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[Chest computed tomography in children: Indications, efficiency and effective dose.]

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New multidetector row computed tomography (CT) has made the imaging of younger children more feasible and extending CT indications to a wide range of pediatric respiratory diseases in the last few years. However, CT is a source of radiation exposure. The aim of this study was to evaluate the main indications and the contribution of chest CT in pediatric pulmonology as well as induced radiation.

METHODS: This was an observational, prospective study. Children whose chest CTs were analyzed during multidisciplinary meetings (radiologist, pulmonary pediatrician) were included from November 2009 to April 2010. We collected demographic data, CT results, contribution of CT to diagnosis and management, and radiation doses (dose-length product [DLP] and effective dose). Radiation doses were compared according to the CT scans (Lille University Hospital with 128-slice dual-source CT or Lille University Hospital single-source 64-slice CT, or CT performed outside the university hospital).

RESULTS: One hundred thirty-five patients were included. The mean age was 6.4 years old. The main indications were analysis of bronchial disease (44%), infectious disease (16%), interstitial disease (14%), or a malformation (9%). The aim of CT was diagnosis (61%) or follow-up of previous lung diseases (39%). Diagnosis chest-CT directly contributed to diagnosis in 48% of cases and to treatment in 24%. Follow-up CT contributed to diagnosis in 38% and treatment in 19% of cases. DLP and effective doses were significantly lower for CT performed in the university hospital, especially with the 128-slice CT compared to the others (P<0.001). The effective doses were: 128-slice CT, 0.61mSv±0.32; 64-slice CT, 1.24mSv±0.97; outside university hospital, 2.56mSv±1.98.

CONCLUSION: This study confirms the role played by chest CT in children, which contributes to diagnosis and management of lung diseases. The main concern of CT application, especially in children, is the radiation burden. Children are more susceptible to the effects of radiation than adults and have a longer life expectancy to develop complications. Both radiologists and pediatricians should be aware of a potential risk and have to conjugate their efforts in reducing this risk. The wide range of radiation doses in this study for the same CT procedures underlines the extensive efforts still needed to limit radiation exposure in children.

Genetic predictors associated with improvement of asthma symptoms in response to inhaled corticosteroids.

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To date, genome-wide association studies (GWASs) of inhaled corticosteroid (ICS) response in asthmatic patients have focused primarily on lung function and exacerbations.

OBJECTIVE: We hypothesized that GWAS analysis could identify novel genetic markers predicting a symptomatic response to ICSs.

METHODS: We analyzed differences in asthma symptoms in response to ICSs in 124 white children from the Childhood Asthma Management Program (CAMP) trial using scores from diary cards. Of the 440,862 single nucleotide polymorphisms (SNPs) analyzed, the top 100 ranked SNPs were pursued for replication initially in subjects from the pediatric Childhood Asthma Research and Education trials (77 white children) and then in subjects from the adult Asthma Clinical Research Network (110 white adults) and Leukotriene Modifier or Corticosteroid or Corticosteroid-Salmeterol trials (110 white adults).

RESULTS: The lowest P value for GWAS analysis in the CAMP trial was 8.94 × 10(-8) (rs2388639). Of the 60 SNPs available in the Childhood Asthma Research and Education Network trials, rs1558726 (combined P = 1.02 × 10(-5)), rs2388639 (combined P = 8.56 × 10(-9)), and rs10044254 (combined P = 9.16 × 10(-8)) independently replicated. However, these 3 SNPs were not additionally replicated in the adult asthmatic patients of the remaining trials. rs10044254 lies in the intronic region of F-box and leucine-rich repeat protein 7 (FBXL7) and is associated with decreased expression in immortalized B cells derived from CAMP participants.

CONCLUSIONS: We have identified a novel SNP, rs10044254, associated with both decreased expression of FBXL7 and improved symptomatic response to ICSs in 2 independent pediatric cohorts. Our results suggest that there might be a specific genetic mechanism regulating symptomatic response to ICSs in children that does not carry over to adults.

Diffuse granulomatous lung disease: combined pathological-HRCT approach.

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Granulomatous lung diseases include a large number of conditions among granulomas are the pathological hallmark. Some of these conditions are frequently encountered in clinical practice.

