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Effectiveness of magnesium sulfate as initial treatment of acute severe asthma in children, conducted in a tertiary-level university hospital: A randomized, controlled trial.

Arch Argent Pediatr. 2012 Aug;110(4):291-6

Authors: Torres S, Sticco N, Bosch JJ, Iolster T, Siaba A, Rocca Rivarola M, Schnitzler E

Abstract
Introduction. Magnesium sulfate is a calcium antagonist that inhibits bronchial smooth muscle contraction promoting bronchodilation. It is used for the management of acute severe asthma in children; however most of the studies have been performed in adults. Objective. To evaluate the effectiveness of intravenous magnesium sulfate for the treatment of pediatric patients with acute severe asthma exacerbations. Population and Methods. A clinical, randomized, controlled trial was conducted between March 2006 and March 2011 at Hospital Universitario Austral. Children with acute severe asthma admitted to the emergency department were randomized into two groups. Group A (control group): standard protocol for the initial treatment of acute asthma exacerbation. Group B: treatment protocol with magnesium sulphate for acute severe asthma exacerbation. The primary outcome was the requirement of invasive or non invasive mechanical ventilation support. Results. One hundred and forty three patients randomized into 2 groups were analyzed. The treatment group included 76 patients receiving magnesium sulfate within the first hour of the initiation of rescue treatment at the hospital, and the control group included 67 patients not treated with magnesium sulphate. Among the patients in the control group, 33% (n= 22) required mechanical ventilation support, compared to only 5% (n= 4) of the patients in the treatment group (p = 0.001). Conclusions. Intravenous infusion of magnesium sulfate during the first hour of hospitalization in patients with acute severe asthma significantly reduced the percentage of children who required mechanical ventilation support.

PMID: 22859321 [PubMed - in process]

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Household mold and dust allergens: Exposure, sensitization and childhood asthma morbidity.

Environ Res. 2012 Aug 2;

Authors: Gent JF, Kezik JM, Hill ME, Tsai E, Li DW, Leaderer BP

Abstract
BACKGROUND: Few studies address concurrent exposures to common household allergens, specific allergen sensitization and childhood asthma morbidity. OBJECTIVE: To identify levels of allergen exposures that trigger asthma exacerbations in sensitized individuals. METHODS: We sampled homes for common indoor allergens (fungi, dust mites (Der p 1, Der f 1), cat (Fel d 1), dog (Can f 1) and cockroach (Bla g 1)) for levels associated with respiratory responses among school-aged children with asthma (N=1233) in a month-long study. Blood samples for allergy testing and samples of airborne fungi and settled dust were collected at enrollment. Symptoms and medication use were recorded on calendars. Combined effects of specific allergen sensitization and level of exposure on wheeze, persistent cough, rescue medication use and a 5-level asthma severity score were examined using ordered logistic regression. RESULTS: Children sensitized and exposed to any Penicillium experienced increased risk of wheeze (odds ratio [OR] 2.12 95% confidence interval [CI] 1.12, 4.04), persistent cough (OR 2.01 95% CI 1.05, 3.85) and higher asthma severity score (OR 1.99 95% CI 1.06, 3.72) compared to those not sensitized or sensitized but unexposed. Children sensitized and exposed to pet allergen were at significantly increased risk of wheeze (by 39% and 53% for Fel d 1>0.12μg/g and Can f 1>1.2μg/g, respectively). Increased rescue medication use was significantly associated with sensitization and exposure to Der p 1>0.10μg/g (by 47%) and Fel d 1>0.12μg/g (by 32%). CONCLUSION: Asthmatic children sensitized and exposed to low levels of common household allergens Penicillium, Der p 1, Fel d 1 and Can f 1 are at significant risk for increased morbidity.

PMID: 22863552 [PubMed - as supplied by publisher]

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Atopic diseases, such as asthma and allergic rhinitis, are common conditions that can influence sleep and subsequent daytime functioning. Children and patients with allergic conditions from ethnic minority groups might be particularly vulnerable to poor sleep and compromised daytime functioning because of the prevalence of these illnesses in these groups and the high level of morbidity.

Research over the past 10 years has shed light on the pathophysiologic mechanisms (eg, inflammatory mediators) involved in many atopic diseases that can underlie sleep disruptions as a consequence of the presence of nocturnal symptoms. Associations between nocturnal symptoms and sleep and poorer quality of life as a result of missed sleep have been demonstrated across studies. Patients with severe illness and poor control appear to bear the most burden in terms of sleep impairment. Sleep-disordered breathing is also more common in patients with allergic diseases. Upper and lower airway resistance can increase the risk for sleep-disordered breathing events. In patients with allergic rhinitis, nasal congestion is a risk factor for apnea and snoring. Finally, consistent and appropriate use of medications can minimize nocturnal asthma or allergic symptoms that might disrupt sleep. Despite these advances, there is much room for improvement in this area.

A summary of the sleep and allergic disease literature is reviewed, with methodological, conceptual, and clinical suggestions presented for future research.

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BACKGROUND: Asthma is a chronic inflammatory disease noteworthy for its vulnerability to stress and emotion-induced symptom intensification. The fact that psychological stress and mood and anxiety disorders appear to increase expression of asthma symptoms suggests that neural signaling between the brain and lung at least partially modulates the inflammatory response and lung function. However, the precise nature of the neural pathways implicated in modulating asthma symptoms is unknown. Moreover, the extent to which variations in neural signaling predict different phenotypes of disease expression has not been studied.

METHODS AND RESULTS: We used functional magnetic resonance imaging to measure neural signals in response to asthma-specific emotional cues, following allergen exposure, in asthmatics with a dual response to allergen challenge (significant inflammation), asthmatics with only an immediate response (minimal inflammation), and healthy controls. The anterior insular cortex was differentially activated by asthma-relevant cues, compared to general negative cues, during the development of the late phase of the dual response in asthmatics. Moreover, the degree of this differential activation predicted changes in airway inflammation.

CONCLUSIONS: These findings indicate that neurophenotypes for asthma may be identifiable by neural reactivity of brain circuits known to be involved in processing emotional information. Those with greater activation in the anterior insula, in response to asthma-relevant psychological stimuli, exhibit greater inflammatory signals in the lung and increased severity of disease and may reflect a subset of asthmatics most vulnerable to the development of psychopathology. This approach offers an entirely new target for potential therapeutic intervention in asthma.