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1.
Pulm Med ; 2023: 1532443, 2023.
Article En | MEDLINE | ID: mdl-36760693

Aim: It is known that children and adolescents with obesity are more prone to obstructive sleep apnea syndrome (OSAS) and that their lung function may show some disturbance. Literature is scarce about potential associations; therefore, we aimed to study the relationship between OSAS, lung function, and adiposity in a population of children suspected of OSAS. Material and Methods. We performed home respiratory polygraphy and spirometry in all subjects. The relationships between body mass index z-score (zBMI), polygraphy, and spirometry data were analyzed. Results: We recruited 81 subjects aged between 5 and 16 years, 63% being obese. 43.2% of subjects were diagnosed with OSAS (32.1% mild, 4.9% moderate, and 6.2% severe). We found no correlation between respiratory polygraphy and the zBMI. The mean spirometric value FEV1, FVC, and FEV1/FVC ratio z's were normal in all subjects, whereas FVC z's and FEV1/FVC ratio z's were significantly positively related for obesity and negatively for normal weight (p < 0.05). FEV1 z's was inversely correlated to the percentage of analyzed time passed below 90% of SpO2 (r = -0.224, p = 0.044). All subjects with FEV1 (n = 8) and/or FVC (n = 9) z's below the lower limit for normal (LLN) had an AHI ≥ 1 (FEV1: p = 0.001; FVC: p < 0.001), especially subjects with normal weight (FEV1: p = 0.003; FVC: p = 0.010). Conclusion: When comparing normal-weight children and adolescents with obesity, the prevalence of OSAS but not spirometric values was strongly related to BMI z-score, probably because obesity engenders advanced puberty and an accelerated growth spurt. FEV1 was more frequently

Pediatric Obesity , Sleep Apnea, Obstructive , Adolescent , Humans , Child , Child, Preschool , Forced Expiratory Volume , Spirometry , Body Mass Index , Sleep Apnea, Obstructive/diagnosis , Vital Capacity
2.
Chest ; 158(6): e295-e298, 2020 12.
Article En | MEDLINE | ID: mdl-33280772

CASE PRESENTATION: A 13-year-old male was referred after incidental finding of cardiomegaly on chest radiograph and signs of pulmonary hypertension on subsequent cardiology consult. He was diagnosed with idiopathic pulmonary hypertension, and came to our center for a second opinion. He was born from consanguineous parents. He reported to be asymptomatic in his daily life. He was not on medications. Family history was not contributive.


Portal Vein/abnormalities , Pulmonary Arterial Hypertension/etiology , Vascular Malformations/complications , Vena Cava, Inferior/abnormalities , Adolescent , Angiography , Diagnosis, Differential , Humans , Male , Portal Vein/diagnostic imaging , Pulmonary Arterial Hypertension/diagnosis , Tomography, X-Ray Computed , Vascular Malformations/diagnosis , Vena Cava, Inferior/diagnostic imaging
5.
Eur J Pediatr ; 171(1): 159-66, 2012 Jan.
Article En | MEDLINE | ID: mdl-21674140

UNLABELLED: The true burden of influenza in children is difficult to assess and is probably underestimated as clinical signs are usually nonspecific, and formal viral identification is rarely searched. In this study, we compare the clinical features of infections related to the new H1N1/09 influenza virus with infections due to other respiratory viruses in children consulting in a tertiary care pediatric hospital in Geneva. Between October 1, 2009 and February 10, 2010, 109 patients were recruited, with a median of age of 7 years (range 0.1-18). There were 75 H1N1/09-positive patients (69%), and 32 (43%) had identified risk factors such as asthma or a history of wheezing. Fever (87%), cough (92%), and rhinitis (85%) were the most frequent reported presenting symptoms in both patient groups. H1N1/09-positive patients were significantly older (median of 8.2 vs. 4.6 years) and were more likely to have risk factors (43% vs. 24%) and myalgias (41% vs. 20%). H1N1/09-negative patients had more wheezing episodes (29% vs. 9%), higher rates of dyspnea (28% vs. 20%) and of hospital admissions (35% vs. 16%). CONCLUSION: Clinical signs cannot reliably differentiate H1N1/09-positive and H1N1/09-negative patients, although we found a higher proportion of myalgias in H1N1/09-positive patients. Severity of disease was lower in H1N1/09-positive than in H1N1/09-negative patients, mostly because of a higher proportion of asthma/wheezing episodes among H1N1/09-negative patients.


