Marzia Duse

Prevalence and risk factors for atopic disease in a population of preschool children in Rome: Challenges to early intervention

Background: Allergic diseases are complex identities determined by an interplay of genetic and environmental factors, resulting in the clinical manifestation of the disease. So far in Italy, updated data about the prevalence and risk factors of respiratory and allergic diseases in preschool children are not available. Methods: Children aged 3–5 years, attending four different nursery schools in an urban district of the city of Rome. A standardized questionnaire developed under the SIDRIA-2 protocol was administered to the parents of the children for the assessment of the potential risk factors and the outcomes. Results: A total of 494 children were enrolled in the study; 289 of them (60.3%) performed a skin prick test (SPT). In the 12 months preceding the interviews, 15% of children experienced at least one episode of wheezing, 5.5% of allergic rhinitis, 11% of children had a doctor diagnosis of asthma, 12% of children who underwent the SPT were positive to at least one of the tested allergens, being diagnosed as atopic. The univariate analysis for the health outcomes of the study shows that asthma was positively associated with daycare attendance, mother’s history of atopy, siblings’ history of atopy, recurrent siblings’ bronchitis, and dermatitis. Atopy was positively associated with mother’s history of atopy and dermatitis, whereas there is a borderline protective association with recurrent siblings’ bronchitis. Conclusions: This study represents a first comprehensive epidemiological evaluation of prevalence of respiratory and allergic diseases in children aged 3–5 years in the city of Rome and an updating of the evolution of allergic diseases.

Severe asthma is really uncommon

We describe the case of a 10-year-old girl with a history of severe persistent asthma and exercise-induced-asthma, controlled using an appropriate treatment with inhaled corticosteroid-long-acting beta-2 adrenergic agonists (ICS+LABA) and leukotriene receptor antagonists. She was healthy until the age of 8 years, when she presented two episodes of radiologically diagnosed pneumonia. After that, she began to present persistent cough, also nocturnal, stridor, dyspnea and respiratory distress and she was sent by pediatrician to our hospital. She performed a global spirometry which shows an obstructive and restrictive phenotype (FEV1: 75,3% and MEF50: 57,6%), without a significantly dilatation after inhaled salbutamol (400 mcg). She underwent to a systemic therapy with oral corticosteroid, with not benefit. She had no fever neither upper respiratory tract infections. We excluded gastro-esophageal reflux disease, cystic fibrosis, mycoplasma and chlamydia pneumonia. Cardiological examination was negative. During hospitalization, she spontaneously expectorated a thick fibrinous mucoid formation. A chest X-ray and a computed tomography (CT) scan showed atelectasis of both lung, widespread hyperlucency, and occlusion of the right main bronchus, compatible with a diagnosis of plastic bronchitis. Plastic bronchitis is a rare disease characterized by the formation of large gelatinous or rigid branching airway casts. The prevalence and etiology of plastic bronchitis are still unknown and the symptoms may also overlap with those of other diseases such as severe asthma, in the severe mucus plugging sometimes seen in allergic bronchopulmonary aspergillosis (ABPA) or in middle lobe syndrome. In the pathogenesis of the disease the inflammation is usually present and initiates cast formation. Treatment includes bronchodilators, inhaled and oral corticosteroids, mucolytics, airway clearance therapy and antibiotics. Other therapies can include inhaled heparin, urokinase, tissue plasminogen activator (TPA), dornase alfa and oral macrolide antibiotics as mucoregulatory therapy 2.

Influence of physical activity in asthmatic children

Methods We compared functional respiratory testing in 72 asthmatic children (mean age 11.4±2.6 years) and in 70 healthy subjects (mean age 12.5±2.5 years). Each group was divided in 2 subgroups using a physical activity level cut-off ( 3 hours spent for week), that way generating 4 study groups: asthmatic trained children, non asthmatic trained children, trained controls, non trained controls. We investigated type of preparticipation screening (noncompetitive or competitive) and functional characterizes. All subjects underwent a maximal treadmill exercise test, determining maximal oxygen uptake by indirect method, metabolic equivalents and exercise time, and performed spirometry pre and post exercise.

A surprising finding in an adolescent athlete affected by diffuse congenital cystic adenomatoid malformation (CCAM).