Differentiating infectious from noninfectious forms is a priority for the different specialists approaching these diseases, given the different implications for management and treatment. However, differential diagnosis is not always straightforward and the diagnosis of granulomatous disease, considering separately the clinical, radiological and pathological aspects, is at times incomplete or uncertain and requires multidisciplinary assessment.

In this paper, we propose a combined HRCT-pathological approach to assess both the topographical and morphological features of the lesions. Based on topography, we can distinguish between granulomatous lesions distributed along the lymphatic vessels, with random distribution or centred on the airways. The prototype of the disease with lymphatic granulomas is sarcoidosis. In contrast, diseases exhibiting a random distribution of granulomas are those with haematogenous spread, the most typical of which is miliary tuberculosis (TB). Many diseases have distribution along the airways including hypersensitivity pneumonia and granulomatous bronchiolitis (including infections with bronchial spread, especially mycobacteriosis).

The anatomical approach is completed by the assessment of the morphological aspects of the lesions and associated signs, reflecting both the possible mechanisms of spread and the different types of pathological and/or reparative tissue related to the disease.

Cigarette smoke toxins deposited on surfaces: implications for human health.

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Cigarette smoking remains a significant health threat for smokers and nonsmokers alike. Secondhand smoke (SHS) is intrinsically more toxic than directly inhaled smoke.

Recently, a new threat has been discovered - Thirdhand smoke (THS) - the accumulation of SHS on surfaces that ages with time, becoming progressively more toxic. THS is a potential health threat to children, spouses of smokers and workers in environments where smoking is or has been allowed.

The goal of this study is to investigate the effects of THS on liver, lung, skin healing, and behavior, using an animal model exposed to THS under conditions that mimic exposure of humans.

THS-exposed mice show alterations in multiple organ systems and excrete levels of NNAL (a tobacco-specific carcinogen biomarker) similar to those found in children exposed to SHS (and consequently to THS). In liver, THS leads to increased lipid levels and non-alcoholic fatty liver disease, a precursor to cirrhosis and cancer and a potential contributor to cardiovascular disease. In lung, THS stimulates excess collagen production and high levels of inflammatory cytokines, suggesting propensity for fibrosis with implications for inflammation-induced diseases such as chronic obstructive pulmonary disease and asthma. In wounded skin, healing in THS-exposed mice has many characteristics of the poor healing of surgical incisions observed in human smokers. Lastly, behavioral tests show that THS-exposed mice become hyperactive.

The latter data, combined with emerging associated behavioral problems in children exposed to SHS/THS, suggest that, with prolonged exposure, they may be at significant risk for developing more severe neurological disorders.

These results provide a basis for studies on the toxic effects of THS in humans and inform potential regulatory policies to prevent involuntary exposure to THS.

What role do viruses play in nosocomial pneumonia?

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PURPOSE OF THE REVIEW: Viruses are an increasingly recognized cause of community-acquired pneumonia (CAP), but their exact role in nosocomial pneumonia is still debated. This review focuses on the role of viruses as a cause of nosocomial pneumonia.

RECENT FINDINGS: Respiratory viruses may be responsible for healthcare-associated pneumonia, because affected patients and those with CAP have the same risk factors for viral disease. In mechanically ventilated patients, viruses belonging to the Herpesviridae family, namely herpes simplex virus (HSV) and cytomegalovirus, can be reactivated and cause bronchopneumonitis or ventilator-associated pneumonia, respectively. Recent results confirmed the high rate of HSV reactivation in the distal airways of mechanically ventilated patients, and that patients with high virus loads (>10 copies/ml of bronchoalveolar lavage fluid) have poorer outcomes than those with low or no virus load. However, the responsibility of mimivirus, initially described as a possible cause of pneumonia, was not confirmed for nosocomial pneumonia.

SUMMARY: Respiratory viruses are mainly responsible for CAP, but they may also cause healthcare-associated pneumonia. HSV bronchopneumonitis and cytomegalovirus pneumonia are not rare diseases, and patients with Herpesviridae lung infections have worse prognoses than those without. Whether or not those Herpesviridae infections are responsible for true morbidity or morbidity remains to be determined.

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