Influenza A Virus, H1N1 Subtype/isolation & purification , Influenza, Human/virology , Adolescent , Antiviral Agents/therapeutic use , Asthma/complications , Case-Control Studies , Child , Child, Preschool , Diagnosis, Differential , Hospitalization , Humans , Infant , Influenza, Human/complications , Influenza, Human/diagnosis , Influenza, Human/drug therapy , Oseltamivir/therapeutic use , Prospective Studies , Respiratory Sounds/etiology , Risk Factors , Seizures, Febrile/etiology
6.
Am J Physiol Lung Cell Mol Physiol ; 299(3): L312-22, 2010 Sep.
Article En | MEDLINE | ID: mdl-20382751

Bcl-2 is an anti-apoptotic molecule preventing oxidative stress damage and cell death. We have previously shown that Bcl-2 is able to prevent hyperoxia-induced cell death when overexpressed in a murine fibrosarcoma cell line L929. We hypothesized that its specific overexpression in pulmonary epithelial type II cells could prevent hyperoxia-induced lung injury by protecting the epithelial side of the alveolo-capillary barrier. In the present work, we first showed that in vitro Bcl-2 can rescue murine pulmonary epithelial cells (MLE12) from oxygen-induced cell apoptosis, as shown by analysis of LDH release, annexin V/propidium staining, and caspase-3 activity. We then generated transgenic mice overexpressing specifically Bcl-2 in lung epithelial type II cells under surfactant protein C (SP-C) promoter (Tg-Bcl-2) and exposed them to hyperoxia. Bcl-2 did not hinder hyperoxia-induced mitochondria and DNA oxidative damage of type II cell in vivo. Accordingly, lung damage was identical in both Tg-Bcl-2 and littermate mice strains, as measured by lung weight, bronchoalveolar lavage, and protein content. Nevertheless, we observed a significant lower number of TUNEL-positive cells in type II cells isolated from Tg-Bcl-2 mice exposed to hyperoxia compared with cells isolated from littermate mice. In summary, these results show that although Bcl-2 overexpression is able to prevent hyperoxia-induced cell death at single cell level in vitro and ex vivo, it is not sufficient to prevent cell death of parenchymal cells and to protect the lung from acute damage in mice.


Acute Lung Injury/prevention & control , Epithelial Cells/metabolism , Hyperoxia/complications , Hyperoxia/metabolism , Lung/metabolism , Proto-Oncogene Proteins c-bcl-2/metabolism , Acute Lung Injury/etiology , Animals , Apoptosis , Cell Death , Cells, Cultured , DNA Damage , Epithelial Cells/classification , Hyperoxia/pathology , Hyperoxia/physiopathology , Lung/physiopathology , Mice , Mice, Inbred C57BL , Mice, Transgenic , Mitochondria/pathology , Oxidative Stress , Proto-Oncogene Proteins c-bcl-2/genetics , Up-Regulation
7.
Ann Thorac Surg ; 78(4): 1446-8, 2004 Oct.
Article En | MEDLINE | ID: mdl-15464513

A 9-month-old girl presented with life-threatening acute respiratory failure 1 week after the surgical correction of a double aortic arch, which was due to a severe bulging of the pars membranacea into the lumen of the trachea that produced a complete obstruction of the lower trachea. Under cardiopulmonary bypass, a Y-shaped posterior biodegradable splint was placed behind the trachea and sutured to the posterior trachea, and a simultaneous right aortic arch aortopexy was performed. Thereafter, the child recovered normal respiratory function. Follow-up bronchoscopy showed a posterior dip at the splint level and an asymptomatic persistent posterior compression of the right main bronchus.


Absorbable Implants , Respiratory Insufficiency/surgery , Splints , Tracheal Diseases/surgery , Airway Obstruction/etiology , Aorta, Thoracic/abnormalities , Aorta, Thoracic/surgery , Cardiopulmonary Bypass , Child , Equipment Design , Female , Humans , Postoperative Complications/etiology , Postoperative Complications/surgery , Reoperation , Respiratory Insufficiency/etiology , Tracheal Diseases/complications
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