Minna Lukkarinen

Prednisolone reduces recurrent wheezing after first rhinovirus wheeze: a 7-year follow-up.

To better understand the role of human rhinovirus‐associated wheeze as a risk factor for childhood recurrent wheezing, a cohort of young children experiencing their first wheezing episode was followed until school age.

Rhinovirus-induced first wheezing episode predicts atopic but not nonatopic asthma at school age

Background: Persistent childhood asthma is mainly atopy driven. However, limited data exist on the risk factors for childhood asthma phenotypes. Objective: We sought to identify risk factors at the first severe wheezing episode for current asthma 7 years later and separately for atopic and nonatopic asthma. Methods: One hundred twenty‐seven steroid‐naive children with the first severe wheezing episode (90% hospitalized/10% emergency department treated) were followed for 7 years. The primary outcome was current asthma at age 8 years, which was also analyzed separately as atopic and nonatopic asthma. Risk factors, including sensitization, viral cause, and other main asthma risk factors, were analyzed. Results: At study entry, median age was 11 months (interquartile range, 6‐16 months); 17% were sensitized, and 98% were virus positive. Current asthma (n = 37) at 8 years was divided into atopic (n = 19) and nonatopic (n = 18) asthma. The risk factors for current atopic asthma at study entry were sensitization (adjusted odds ratio [OR], 12; P < .001), eczema (adjusted OR, 4.8; P = .014), and wheezing with rhinovirus (adjusted OR, 5.0; P = .035). The risk factors for nonatopic asthma were the first severe respiratory syncytial virus/rhinovirus–negative wheezing episode (adjusted OR, 8.0; P = .001), first wheezing episode at age less than 12 months (adjusted OR, 7.3; P = .007), and parental smoking (adjusted OR, 3.8; P = .028). Conclusions: The data suggest diverse asthma phenotypes and mechanisms that can be predicted by using simple clinical markers at the time of the first severe wheezing episode. These findings are important for designing early intervention strategies for secondary prevention of asthma.

Sensitization at the first wheezing episode increases risk for long-term asthma therapy

mended that ASST be carried out in conjunction with the basophil histamine-release assay to demonstrate autoantibody specificity (6). The assay was negative in our patients, which could suggest a different possible cause of autoreactivity, although there were no other signs of chronic inflammatory or autoimmune disease. There have been no previous reports of IA with HI in a pediatric patient. Whether this is pure coincidence or the result of a common underlying pathogenetic mechanism remains to be seen. Histamine is a biogenic amine, affecting human organs and systems in multiple ways. Symptoms of excessive histamine in plasma manifest as acute pseudoallergic illness with skin rash, vomiting, diarrhea, abdominal pain, and/or respiratory distress. HI describes a state where catabolic capacity for endogenously released or exogenously administered histamine is insufficient, leading to histamine-mediated adverse reactions. People with low intestinal histamine inactivation or inhibition of this activity suffer from HI. This diagnosis is based on the careful recording of symptoms and the identification of intestinal or serum activities of DAO and histamine N-methyltransferase (HMT). It may be complemented by an analysis of DAO and HMT gene polymorphisms to identify a possible genetic predisposition. We measured DAO by enzyme immunoassay analysis in serum samples (10). For evaluation, we used the manufacturer’s recommended reference values, and all our patients had highly reduced activity of DAO <40 HDU/ml. The only effective therapy for HI is the avoidance of histamine-containing food, and our patients were advised to follow a histamine-free diet. Controlled trials demonstrating the efficacy of DAO substitution with fresh encapsulated enzymes are still lacking. It has been demonstrated that DAO activity increases in patients on a histamine-free diet, which could be a possible explanation for improvement and remission in case 1 and case 3, respectively. Symptomsandclassifications of IA in thepediatric population are the sameas those inadults, andadult treatment regimenshave been applied to children (2, 3). Two patients were considered to have generalized infrequent IA, and the third had generalized frequent IA (2, 3). Patients were instructed to carry epinephrine and were taught to self-administer it. We suggested prednisone therapy with antihistamine for the third patient, but the parents, fearing the side effects of corticosteroid, accepted only antihistamine daily. The girl has been in remission for 6 months. Idiopathic anaphylaxis has been classified and treated successfully, but the underlying mechanism of this disorder has yet to be revealed. The observation that IA is a steroidresponsive disorder indicates a possible autoimmune etiology. Pediatric IA can show up at any age; therefore, it is important to recognize it so that it may be appropriately treated. This potentially life-threatening syndrome can be successfully managed, and in the majority of patients with IA, the frequency of episodes often declines with age.

