanding and Key Issues in Diagnosis and Treatment.

Curr Allergy Asthma Rep. 2012 Jul 20;

Authors: Dinakar C

Abstract
Anaphylaxis is a severe allergic reaction that is rapid in onset and may cause death. Since it is unpredictable and potentially fatal, prompt recognition and treatment are vital to maximize a positive outcome. The occurrence of anaphylaxis is increasing across all ages in the United States, with increased risk of worse outcome in teenagers/young adults and in those with comorbid conditions such as asthma. Gaps in the assessment of patient-specific risk factors, identification and prevention of triggers, recognition of signs/symptoms, and pharmacologic treatment of anaphylaxis have been identified at the physician and caregiver/patient level. A PubMed literature search (January 2000-December 2011) was conducted to identify publications on childhood anaphylaxis using the following terms: food allergy, food allergens, food hypersensitivity, epinephrine, epinephrine auto-injectors, anaphylactic triggers, and anaphylaxis. This review will critically appraise these key issues and highlight strategies that might result in improved management of anaphylaxis in children.

PMID: 22815131 [PubMed - as supplied by publisher]

Asthma and Adolescents: Review of Strategies to Improve Control.

J Sch Nurs. 2012 Jul 18;

Authors: Hennessy-Harstad E

Abstract
One of every 10 adolescents in the United States has asthma. Adolescents who lack asthma control are at increased risk for severe asthma episodes and death. The National Heart, Lung, and Blood Institute 2007 asthma guidelines and research studies indicated that school nurses are instrumental in assisting adolescents to monitor their asthma, learn asthma self-management skills, and improve health outcomes. This integrative review examines the research from 2005 to 2011 to identify strategies for school nurses to employ with adolescents to foster self-management skills. The research reviewed here supports the need for school nurses to engage adolescents with asthma to practice self-management behaviors. They should educate the adolescent for asthma, monitor how well the adolescent controls asthma, manage acute asthma episodes by using an asthma action plan, and coordinate care by obtaining written consent from parents to share health information with health care providers.

PMID: 22815347 [PubMed - as supplied by publisher]

Related Articles

Passive stiffness of airway smooth muscle: The next target for improving airway distensibility and treatment for asthma?

Pulm Pharmacol Ther. 2012 Jul 6;

Authors: Seow CY

Abstract
Reduced airway distensibility due to increased airway stiffness is a characteristic of asthma. Airway stiffness is determined by the property and structural organization of the various elements of the airway wall, and is often divided into active and passive components. Active stiffness is thought to be associated with activation of muscle cells in the airway wall. This component of stiffness can be inhibited when active force produced by the muscle is abolished. Passive stiffness, on the other hand, is thought to stem from non-muscle component of the airway wall, especially the collagen/elastin fibrous network of the extracellular matrix within which the muscle cells are embedded. In this brief review, the notion that passive stiffness is exclusively extracellular in origin is challenged. Recent evidence suggests that a substantial portion of the passive stiffness of an in vitro preparation of tracheal smooth muscle is calcium sensitive and is regulated by Rho-kinase, although the underlying mechanism and the details of regulation for the development of this intracellular passive stiffness are still largely unknown. To reduce airway stiffness different lines of attack must be tailored to different components of the stiffness. The regulatable passive stiffness is distinct from the relatively permanent stiffness of the extracellular matrix and the stiffness associated with active muscle contraction. To improve airway distensibility during asthma exacerbation, a comprehensive approach to reduce overall airway stiffness should therefore include a strategy for targeting the regulatable passive stiffness.

PMID: 22776694 [PubMed - as supplied by publisher]

Chronic respiratory disease, inhaled corticosteroids and risk of non-tuberculous mycobacteriosis.

Thorax. 2012 Jul 10;

Authors: Andréjak C, Nielsen R, Thomsen VO, Duhaut P, Sørensen HT, Thomsen RW

Abstract
BACKGROUND: Chronic respiratory disease and inhaled corticosteroid (ICS) therapy for chronic obstructive pulmonary disease (COPD) increase the risk of pneumonia. Few data are available on the association of these risk factors with non-tuberculous mycobacterial (NTM) pulmonary disease. METHODS: This study examined chronic respiratory diseases and ICS use as risk factors in a population-based case-control study encompassing all adults in Denmark with microbiologically confirmed NTM pulmonary disease between 1997 and 2008. The study included 10 matched population controls per case. Conditional logistic regression was used to compute adjusted ORs for NTM pulmonary disease with regard to chronic respiratory disease history. RESULTS: Overall, chronic respiratory disease was associated with a 16.5-fold (95% CI 12.2 to 22.2) increased risk of NTM pulmonary disease. The adjusted OR for NTM disease was 15.7 (95% CI 11.4 to 21.5) for COPD, 7.8 (95% CI 5.2 to 11.6) for asthma, 9.8 (95% CI 2.03 to 52.8) for pneumoconiosis, 187.5 (95% CI 24.8 to 1417.4) for bronchiectasis, and 178.3 (95% CI 55.4 to 574.3) for tuberculosis history. ORs were 29.1 (95% CI 13.3 to 63.8) for patients with COPD on current ICS therapy and 7.6 (95% CI 3.4 to 16.8) for patients with COPD who had never received ICS therapy. Among patients with COPD, ORs increased according to ICS dose, from 28.1 for low-dose intake to 47.5 for high-dose intake (more than 800 μg/day). The OR was higher for fluticasone than for budesonide. CONCLUSION: Chronic respiratory disease, particularly COPD treated with ICS therapy, is a strong risk factor for NTM pulmonary disease.

PMID: 22781123 [PubMed - as supplied by publisher]