Data from large population registries suggest an incidence of congenital lung cysts in the range of 1 per 8300–35 000 live births (1). Congenital cystic adenomatoid malformation (CCAM) is a developmental, non-hereditary hamartomatous abnormality of the lung with adenomatoid cyst proliferation, firstly described in 1949 by Ch’in and Tang (2). It is believed to be the result of a bronchial atresia or maturation arrest in bronchopulmonary segments at/before the seventh gestational week, producing dysplastic lung growth beyond the atretic segments (3) and cystic distortion of the lung architecture. Most CCAMs are detected antenatally by ultrasound, presenting with respiratory distress in the neonatal period; infants with large lesions may have respiratory insufficiency. The malformation is usually unilateral and sublobar or lobar in size, but occasionally, it can be multilobar or even bilateral with no special predilection for any lobe (4, 5). Only 10% of primary diagnoses are made after the first year of life (5, 6), and rarely the presentation of CCAM is delayed until adulthood. Computed tomography (CT) scan is the investigation of choice with a good accuracy (66.7%) in characterising the various types of CCAM. CCAMs symptoms include frequent chest infections, bronchiectasis, lung abscess, haemoptysis, pneumothorax, air embolism, haemothorax, pyopneumothorax, steroid resistant bronchospasm or rarely bronchioloalveolar carcinoma, blastomas and rhabdomyosarcoma. The treatment is usually surgical, involving complete resection of the affected parenchyma. This prevents recurrent infections and development of neoplastic transformation. The CCAMs Stocker classification (7) was based on the clinical and histological features and originally divided into three types (1, 2 and 3). CCAMs Type 1 account for 70% of cases, and are characterised by single or multiple cysts more than 3 cm in diameter; the cyst wall contains elastic tissue, smooth muscle and fibrovascular connective tissue. CCAMs Type 2 (approximately the 20–25% of cases) are characterised by multiple small cysts, 2 cm in diameter (rarely larger); mucous cells and cartilage are absent, and striated muscle fibres may occasionally be seen. CCAMs Type 3 are rare (approximately the 8% of cases) and characterised by cysts not larger than 1.5 cm in diameter; mucous cells, cartilage and striated muscle fibres are absent. Usually, CCAMs Type 3 involve a lobe of lung and have a spongy-like appearance, constructed by bulk gland-like structures. Types 0 and 4 CCAMs were subsequently proposed (8), and the term congenital pulmonary airway malformation was proposed instead of CCAM. CCAMs Type 0 account <2% of cases, and are the less frequently observed among CCAM lesions and incompatible with life. Clinically, infants present cyanosis and severe respiratory distress at birth and survive only few hours unless treated with extracorporeal membrane oxygenation; they are unable to survive without this support. Microscopically, the tissue consists entirely of bronchial-like structures with muscle, glands, numerous cartilage plates and small cysts (<0.5 mm); more distal components, such as proximal bronchioles, are only rarely seen. CCAMs Type 4 account between 10% and 15% of cases, and consist of multiple large cysts (up to 15 cm) lined only with Type 1 and 2 alveolar cells. Children with this malformation vary in age at presentation from 1 day to 4 years and display various degrees of respiratory distress. It may involve more than one lobe in 20% of cases, and resection is usually curative even with bilateral involvement (9). We report a case of diffuse, bilateral CCAM associated with allergic bronchial asthma, discovered in an adolescent with few symptoms. A 13-year-old Caucasian boy, sensitised to dust mites and grass pollen with a clinical history of respiratory distress at birth, was resolved in the second day of life with oxygen therapy. In the first year of life, he showed recurrent episodes of cough and bronchospasm treated with bronchodilators. In the subsequent years, he was healthy and reported wheezing only after intense physical exercise; he practiced daily martial arts. The boy came to our department for the Pre-Competition Medical Assessment when he was 12 years old. Pulmonary function tests showed severe airflow obstruction [forced expiratory volume in 1 s (FEV1) 49.0%, FEV1/ forced vital capacity 70.0% and maximum expiratory flow 50 24.7% of the predicted values] reversible after inhalation of 400 mcg of salbutamol (FEV1 + 16.3%). For this reason, he started a daily antiasthmatic therapy The Clinical Respiratory Journal