Prednisolone for the first rhinovirus-induced wheezing and 4-year asthma risk: a randomized trial

Previous findings show that corticosteroid treatment during the first acute wheezing episode may reduce recurrent wheezing in children with high rhinovirus genome load at 12‐month follow‐up. Longer‐term effects have not been investigated prospectively.

Physical exercise increases nasal patency in asthmatic and atopic preschool children.

Background Physical exercise causes a decrease in nasal mucosal congestion and hence an increase in nasal patency. This nasal response has been studied only in adults. A correlation between nasal obstruction and asthma or allergic rhinitis has been previously found. This study evaluates the influences of atopy and asthma on nasal patency and the changes in nasal patency induced by physical exercise in preschool children. Methods An 8-minute exercise challenge test was conducted in 31 children aged between 4.1 and 6.4 years: 13 children had asthma, 17 were atopic, and 13 had neither asthma nor atopy. Nasal patency was measured with acoustic rhinometry at baseline and 10 minutes after the exercise. Results At baseline, the total acoustic values were 17–25% larger in nonasthmatic children than in asthmatic children. Accordingly, the acoustic values in nonatopic children were 16–35% larger than in atopic children. After physical exercise, there was an overall increase in mean total nasal volume from 2.973 (SD = 0.647) to 3.405 cm3 (SD = 0.705), indicating an improvement of 15% in nasal volume (p = 0.025). The increase in nasal patency was similar in asthmatic and nonasthmatic children, as well as in atopic and nonatopic children. Conclusion A significant increase in total nasal volume after physical exercise was found in all preschool children. The minimal cross-sectional areas remained smaller in asthmatic and atopic children after exercise, indicating partly irreversible nasal mucosal congestion in these children.

Exercise simultaneously increases nasal patency and bronchial obstruction in asthmatic children.

We found that simultaneous post‐exercise increase in nasal patency and bronchial obstruction occurs only in children with atopic asthma, but not in sensitized children without asthma. In healthy children, the increase in nasal patency is accompanied by bronchial dilatation.

Toward Primary Prevention of Asthma: Role of Corticosteroids for the First Rhinovirus Wheeze

have indicated that correlations between inflammation and symptoms are weak or absent in patients with asthma (9, 10), suggesting these reflect different aspects of asthma. We speculate that common exposures, specifically viral airway infections, may transiently alter the relationship between inflammation and symptoms in children with asthma. We conclude that discordant phenotypes were common and often unstable in children with asthma. FENO-guided treatment was not more effective in children with discordant phenotypes. n

Irreversible airway obstruction due to innominate artery compression of the trachea.

A 12-year-old girl presented with occasional cough and minor exercise intolerance. Peak expiratory flow (PEF) follow-up suggested asthma and irreversible expiratory obstruction was demonstrated by spirometry. Treatment with inhaled corticosteroids alleviated the symptoms, but a slight obstruction in spirometry persisted (figure 1A). Three years later, a CT of the thorax was performed due to the unusual shape of the flow/volume curve. The innominate artery (figure 1B, white arrow) was detected to compress the trachea and cause a 30% reduction in tracheal diameter (figure 1C, black arrow). This finding was consistent with the characteristic change in the flow/volume curve: a sudden and temporary drop in expiratory flow immediately after PEF (figure 1A). Minor compression of the trachea did not cause the asthmatic symptoms but mislead physicians to treat irreversible obstruction as asthma. The asthma medication was discontinued and the girl remained symptom free.